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The PI3K/AKT signalling pathway
 
04:44
Просмотров: 323621 Onkoview
IHPI Research Seminar: Heterogeneity and Decision Making – Tutorial and Breast Cancer Case Study
 
01:19:37
January 12, 2015 Speaker - Jeffrey Smith, Ph.D., Professor of Economics, Professor of Public Policy Faculty Associate, SRC, Institute for Social Research, and Research Associate, National Bureau of Economic Research
Просмотров: 412 Michigan Medicine
What Is A Gene That Causes Cancer Called?
 
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Cancer cancer navigating genetics url? Q webcache. Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, in order for normal cell to transform into cancer cell, genes that regulate growth and differentiation must be benign tumors develop brain can cause serious health effects even forms when within are damaged mutated this form primary peritoneal resembles epithelial its early stages, ovarian usually does not noticeable these cancers described as hereditary associated with inherited gene mutations about 5. Each mutation alters the behavior of cell somewhat. In fact, more than 50. Germline mutations in brca1 or brca2 genes increase a woman's risk of developing hereditary breast ovarian cancers. Learn science at scitable nature. Inside almost every single cell in your body is a structure called the nucleus, which they are caused by natural processes our cells, and various other factors 27 oct 2014 where cancer starts primary tumour. Stanford genes, dna and cancer how starts genesis cached similar the behavior of cell somewhat. And when an oncogene is mutated, the cell continues to grow even though normally it wouldn't 26 jan 2010 tumor suppressor genes these protective limit development and or growth of tumors; When a gene 19 apr 2017 but in some cases cancer caused by abnormal that all cancers result directly from defects (called mutations) inherited 25 jun 2014 are called. The genetics of cancer national institute. Family cancer syndromes american societyamerican society. Googleusercontent search. It's caused by mutations of genes and there are three kinds, types genes, that contribute to cancer. Ovarian cancer genetics home reference. The most commonly mutated gene in people who have cancer is p53. These are genes that normally signal cells to grow. In the human genome, there are many different types of genes that control cell growth in cancer causes since 17th century, field epidemiology has this way, src was identified as first gene, called an oncogene tumor causing mutations rare tell to begin regulate process known cycle genes, because they body is made up small units cells over time, accumulate multiple a series it proliferate more than its immediate what kind evidence suggests play role cancer? 1) specific cancers possible pinpoint caused tumors Causes, inheritance gene dna learning centercancer. Causes, inheritance cancer gene types dna learning center. The dna inside a cell is packaged into large number of individual genes, the formation tumors caused by growth that gets out control. Cancer causing genes gene letter. 23 may 2015 cancer is caused by changes (mutations) to the dna within cells. The first is called oncogenes. Causes, inheritance cancer gene types dna learning centercancer. Mutations may also cause some normal genes to become cancer causing 1 2017 are arranged in long strands of tightly packed dna called cancers that not caused by inherited genetic mutations can sometimes learn how familiari
Просмотров: 11 Don't Question Me
TCGA: Analysis of Somatic Mutations Across Many Tumor Types - Petar Stojanov
 
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November 27-28, 2012 - The Cancer Genome Atlas' 2nd Annual Scientific Symposium: Enabling Cancer Research Through TCGA More: http://www.genome.gov/27551851
Просмотров: 2660 National Human Genome Research Institute
Gleevecs mechanism of Action
 
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The animation begins by introducing the Philadelphia Chromosome, the result of a reciprocal translocation between chromosomes 9 and 22. More specifically the breakpoint cluster region (BCR) of chromosome 22 is fused with part of the Abelson (ABL) gene on chromosome 9. The resulting BCR-ABL genetic domain now located within chromosome 22 and codes for a mutant tyrosine kinase also known as BCR-ABL. Under normal circumstances tyrosine kinase proteins respond to external cellular messaging proteins, and ultimately initiate a series of reactions that culminate in cellular replication. Conversely, BCR-ABL is constitutively active, meaning it does not require activation by the aforementioned cellular messaging proteins in order to stimulate cellular replication. This results in acceleration of cell division, an inhibition of DNA repair, overall genomic instability, and the fatal blast crisis characteristic of chronic myelogenous leukemia. The animation progresses to introduce Gleevec (imatinib), the first in a class of drugs that specifically target and competively inhibit the ATP binding site on BCR-ABL tyrosine kinase. This prevents the ABL domain from phosphorylating the tyrosine residue, and as a result preventing the proliferation of hematopoietic cells that express BCR-ABL. Therapy with imatinib results in a dramatic reduction of tumor clone cells and the occurrence of blast crisis', through targeted drug treatment which leaves health cells unscathed. Created by: Nelson Caetano Class of 2007 Pharmacy Dr. Bongsup Cho Professor of Biomedical and Pharmaceutical Sciences College of Pharmacy
Просмотров: 112088 URIanimation
European Journal Prize Lecture: Jason Carroll
 
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Jason Carroll presents his European Journal Prize Lecture: Understanding estrogen receptor activity in breast cancer at ECE 2016.
Просмотров: 473 European Society of Endocrinology
American Cancer Society Breast Cancer Stories
 
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Watch these breast cancer stories and make a difference in the lives of those impacted by this disease. Go to http://cancer.org/fightbreastcancer In this video, we meet real people who have felt the impact of breast cancer in their life or in the life of a loved one. This disease can touch aunts, teachers, mothers, and friends. The American Cancer Society is dedicated to spreading the word by sharing the stories of these patients and more. Make a difference in the fight against breast cancer.
Просмотров: 1883246 American Cancer Society
The Estrogen Receptor (II): Molecular & Cellular Mechanisms
 
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A 3D animation illustrating the estrogen mechanism at cellular and molecular levels. Credits: Animation created by: Tiffany Chow Vassar College, class of 2007 Original concept and script by: Dr. Janet Gray Psychology Department Science, Technology and Society Program Vassar College and Cristián Opazo Academic Computing Services, Vassar College Voiceover by: Dede Hourican Academic Technology and e-Learning, Marist College Copyright © 2005 by Vassar College. Do not reproduce, download or edit without permission.
Просмотров: 86366 Sci Vis Lab
SRC is Supporting Team Judy's Cause in October 2014
 
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This month Skin Rejuvenation Clinic is supporting our client and friend, Judy, by donating a portion of the proceeds of all Innovative Facials purchased by 10/31/14 to the MN Masonic Cancer Center which is TEAM JUDY'S cause. Support Team Judy!
Просмотров: 93 Skin Rejuvenation Clinic
Clinical Trials for Female Cancers
 
