细胞粘附、信号和癌症 - MARy Beckerle P1
本视频由科普中国和生物医学大讲堂出品
MARy Beckerle (University of Utah) PARt 1: Adhesion, Signaling and Cancer
Cell-substratum adhesion is mediated by integrins, a family of transmembrane, heterodimeric, extracellulAR matrix receptors that ARe concentrated at focal adhesions. Integin engagement influences a vARiety of signaling pathways and regulates cell behaviors including motility, proliferation, and survival. Disturbance of normal integrin function is associated with a vARiety of pathologic conditions including cancer. In the first segment of my seminAR, I provide a broad overview of the cancer problem for a lay audience. Advances in our understanding of cancer as a genetic disease ARe discussed. The influence of cell adhesion on control of cell growth is reviewed. See more at http://www.ibiology.org
粘着蛋白的发现和表征 - MARy Beckerle P2
本视频由科普中国和生物医学大讲堂出品
MARy Beckerle (University of Utah) PARt 2: Discovery and ChARacterization
In the second segment, I describe the identification of the focal adhesion protein, zyxin, by my lab. Recent work revealed that zyxin is down-regulated upon expression of the Ewing sARcoma oncoprotein, EWS-FLI. Loss of zyxin expression results in enhanced cell motility and is also associated with failed apoptotic signaling. Evidence that zyxin shuttles between focal adhesions and the nucleus is presented. The impact of reduced zyxin expression on tumor progression is discussed. See more at http://www.ibiology.org
焦点粘连作为压力传感器 - MARy Beckerle P3
本视频由科普中国和生物医学大讲堂出品
MARy Beckerle (University of Utah) PARt 3: Focal Adhesions as Stress Sensors
In the third segment of my seminAR, I address a new frontier in cell biology, that is how cells respond to mechanical information. Cells and tissues ARe exposed to physical forces in vivo and excessive mechanical stress leads to a vARiety of pathological consequences. I describe a system for exposing cells to controlled mechanical stress and discuss the stretch response. We have discovered that the focal adhesion protein, zyxin, is exquisitely sensitive to mechanical stimulation and is required for the ability of cells to reinforce the actin cytoskeleton when challenged by exposure to cyclic stretch. See more at http://www.ibiology.org
化学糖生物学 - CARolyn Bertozzi P1
本视频由科普中国和生物医学大讲堂出品
CARolyn Bertozzi (UC Berkeley) PARt 1: Chemical Glycobiology
PARt 1 A lARge pARt of an organism's complexity is not encoded by its genome but results from post-translational modification. Glycosylation, or the addition of sugAR molecules to a protein is an example of such a modification. These sugARs, or glycans, ARe often complex, branched molecules specific to pARticulAR cells. Cell surface glycans determine human blood types, allow viral infections and play a key role in tissue inflammation. See more at http://www.ibioseminARs.org
生物糖组成像方法 - CARolyn Bertozzi P2
本视频由科普中国和生物医学大讲堂出品
CARolyn Bertozzi (UC Berkeley) PARt 2: Imaging the Glycome
Since glycans cannot be labeled with genetically-encoded reporters such as GFP, bioorthoganal reactions have been developed to allow their labeling and imaging. In this lecture, Bertozzi describes the chemistry and imaging methodology used to view glycoproteins in cells and whole organisms. See more at http://www.ibioseminARs.org
病毒结构的一般原则 - Stephen HARrison P1
本视频由科普中国和生物医学大讲堂出品
Stephen HARrison (HARvARd) PARt 1: Virus structures: General principles
HARrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses ARe symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins ARe correctly placed. This ARrangement results in symmetrically shaped viruses.
In PARt 1, HARrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the moleculAR mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in PARt 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of PARt 3. Using rotavirus as a model, HARrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
病毒的膜融合 - Stephen HARrison P2
本视频由科普中国和生物医学大讲堂出品
Stephen HARrison (HARvARd) PARt 2: Viral membrane fusion
HARrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses ARe symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins ARe correctly placed. This ARrangement results in symmetrically shaped viruses.
In PARt 1, HARrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the moleculAR mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in PARt 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of PARt 3. Using rotavirus as a model, HARrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
非包膜病毒如何侵入细胞 - Stephen HARrison P3
本视频由科普中国和生物医学大讲堂出品
Stephen HARrison (HARvARd) PARt 3: Non-enveloped virus entry
HARrison begins his talk by asking why most non-enveloped viruses and some enveloped viruses ARe symmetrical in shape. He proceeds to show us lovely images of the structures obtained by x-ray crystallography of numerous viral coat proteins. Deciphering these structures allowed scientists to understand that viral coat proteins form multimers, such as dimers and pentamers, which in turn interact with a scaffold that ensures that the coat proteins ARe correctly placed. This ARrangement results in symmetrically shaped viruses.
In PARt 1, HARrison also explains that enveloped viruses infect cells by inducing the fusion of the viral and host cell membranes. He delves deeper into the moleculAR mechanism of membrane fusion driven by the hemagglutinin or HA protein of the influenza virus in PARt 2 of his talk.
Non-enveloped viruses, on the other hand, must enter cells by a mechanism other than membrane fusion. This is the focus of PARt 3. Using rotavirus as a model, HARrison and his colleagues have used a combination of Xray crystallography and electron cryomicroscopy to decipher how the spike protein on the viral surface changes its conformation and perforates the cell membrane allowing the virus to enter the cell.
病毒与宿主细胞表面结合的方式 - ARi Helenius P1
本视频由科普中国和生物医学大讲堂出品
ARi Helenius (ETH Zurich) PARt 1: Virus entry
Viruses ARe extremely simple and small yet they ARe responsible for many of the worlds diseases. A virus pARticle consists of only a genome, a protein coat or capsid, and sometimes a surrounding lipid envelope. To replicate, a virus must successfully enter a host cell, uncoat its genome, and appropriate the host cell machinery to replicate its genome and produce viral proteins. PARt 1 of this lecture will discuss ways in which viruses bind to the surface of host cells. Simian Virus 40 which binds to specific cell surface glycolipids, and Human Papilloma Virus-16 which binds to sites on filoipodia, ARe examples of different binding mechanisms. Attachment of viruses to the plasma membrane activates cell signaling resulting in endocytosis of the viral pARticles. This lecture is appropriate for upper level undergraduate and graduate classes studying virology or endocytosis.
牛痘病毒如何进入细胞 - ARi Helenius P3
本视频由科普中国和生物医学大讲堂出品
ARi Helenius (ETH Zurich) PARt 3: Open Sesame: Cell Entry and Vaccinia Virus
PARt 3 focuses on a single virus, the Vaccinia virus, as a model for cell binding, signaling and endocytosis. Fluorescently labeled Vaccinia viruses bind to and surf along host cell filopodia. Helenius lab members noticed that when Vaccinia, unlike other viruses, reached the surface of the cell body it caused the plasma membrane to form blebs. Further experiments showed that the virus tricks the cell into thinking it is apoptotic debris. This induces blebbing and subsequent uptake of the virus by macropinocytosis. Additionally, automated high throughput siRNA screening was used to screen a lARge number of infected cells for host genes required for Vaccinia virus uptake. Analysis of the genes identified allowed host factors and processes critical to viral infection to be identified. Expansion of this technique may provide a new source of information on pathogen-host interactions.