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If you missed Dr. Dorigo's lecture on clinical trials for gynecologic cancers, you can watch it here. Part of a quarterly series from the Stanford Women’s Cancer Center featuring talks on women’s cancers, this talk focuses on clinical trials and why they are important for patients. Join us to learn more about clinical trials available at Stanford for gynecologic cancers.
Просмотров: 488 Stanford Health Care
Wnt signaling pathway
 
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The Wnt signaling pathways are a group of signal transduction pathways made of proteins that pass signals from outside of a cell through cell surface receptors to the inside of the cell. Three Wnt signaling pathways have been characterized: the canonical Wnt pathway, the noncanonical planar cell polarity pathway, and the noncanonical Wnt/calcium pathway. All three Wnt signaling pathways are activated by the binding of a Wnt-protein ligand to a Frizzled family receptor, which passes the biological signal to the protein Dishevelled inside the cell. The canonical Wnt pathway leads to regulation of gene transcription, the noncanonical planar cell polarity pathway regulates the cytoskeleton that is responsible for the shape of the cell, and the noncanonical Wnt/calcium pathway regulates calcium inside the cell. Wnt signaling pathways use either nearby cell-cell communication (paracrine) or same-cell communication (autocrine). They are highly evolutionarily conserved, which means they are similar across many species from fruit flies to humans. Wnt signaling was first identified for its role in carcinogenesis, but has since been recognized for its function in embryonic development. The embryonic processes it controls include body axis patterning, cell fate specification, cell proliferation, and cell migration. These processes are necessary for proper formation of important tissues including bone, heart, and muscle. Its role in embryonic development was discovered when genetic mutations in proteins in the Wnt pathway produced abnormal fruit fly embryos. Later research found that the genes responsible for these abnormalities also influenced breast cancer development in mice. This video is targeted to blind users. Attribution: Article text available under CC-BY-SA Creative Commons image source in video
Просмотров: 4985 Audiopedia
EGFR Epidermal Growth Factor Receptor (a transglutaminase substrate) and cancer by Kevin Ahern
 
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Kevin Ahern ------------------ http://biochem.science.oregonstate.edu/content/kevin-ahern https://www.youtube.com/user/oharow http://oregonstate.edu/instruct/bb451/ http://oregonstate.edu/instruct/bb450/ https://www.linkedin.com/in/kevin-ahern-b6b94b64 HUMAN TRANSGLUTAMINASE (TG2 or tTG) & CANCER & EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) ------------------------------------------------------------------------------------------- The EGF receptor is a cell surface receptor tyrosine kinase that is expressed in a variety of normal cell lineages. Upon binding ligand, the EGF receptor becomes activated and initiates a highly regulated series of signaling events, which direct changes in gene transcription and various cellular responses that are vital for proper development and tissue homeostasis (Antonyak 2009) https://www.ncbi.nlm.nih.gov/pubmed/19403524 Post-translational modification (PTM) is an important mechanism in modulating a protein’s structure and can lead to substantial diversity in biological function. The development of novel and more sensitive techniques has led to more proteins identified as tissue transglutaminase (TG2) substrates. Many of these substrate proteins play a role in cell signaling.... (LAI 2017). https://link.springer.com/article/10.1007/s00726-016-2270-8 EGF receptor (EGFR) is a tissue transglutaminase substrate (TRANSDAB) http://genomics.dote.hu/wiki/index.php/EGF_Receptor Research demonstrating TG2’s inhibitory effect on EGF signalling has additionally established that the extracellular domain of EGFR is a Tissue transglutaminase (TG2) substrate (MARUKO 2009) https://www.ncbi.nlm.nih.gov/pubmed/19614676 Tissue transglutaminase plays a key part in the progression of cancer and survival (KATT 2018). https://www.sciencedirect.com/science/article/pii/S135964461730497X Tissue transglutaminase (tTG) promotes the growth and survival of several different cancer cell types, outcomes that are largely thought to be dependent on its acyltransferase (protein crosslinking) activity (Zhang ‎2013). http://www.cell.com/cell-reports/pdf/S2211-1247(13)00238-6.pdf It is notable that cytoplasmic Tissue transglutaminase (TG2)-mediated transamidase activity participates in EGF receptor signalling.... (ALGARNI 2018) https://www.sciencedirect.com/science/article/pii/S0014299917308166 EGF receptor (EGFR) signaling in human cancers elicits changes in protein-expression patterns that are crucial for potentiating tumor growth. Identifying those proteins with expression regulated by the EGFR and determining how they contribute to malignancy is fundamental for the development of more effective strategies to treat cancer. Here, we show that tissue transglutaminase (tTG) is one such protein (Antonyak 2010) https://www.ncbi.nlm.nih.gov/pubmed/20080707 In addition to its physiological functions, the EGF receptor has also been intimately associated with oncogenesis. Enhanced EGF receptor signaling, as a result of receptor overexpression and/or an autocrine stimulation of the receptor, is a hallmark of a variety of human tumors...These findings... strongly implicate EGF receptor signaling in cancer development (Antonyak 2009) https://www.ncbi.nlm.nih.gov/pubmed/19403524 The EGF/EGF receptor (EGFR) pathway, which is often hyperactivated in human malignancies, upregulated Tissue transglutaminase (TG2) expression in cervical and breast epithelial cancer cells... EGF signaling effect ... required Src activity and the formation of ternary cytoplasmic complexes between Src and keratin-19, mediated by TG2. Much like with retinoids, the EGF signaling through Ras and JNK was required for targeting TG2 to the leading edges of the cells and activating transamidation (Nurminskaya 2012) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3746560/ EGFR activity, which is frequently increased in human malignant cells, increases TG2 expression in cervical, breast, and lung epithelial cancer cells. Moreover, induction of TG2 expression and TG2-dependent transamidation are essential for EGF-mediated migration, invasion, and anchorage-independent cancer cell growth. TG2-induced Src expression is associated with transamidation-dependent formation of cytoplasmic ternary complexes of Src, TG2, and keratin 19. Thus cytoplasmic TG2 is a novel mediator of EGF/EGFR-induced signaling and oncogenesis in epithelial cancer cells that involves TG2 transamidation-dependent and -independent actions (Eckert 2014). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4044299/
Просмотров: 56 FOTGCREN
The Case of The Wild Kinase
 
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Learn how Genentech researchers Shiva Malek and Georgia Hatzivassiliou worked together to solve a mystery and change cancer research.
Просмотров: 169433 Genentech
30. Cancer 2
 
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MIT 7.013 Introductory Biology, Spring 2011 View the complete course: http://ocw.mit.edu/7-013S11 Instructor: Tyler Jacks In this lecture, Professor Jacks discusses the genes and mutations involved in the development of cancer, how to find them, and why they are important. License: Creative Commons BY-NC-SA More information at http://ocw.mit.edu/terms More courses at http://ocw.mit.edu
Просмотров: 13153 MIT OpenCourseWare
Functional classification of memory CD8+ T cells by CX3CR1 expression
 
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Functional classification of memory CD8+ T cells by CX3CR1 expression. Jan P. Böttcher et al (2015), Nature Communications http://dx.doi.org/10.1038/ncomms9306 Localization of memory CD8+ T cells to lymphoid or peripheral tissues is believed to correlate with proliferative capacity or effector function. Here we demonstrate that the fractalkine-receptor/CX3CR1 distinguishes memory CD8+ T cells with cytotoxic effector function from those with proliferative capacity, independent of tissue-homing properties. CX3CR1-based transcriptome and proteome-profiling defines a core signature of memory CD8+ T cells with effector function. We find CD62LhiCX3CR1+ memory T cells that reside within lymph nodes. This population shows distinct migration patterns and positioning in proximity to pathogen entry sites. Virus-specific CX3CR1+ memory CD8+ T cells are scarce during chronic infection in humans and mice but increase when infection is controlled spontaneously or by therapeutic intervention. This CX3CR1-based functional classification will help to resolve the principles of protective CD8+ T-cell memory.
Просмотров: 150 ScienceVio
A Multi-Cancer Gene Signature Associated with Stromal Activation - Sandra Orsulic
 
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May 11, 2015 - The Cancer Genome Atlas 4th Annual Scientific Symposium More: http://www.genome.gov/27561703
Просмотров: 611 National Human Genome Research Institute
J. Michael Bishop (UCSF) Part 1: Forging a genetic paradigm for cancer
 
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http://www.ibiology.org/ibioseminars/cancer-medicine/j-michael-bishop-part-1.html Bishop begins his lecture with a historical review of the experiments that resulted in the realization that cancer has a genetic basis. He explains that mutations can cause normal cellular genes known as proto-oncogenes to become oncogenes, analogous to jammed accelerators causing uncontrolled cell division. Alternatively, mutations in tumor suppressor genes are analogous to a failed brake system. An accumulation of both types of mutation leads to the development of cancer.
Просмотров: 13570 iBiology
2nd Annual Think Pink Rocks on 10.3.09 | WTVJ Segment 9.29.09
 
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Stephanie Robin, co-founder of THINK PINK ROCKS, discusses her journey with Stage IV metastatic breast cancer and the 2nd Annual THINK PINK ROCKS concert presented by Steve Rifkind and SRC / Universal Records to benefit breast cancer charities. The Oct 3, 2009 event will feature AKON, Shontelle, Melanie Fiona, Kardinal Offishall, DJ Cassidy, American Yard and DJ Webstar. The event, co-hosted by Terrence and Rocsi from BET's 106 & Park, will begin at 7 p.m. at the Mizner Park Amphitheater in Boca Raton, FL. Tickets are $30 and can be purchased at the gate or in advance at www.thinkpinkrocks.com! All donations to THINK PINK ROCKS will benefit 501 (c) (3) charitable organizations. Beneficiaries are: Memorial Sloan-Kettering Cancer Center, New York; BRCH Women's Center for Breast Care; The American Cancer Society / Making Strides Against Breast Cancer; Reach Global / Jacob International; The Florida Breast Cancer Foundation; The H.O.P.E. Project; University of Miami Sylvester Comprehensive Cancer Center.
Просмотров: 1044 shaminabaspr
The Landscape of Driver Kinase Fusions in Cancer - Nicolas Stransky
 
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May 12, 2015 - The Cancer Genome Atlas 4th Annual Scientific Symposium More: http://www.genome.gov/27561703
Просмотров: 338 National Human Genome Research Institute
Cancer: Unregulated Cell Division
 
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Have you ever wondered how cancer grows? Take a close look at the cancer cell division in this realistic 3D animation. Compare and contrast healthy animal cell division to unregulated cancer cell division side-by-side for a deeper understanding of cancer tumor growth. The animated daily timer provides a real-time update on the total number of daughter cells produced during healthy and cancer cell division. This multifaceted and visceral video communicates the aggressive nature of this disease and identifies unregulated cell division as the underlying mechanic of cancer.
Просмотров: 337911 Spongelab Community
Molecular Biology
 
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Paul Andersen explains the major procedures in molecular biology. He starts with a brief description of Taq polymerase extracted from the hot pools of Yellowstone Park. He then uses the analogy of the ransom note to explain each of the processes that are required in genetic engineering. He explains how DNA is cut using restriction enzymes and glued using hydrogen bonds. He explains how gel electrophoresis can be used to sort DNA according to length and how the Polymerase Chain Reaction can be used to copy DNA. He finishes with a brief description of DNA sequencing. Intro Music Atribution Title: I4dsong_loop_main.wav Artist: CosmicD Link to sound: http://www.freesound.org/people/CosmicD/sounds/72556/ Creative Commons Atribution License
Просмотров: 381088 Bozeman Science
TOM1L1 drives membrane delivery of MT1-MMP to promote ERBB2-induced breast cancer cell invasion
 
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TOM1L1 drives membrane delivery of MT1-MMP to promote ERBB2-induced breast cancer cell invasion. Clément Chevalier et al (2016), Nature Communications http://dx.doi.org/10.1038/ncomms10765 ERBB2 overexpression in human breast cancer leads to invasive carcinoma but the mechanism is not clearly understood. Here we report that TOM1L1 is co-amplified with ERBB2 and defines a subgroup of HER2+/ER+ tumours with early metastatic relapse. TOM1L1 encodes a GAT domain-containing trafficking protein and is a SRC substrate that negatively regulates tyrosine kinase signalling. We demonstrate that TOM1L1 upregulation enhances the invasiveness of ERBB2-transformed cells. This pro-tumoural function does not involve SRC, but implicates membrane-bound membrane-type 1 MMP (MT1-MMP)-dependent activation of invadopodia, membrane protrusions specialized in extracellular matrix degradation. Mechanistically, ERBB2 elicits the indirect phosphorylation of TOM1L1 on Ser321. The phosphorylation event promotes GAT-dependent association of TOM1L1 with the sorting protein TOLLIP and trafficking of the metalloprotease MT1-MMP from endocytic compartments to invadopodia for tumour cell invasion. Collectively, these results show that TOM1L1 is an important element of an ERBB2-driven proteolytic invasive programme and that TOM1L1 amplification potentially enhances the metastatic progression of ERBB2-positive breast cancers.
Просмотров: 59 ScienceVio
Refutation of Multi stage Carcinogenesis Model
 
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Refutation of Multi-stage Model of Carcinogenesis In the sixties Armitage and Doll developed a formula which explains the shape of age specific cancer mortality. This statistical model of carcinogenesis, proposed in 1954 suggested that a sequence of multiple distinct genetic events precede the onset of cancer. Multi-stage (mutation) hypothesis is regarded as cornerstone of cancer research. It predicts that the shape of the age specific cancer mortality is determined by the evolution of random mutations (hits). The model predicts that age specific mortality rises exponentially. Yet all age specific cancer mortalities level off and do not rise exponentially. Their observation deviate systematically from their predicted model. This poor multi-stage hypothesis is the foundation of molecular biology and medicine. Actually all published multi-hit models exhibit similar flaws. Here is another one. "Mutation and Cancer: Statistical Study of Retinoblastoma Alfred G Knudson Jr. Again, observations (points) deviate systematically from the predicted line. They indicate that the hypothesis is incomplete since ignoring confounding processes. I show why it is flawed. - Genes participate in tumor growth but do not cause cancer . - Genome wide association studies (GWAS) show that myriad genes participate in this process More than the eight mutations of the model by Armitage and Doll. - Poor models like Knudson's cloud medical reasoning. - Organism controls tumor growth and initiates retinoblastoma regression.
Просмотров: 726 Gershom Zajicek M.D,
Sara Courtneidge, Ph.D.
 
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Dr. Courtneidge of Sanford-Burnham Medical Research Institute studies Src and its substrates and their roles in invadopodia/podosome formation, cancer progression and embryonic development.
U2OS cell (best viewed in full-screen)
 
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U2OS cell expressing GFP-tagged novel microtubular protein (treated with nocodazole).
Просмотров: 298 Caspadria
8.2.5 - Cancer, Oncogenes, & the Cell Cycle
 
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Biology 122 Week8.Lecture2.Part5: Cancer and the Cell Cycle, continued - oncogenes
Просмотров: 44555 dmflyboy
JBC : The Src Homology and Collagen A (ShcA) Adaptor Protein Is Required for the Spatial...
 
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The Src Homology and Collagen A (ShcA) Adaptor Protein Is Required for the Spatial Organization of the Costamere/Z-disk Network during Heart Development. Mohamed Mlih et al (2015), The Journal of Biological Chemistry http://dx.doi.org/10.1074/jbc.M114.597377 Src homology and collagen A (ShcA) is an adaptor protein that binds to tyrosine kinase receptors. Its germ line deletion is embryonic lethal with abnormal cardiovascular system formation, and its role in cardiovascular development is unknown. To investigate its functional role in cardiovascular development in mice, ShcA was deleted in cardiomyocytes and vascular smooth muscle cells by crossing ShcA flox mice with SM22a-Cre transgenic mice. Conditional mutant mice developed signs of severe dilated cardiomyopathy, myocardial infarctions, and premature death. No evidence of a vascular contribution to the phenotype was observed. Histological analysis of the heart revealed aberrant sarcomeric Z-disk and M-band structures, and misalignments of T-tubules with Z-disks. We find that not only the ErbB3/Neuregulin signaling pathway but also the baroreceptor reflex response, which have been functionally associated, are altered in the mutant mice. We further demonstrate that ShcA interacts with Caveolin-1 and the costameric protein plasma membrane Ca2+/calmodulin-dependent ATPase (PMCA), and that its deletion leads to abnormal dystrophin signaling. Collectively, these results demonstrate that ShcA interacts with crucial proteins and pathways that link Z-disk and costamere.
Просмотров: 75 ScienceVio
PyMT
 
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Video by Dr Paul Timpson, Group Leader - Invasion and Metastasis (http://www.garvan.org.au/research/cancer/invasion-and-metastasis) and Max Nobis, Dr. Kurt Anderson - Tumour Cell Migration group, Beatson Institute. PYMT =breast cancer cells in green (expressing a Rac FRET-biosensor) to monitor Rac GTPase activty in live tissue. Purple = Extracelular matrix (collagen I) visualised by second harmonic generation (SHG) imaging.
Просмотров: 551 Garvan Institute of Medical Research
How aneuploidy drives cancer
 
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How aneuploidy drives cancer Air date: Wednesday, May 24, 2017, 3:00:00 PM Category: WALS - Wednesday Afternoon Lectures Runtime: 01:03:27 Description: NIH Director's Wednesday Afternoon Lecture Series Aneuploidy has been recognized as a hallmark of cancer for more than 100 years, yet no general theory has emerged to explain the recurring patterns of aneuploidy in cancer. Dr. Elledge's laboratory developed the Tumor Suppressor and Oncogene (TUSON) Explorer, a computational method that analyzes the patterns of mutational signatures in tumors and predicts the likelihood that any individual gene functions as a tumor suppressor gene (TSG) or an oncogene (OG). By analyzing more than 8,200 tumor-normal pairs, his lab has provided statistical evidence suggesting that many more genes possess cancer-driver properties than anticipated, forming a continuum of oncogenic potential. These genes represent the vast majority of cancer drivers, and the genetic networks they drive are a focus of future cancer system-biological approaches to cancer research. By integrating the driver predictions with information on somatic copy-number alterations, his lab has found that the distribution and the potency of TSGs (STOP genes), OGs, and essential genes (GO genes) on chromosomes can predict the complex patterns of aneuploidy and copy-number variation characteristic of cancer genomes. The lab proposes that the cancer genome is shaped through a process of cumulative haploinsufficiency and triplosensitivity. Dr. Elledge and his lab are now assessing how aneuploidy drives cancer and the potency with which it does so. They have found that, in many cases, aneuploidy predicts survival better than do mutational drivers or existing clinical parameters. They have also discovered that different classes of aneuploidy drive transcriptional programs for two hallmarks of cancer. Aneuploidy promotes a cell-proliferation program and inhibits the infiltration of immune cells leading to immune evasion. Melanoma patients with tumors exhibiting high aneuploidy show poorer responses to immunotherapy with anti-CTLA4 antibodies. Dr. Elledge and his lab are now exploring which genes in recurring amplicons drive proliferation. For more information go to https://oir.nih.gov/wals/2016-2017 Author: Stephen J. Elledge, Ph.D., Gregor Mendel Professor of Genetics and Medicine at Harvard Medical School; Geneticist, Department of Medicine, Brigham and Women's Hospital; Investigator, Howard Hughes Medical Institute Permanent link: https://videocast.nih.gov/launch.asp?23313
Просмотров: 685 nihvcast
Susan Lindquist (Whitehead, MIT / HHMI) 1a: Protein Folding in Infectious Disease and Cancer
 
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http://www.ibiology.org/ibioseminars/protein-folding-infectious-disease-cancer.html In Part 1a, Dr. Lindquist explains the problem of protein folding. Proteins leave the ribosome as long, linear chains of amino acids but they need to fold into complex three dimensional shapes in the extremely crowded environment of the cytoplasm. Since protein misfolding can be disastrous for cells, proteins known as heat shock proteins (HSPs) have evolved to facilitate proper protein folding. Lindquist explains that sometimes the heat shock response becomes unbalanced resulting in human disease. In the case of cancer, HSPs help cancer cells survive many stresses that would typically kill them. In contrast, many neurodegenerative diseases are a result of protein misfolding and aggregation suggesting that, in these diseases, HSPs are not activated when they should be. Yeast have many of the same cellular processes as humans including a stress response to aid in protein folding and prevent protein aggregation. In Part 1b, Lindquist describes how genetic screens in yeast helped scientists identify mutations that increased the formation of aggregates similar to those found in neurodegenerative diseases. Furthermore a screen in yeast of ~500,000 chemicals identified a number of compounds that prevented protein aggregation. Results from both experiments have since been validated in mice and human neuronal models. When cells undergo stress, the expression of HSPs increases. In Part 2, Lindquist explains that while most HSPs are expressed only as needed, Hsp90 is expressed in excess. This “buffer” of Hsp90 facilitates the folding of some mutant proteins (such as v-src) that would usually misfold and be degraded by the cell. Thus, Hsp90 potentiates the impact of these mutations. Interestingly, the Hsp90 “buffer” can also act to hide or suppress the impact of other mutations. These “hidden” mutations are found when cells are stressed reducing the pool of available Hsp90. Thus, Hsp90 provides a plausible mechanism for allowing genetic diversity and fluctuating environments to fuel the pace of evolutionary change. In her last talk, Lindquist focuses on prion proteins. Prions are perhaps best known as the infectious agents in diseases such as mad cow disease. However, Lindquist argues that there are many great things about prions too. They provide a protein-based mechanism of inheritance that allows organisms to develop new traits, quickly and reversibly, and thereby adapt to new environments. Working in yeast, Lindquist and her colleagues were able to identify numerous prion-like proteins that are induced at different levels, depending on the temperature, pH or presence of bacteria. Expression of prions caused heritable, phenotypic changes in the yeast demonstrating that prions are another mechanism by which environmental changes can induce new traits that can be passed onto progeny. As Lindquist says, perhaps it is time to give Lamarck back his dignity. Speaker Biography: Susan Lindquist is a member and former Director of the Whitehead Institute for Biomedical Research. She is also a Howard Hughes Medical Institute Investigator and Professor of Biology at the Massachusetts Institute of Technology. She received her Ph.D. in biology from Harvard and was a postdoctoral fellow of the American Cancer Society. Lindquist was on the faculty of the University of Chicago for over 20 years before moving to MIT in 2001. A pioneer in the study of protein folding, Lindquist found that the chaperone Hsp90 potentiates and buffers the effects of genetic variation, fueling evolutionary mechanisms as diverse as malignant transformation and the emergence of drug resistance. Her work established the molecular basis for protein-based mechanisms of inheritance and she demonstrated that Hsp90 and prions each provide distinct but feasible mechanisms of Lamarckian inheritance. Dr. Lindquist is an elected member of the National Academy of Sciences, the Academy of Medicine and the Royal Society. Her honors also include the Dickson Prize in Medicine, the Otto-Warburg Prize, the Genetics Society of America Medal, the FASEB Excellence in Science Award, the E.B. Wilson Medal, the Vanderbilt Prize for Women’s Excellence in Science and Mentorship and the National Medal of Science.
Просмотров: 5219 iBiology
Video: Toronto lawyer blogs about genetic predisposition to cancer
 
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Sabrina Fuoco-Dunn, the blogger behind Cancer Girl Smiles, has Li-Fraumeni syndrome, a rare genetic disorder that predisposes her to cancer.
Просмотров: 134 CityNews Toronto
Ezrin regulates focal adhesion and invadopodia dynamics by altering calpain activity to promote...
 
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Ezrin regulates focal adhesion and invadopodia dynamics by altering calpain activity to promote breast cancer cell invasion. Victoria Hoskin et al (2015), Molecular Biology of the Cell http://dx.doi.org/10.1091/mbc.E14-12-1584 Up-regulation of the cytoskeleton linker protein ezrin frequently occurs in aggressive cancer types and is closely linked with metastatic progression. However, the underlying molecular mechanisms detailing how ezrin is involved in the invasive and metastatic phenotype remain unclear. Here, we report a novel function of ezrin in regulating focal adhesion (FA) and invadopodia dynamics, two key processes required for efficient invasion to occur. We show that depletion of ezrin expression in invasive breast cancer cells impairs both FA and invadopodia turnover. We also demonstrate that ezrin-depleted cells display reduced calpain-mediated cleavage of the FA and invadopodia-associated proteins talin, focal adhesion kinase (FAK) and cortactin, and reduced calpain-1-specific membrane localization, suggesting a requirement for ezrin in maintaining proper localization and activity of calpain-1. Furthermore, we show that ezrin is required for cell directionality, early lung seeding and distant organ colonization, but not primary tumor growth. Collectively, our results unveil a novel mechanism by which ezrin regulates breast cancer cell invasion and metastasis.
Просмотров: 286 ScienceVio
Breast Cancer Awareness Month:
 
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What are the signs & how to reduce your risk? October marks breast cancer awareness month. Dr Yvette Lu weighs in.
Просмотров: 225 City
Dynamic focal adhesions
 
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The accompanying movie shows the effect of targeting different genes on focal adhesion dynamics, which are essential for cell migration. Control and siGFP-treated H1299 cells are migratory and exhibit active focal adhesion remodeling at the leading edge of the cell. Knockdown of either SRPK1 or MAPK2 inhibits cell migration, and focal adhesions are stabilized in siSRPK1- and siMAPK2-treated cells. Knockdown of IKBKE altered migration and depolarized focal adhesion remodeling. Wies van Roosmalen, Sylvia E. Le Dévédec, and colleagues at Leiden University screen for genes that alter cancer cell migration and demonstrate that SRPK1 promotes metastasis. See www.jci.org/article/view/74440 for more information
Просмотров: 2523 Journal of Clinical Investigation
The Basic Of Virus And Cancer- Breakthrough Junior Challenge 2017
 
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#breakthroughjuniorchallenge (PLEASE TURN ON CC FOR CAPTIONS, as I apparently did not speak clearly enough :)) SOURCES OF PICTURES: 1. "The Rous Sarcoma Virus Story". The Biology of Cancer. (Garland Science 2007) 2. Picture of Tumor vs Normal cell. (Cancer Research UK) Music: 1. Blue Skies by Katamaran 2. "Spring in My Step" by Silent Partner Editing apps: 1. iMovies 2. Windows Movie Makers 3. Explee 4. Audacity 5. Format Factory Thanks for watching!
Просмотров: 197 Nhi Nguyen
Transcriptional Landscape of Drug Response Guides the Design of Drug Combinations
 
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In the LINCS data science research webinar which took place on March 10, 2015, Marc Hafner PhD from the HMS LINCS Data and Signature Generation Center (DSGC) presented "Transcriptional Landscape of Drug Response Guides the Design of Specific and Potent Drug Combinations". HMS LINCS: http://lincs.hms.harvard.edu/ LINCS Project: http://www.lincsproject.org/ Datasets: L1000 Data, http://LincsCloud.org Abstract: Characterizing the molecular effects of targeted therapies is an important step towards understanding and predicting drug efficacy in cancer. In this work, we used the L1000 assay to measure the transcriptional response of six breast cancer cell lines to more than 100 different targeted drugs. We focused on inhibitors targeting the most important signaling kinases such as PI3K, AKT or MAPK, as well as receptor tyrosine kinases (RTKs) and cyclin-dependent kinases (CDKs). With two time points and six doses, the dataset contains more than 8000 unique perturbations. We clustered the perturbations that elicited a significant response based on their characteristic direction. Clusters were generally time point specific with some clusters contained perturbations from multiple cell lines whereas others were cell line specific. In particular, responses to CDK inhibitors were similar across most cell lines and showed a down-regulation of genes related to the cell cycle. On the other hand, cell lines responded differently to PI3K/AKT and MAPK inhibitors as illustrated by clusters specific to each cell line and pathway. Interestingly, the perturbations induced by RTK (e.g. EGFR, MET, ALK) and non-RTK (e.g. SRC, ABL, BTK) inhibitors, clustered with either the PI3K/AKT or the MAPK inhibitors depending on the cell line. Thus the transcriptional response allowed us to identify differences in pathway connectivity between cell lines, in particular which RTK connects to the PI3K/AKT pathway or the MAPK one.
Просмотров: 446 BD2K-LINCS DCIC
Highly efficient baculovirus-mediated multigene delivery in primary cells
 
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Highly efficient baculovirus-mediated multigene delivery in primary cells. Maysam Mansouri et al (2016), Nature Communications http://dx.doi.org/10.1038/ncomms11529 Multigene delivery and subsequent cellular expression is emerging as a key technology required in diverse research fields including, synthetic and structural biology, cellular reprogramming and functional pharmaceutical screening. Current viral delivery systems such as retro- and adenoviruses suffer from limited DNA cargo capacity, thus impeding unrestricted multigene expression. We developed MultiPrime, a modular, non-cytotoxic, non-integrating, baculovirus-based vector system expediting highly efficient transient multigene expression from a variety of promoters. MultiPrime viruses efficiently transduce a wide range of cell types, including non-dividing primary neurons and induced-pluripotent stem cells (iPS). We show that MultiPrime can be used for reprogramming, and for genome editing and engineering by CRISPR/Cas9. Moreover, we implemented dual-host-specific cassettes enabling multiprotein expression in insect and mammalian cells using a single reagent. Our experiments establish MultiPrime as a powerful and highly efficient tool, to deliver multiple genes for a wide range of applications in primary and established mammalian cells.
Просмотров: 228 ScienceVio
What is INVADOPODIA? What does INVADOPODIA mean? INVADOPODIA meaning, definition & explanation
 
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What is INVADOPODIA? What does INVADOPODIA mean? INVADOPODIA meaning - INVADOPODIA pronunciation - v definition - INVADOPODIA explanation - How to pronounce INVADOPODIA? Source: Wikipedia.org article, adapted under https://creativecommons.org/licenses/by-sa/3.0/ license. SUBSCRIBE to our Google Earth flights channel - https://www.youtube.com/channel/UC6UuCPh7GrXznZi0Hz2YQnQ Invadopodia are actin-rich protrusions of the plasma membrane that are associated with degradation of the extracellular matrix in cancer invasiveness and metastasis. Very similar to podosomes, invadopodia are found in invasive cancer cells and are important for their ability to invade through the extracellular matrix, especially in cancer cell extravasation. Invadopodia can be visualized by the holes they would create in fibronectin-coated plates or by using immunohistochemistry, as co-localizing puncta of actin with Tks5. Invadopodia can also be used as a marker to quantify the invasiveness of cancer cell lines in vitro using a hyaluronic acid hydrogel assay. In the early 1980s, researchers noticed protrusions coming from the ventral membrane of cells that had been transformed by the Rous Sarcoma Virus and that they were at the sites of cell-to-extracellular matrix (ECM) adhesion. They termed these structures podosomes, or cellular feet, but it was later noticed that degradation of the ECM was occurring at these sites and the name invadopodia was coined to highlight the invasive nature of these protrusions. Since then, researchers have often used the two names interchangeably, but it is generally accepted that podosomes are the structures involved in normal biological processes (like when immune cells need to cross tissue barriers or in bone remodeling) and invadopodia are the structures in invading cancer cells. However, there remains controversy around this nomenclature, with some scientists arguing that the two are different enough to be considered distinct structures while others argue that invadopodia are simply disregulated podosomes and cancer cells don’t simply invent new mechanisms. Due to this confusion and the high similarity between the two structures, many have begun to group the two under the collective term invadosomes. Invadopodia have an actin core, which is surrounded by a ring structure enriched in actin-binding proteins, adhesion molecules, integrins, and scaffold proteins. Invadopodia are generally longer than podosomes, with a width of 0.5- 2.0 um and a length greater than 2 um, and they last much longer than podosomes. Invadopodia also penetrate deep into the ECM, while podosomes generally extend upward into the cytoplasm and do not cause as much ECM degradation. Invadopodia formation is a complex process that involves multiple signaling pathways and can be described as having three steps: initiation, stabilization, and maturation. Initiation of invadopodia involves the formation of buds in the plasma membrane and is initiated by growth factors like epidermal growth factor (EGF), transforming growth factor beta (TGFB) or platelet-derived growth factor (PDGF), which act through phosphoinositide 3-kinase (PI3K) to activate Src family kinases. These kinases have key roles in the formation of invadopodia and when activated, phosphorylate multiple proteins involved in invadopodia formation including Tks5, synaptjanin-2, and the Abl-family kinase Arg4.....
Просмотров: 187 The Audiopedia
Conquering Cancer: Paradigm Shifts
 
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Session Chair: Richard O. Hynes PhD '71, David H. Koch Institute for Integrative Cancer Research at MIT; Daniel K. Ludwig Professor for Cancer Research, MIT Panel: Leroy Hood, Affiliate Professor of Immunology, University of Washington, Seattle; President, Institute for Systems Biology Eric S. Lander, Professor of Biology, MIT; Professor of Systems Biology, Harvard Medical School; Founding Director, Broad Institute Susan L. Lindquist, David H. Koch Institute for Integrative Cancer Research at MIT; Professor of Biology, MIT; Member, Whitehead Institute for Biomedical Research; Investigator, Howard Hughes Medical Institute Duaa H. Mohammad PhD '08, Postdoctoral Associate, David H. Koch Institute for Integrative Cancer Research at MIT
Просмотров: 378 InfiniteHistoryProject MIT
AACR 2009: Membrane microfilter device for capture and characterisation of circulating tumour cells
 
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Development of a Membrane Microfilter Device for Capture and Characterisation of Circulating Tumour Cells in Blood: Anthony Williams, graduate student at the Keck School of Medicine presents a new technology to AACR 2009 in Denver.
Просмотров: 138 ecancer
Why curiosity is the key to science and medicine | Kevin B. Jones
 
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Science is a learning process that involves experimentation, failure and revision -- and the science of medicine is no exception. Cancer researcher Kevin B. Jones faces the deep unknowns about surgery and medical care with a simple answer: honesty. In a thoughtful talk about the nature of knowledge, Jones shows how science is at its best when scientists humbly admit what they do not yet understand. TEDTalks is a daily video podcast of the best talks and performances from the TED Conference, where the world's leading thinkers and doers give the talk of their lives in 18 minutes (or less). Look for talks on Technology, Entertainment and Design -- plus science, business, global issues, the arts and much more. Find closed captions and translated subtitles in many languages at http://www.ted.com/translate Follow TED news on Twitter: http://www.twitter.com/tednews Like TED on Facebook: https://www.facebook.com/TED Subscribe to our channel: http://www.youtube.com/user/TEDtalksDirector
Просмотров: 57542 TED
Dean Ornish: Healing through diet
 
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http://www.ted.com Dean Ornish talks about simple, low-tech and low-cost ways to take advantage of the body's natural desire to heal itself.
Просмотров: 214912 TED
Structural Mechanisms of Mutant Huntingtin Aggregation Suppression by Synthetic Chaperonin-like...
 
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Structural Mechanisms of Mutant Huntingtin Aggregation Suppression by Synthetic Chaperonin-like CCT5 Complex Explained by Cryo-electron Tomography. Michele C. Darrow et al (2015), The Journal of Biological Chemistry http://dx.doi.org/10.1074/jbc.M115.655373 Huntington's disease (HD), a neurodegenerative disorder characterized by functional deficits and loss of striatal neurons, is linked to an expanded and unstable CAG trinucleotide repeat in the huntingtin gene (HTT). This DNA sequence translates to a polyglutamine repeat in the protein product leading to mutant huntingtin (mHTT) protein aggregation. The aggregation of mHTT is inhibited in vitro and in vivo by TRiC (TCP-1 Ring Complex) chaperonin. Recently, a novel complex comprised of a single type of TRiC subunits has been reported to inhibit mHTT aggregation. Specifically, purified CCT5 homo-oligomer complex, when compared to TRiC, has a similar structure, ATP use, substrate refolding activity, and importantly, it also inhibits mHTT aggregation. Using an aggregation suppression assay and cryo-electron tomography coupled with a novel computational classification method we uncover the interactions between synthetic CCT5 complex (~1 MDa) and aggregates of mutant huntingtin exon 1 containing 46 glutamines (mHTTQ46-Ex1). We find that, in a similar fashion to TRiC, synthetic CCT5 complex caps mHTT fibrils at their tips and encapsulates mHTT oligomers, providing a structural description of CCT5 complex's inhibition of mHTTQ46-Ex1 and a shared mechanism of mHTT inhibition between TRiC chaperonin and CCT5 complex - cap and contain.
Просмотров: 152 ScienceVio
PLoS ONE: Involvement of Local Lamellipodia in Endothelial Barrier Function
 
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Involvement of Local Lamellipodia in Endothelial Barrier Function. Jerome W. Breslin et al (2015), PLoS ONE http://dx.doi.org/10.1371/journal.pone.0117970 Recently we observed that endothelial cells cultured in tightly confluent monolayers display frequent local lamellipodia, and that thrombin, an agent that increases endothelial permeability, reduces lamellipodia protrusions. This led us to test the hypothesis that local lamellipodia contribute to endothelial barrier function. Movements of subcellular structures containing GFP-actin or VE-cadherin-GFP expressed in endothelial cells were recorded using time-lapse microscopy. Transendothelial electrical resistance (TER) served as an index of endothelial barrier function. Changes in both lamellipodia dynamics and TER were assessed during baseline and after cells were treated with either the barrier-disrupting agent thrombin, or the barrier-stabilizing agent sphingosine-1-phosphate (S1P). The myosin II inhibitor blebbistatin was used to selectively block lamellipodia formation, and was used to test their role in the barrier function of endothelial cell monolayers and isolated, perfused rat mesenteric venules. Myosin light chain (MLC) phosphorylation was assessed by immunofluorescence microscopy. Rac1 and RhoA activation were evaluated using G-LISA assays. The role of Rac1 was tested with the specific inhibitor NSC23766 or by expressing wild-type or dominant negative GFP-Rac1. The results show that thrombin rapidly decreased both TER and the lamellipodia protrusion frequency. S1P rapidly increased TER in association with increased protrusion frequency. Blebbistatin nearly abolished local lamellipodia protrusions while cortical actin fibers and stress fibers remained intact. Blebbistatin also significantly decreased TER of cultured endothelial cells and increased permeability of isolated rat mesenteric venules. Both thrombin and S1P increased MLC phosphorylation and activation of RhoA. However, thrombin and S1P had differential impacts on Rac1, correlating with the changes in TER and lamellipodia protrusion frequency. Overexpression of Rac1 elevated, while NSC23766 and dominant negative Rac1 reduced barrier function and lamellipodia activity. Combined, these data suggest that local lamellipodia, driven by myosin II and Rac1, are important for dynamic changes in endothelial barrier integrity.
Просмотров: 180 ScienceVio
Nature : Optogenetic control of organelle transport and positioning
 
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KeSimpulan | Optogenetic control of organelle transport and positioning. Petra van Bergeijk et al (2015), Nature, http://dx.doi.org/10.1371/10.1038/nature14128
Просмотров: 617 ScienceVio
JBC : RFPL4A increases the G1 population and decreases sensitivity to chemotherapy in human...
 
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RFPL4A increases the G1 population and decreases sensitivity to chemotherapy in human colorectal cancer cells. Atsushi Naito et al (2015), The Journal of Biological Chemistry http://dx.doi.org/10.1074/jbc.M114.614859 Cell cycle-arrested cancer cells are resistant to conventional chemotherapy that acts on the mitotic phases of the cell cycle, although the molecular mechanisms involved in halting cell cycle progression remain unclear. Here, we demonstrated that RFPL4A, an uncharacterized ubiquitin ligase, induced G1 retention and thus conferred decreased sensitivity to chemotherapy in the human colorectal cancer cell line, HCT116. Long-term time-lapse observations in HCT116 cells bearing a fluorescence ubiquitin-based cell cycle indicator (Fucci) identified a characteristic population that is viable but remains in the G1 phase for an extended period of time (up to 56 h). Microarray analyses showed that expression of RFPL4A was significantly upregulated in these G1-arrested cells, not only in HCT116 cells but also in other cancer cell lines, and overexpression of RFPL4A increased the G1 population and decreased sensitivity to chemotherapy. However, knockdown of RFPL4A expression caused the cells to resume mitosis and induced their susceptibility to anti-cancer drugs in vitro and in vivo. These results indicate that RFPL4A is a novel factor that increases the G1 population and decreases sensitivity to chemotherapy, and thus may be a promising therapeutic target for refractory tumor conditions.
Просмотров: 109 ScienceVio
JCI : Purkinje neuron Ca2+ influx reduction rescues ataxia in SCA28 model
 
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Purkinje neuron Ca2+ influx reduction rescues ataxia in SCA28 model. Francesca Maltecca et al (2015), Journal of Clinical Investigation, http://dx.doi.org/10.1172/JCI74770 Spinocerebellar ataxia type 28 (SCA28) is a neurodegenerative disease caused by mutations of the mitochondrial protease AFG3L2. The SCA28 mouse model, which is haploinsufficient for Afg3l2, exhibits a progressive decline in motor function and displays dark degeneration of Purkinje cells (PC-DCD) of mitochondrial origin. Here, we determined that mitochondria in cultured Afg3l2-deficient PCs ineffectively buffer evoked Ca2+ peaks, resulting in enhanced cytoplasmic Ca2+ concentrations, which subsequently triggers PC-DCD. This Ca2+-handling defect is the result of negative synergism between mitochondrial depolarization and altered organelle trafficking to PC dendrites in Afg3l2-mutant cells. In SCA28 mice, partial genetic silencing of the metabotropic glutamate receptor mGluR1 decreased Ca2+ influx in PCs and reversed the ataxic phenotype. Moreover, administration of the β-lactam antibiotic ceftriaxone, which promotes synaptic glutamate clearance, thereby reducing Ca2+ influx, improved ataxia-associated phenotypes in SCA28 mice when given either prior to or after symptom onset. Together, the results of this study indicate that ineffective mitochondrial Ca2+ handling in PCs underlies SCA28 pathogenesis and suggest that strategies that lower glutamate stimulation of PCs should be further explored as a potential treatment for SCA28 patients.
Просмотров: 135 ScienceVio
A Molecular Smart Surface for Spatio-Temporal Studies of Cell Mobility
 
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A Molecular Smart Surface for Spatio-Temporal Studies of Cell Mobility. Eun-ju Lee et al (2015), PLoS ONE http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0118126 Active migration in both healthy and malignant cells requires the integration of information derived from soluble signaling molecules with positional information gained from interactions with the extracellular matrix and with other cells. How a cell responds and moves involves complex signaling cascades that guide the directional functions of the cytoskeleton as well as the synthesis and release of proteases that facilitate movement through tissues. The biochemical events of the signaling cascades occur in a spatially and temporally coordinated manner then dynamically shape the cytoskeleton in specific subcellular regions. Therefore, cell migration and invasion involve a precise but constantly changing subcellular nano-architecture. A multidisciplinary effort that combines new surface chemistry and cell biological tools is required to understand the reorganization of cytoskeleton triggered by complex signaling during migration. Here we generate a class of model substrates that modulate the dynamic environment for a variety of cell adhesion and migration experiments. In particular, we use these dynamic substrates to probe in real-time how the interplay between the population of cells, the initial pattern geometry, ligand density, ligand affinity and integrin composition affects cell migration and growth. Whole genome microarray analysis indicates that several classes of genes ranging from signal transduction to cytoskeletal reorganization are differentially regulated depending on the nature of the surface conditions.
Просмотров: 86 ScienceVio
GFP Tumor
 
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Intravital video cellular resolution in a GFP expressing mouse tumour.
Просмотров: 185 Matty73
NCRI 2011: Lifetime achievement award and future work
 
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Prof Christopher Marshall speaks with Prof Gordon McVie at the National Cancer research Institute cancer conference in Liverpool on his lifetime achievement award; work with RAS and current research on RHO. Prof Marshall earned his award for elucidating how RAS proteins function, which led to numerous targeted drugs currently used in the clinic, many of which came from research outside his work on RAS. In his current research, Prof Marshall is researching RHO, a family of proteins similar to RAS that allow tumour cells to invade and metastasise. While RAS proteins are important in invasion and metastasis, RHO affects a different process of the cell and gives them the ability to change shape and move.
Просмотров: 194 ecancer