SurESelect 定制靶向测序--陈巍学基因（23）
Agilent 公司出品的 SurESelect 定制捕获测序 Panel，是一个很好用的目标基因测序试盒。是在肿瘤靶向用药的伴随诊断上的一个先进技术手段。
许多专业的测序公司提供基于 SurESelect Panel 的定制测序服务。
本视频介绍了客户自行定制 SurESelect Panel 的方法。
秦正红：DRAM1 regulatES autophagy flux and Bid-mediated cell death via lysosomES
秦正红，博士，教授，神经药理专业博士生导师。1994年在美国宾州医学院研究生院获博士学位，先后在美国国家卫生研究院(NIH)及麻省总医院和哈佛大学医学院从事研究工作。2003年从哈佛大学引进，现为苏州大学医学部基础医学与生物科学学院科研中心实验室主任，中国药理学会生化药理学专业委员会委员，中国药理学会神经药理学专业委员会委员，美国神经科学学会会员。
Damage-regulated autophagy modulator1 (DRAM1), a novel TP53 target gene, is an evolutionarily conserved lysosomal protein and plays an ESsential role in TP53-dependent autophagy activation and apoptosis (Crighton et al, 2006). However, the mechanisms by which DRAM1 promotES autophagy and apoptosis are not clear.
3-Nitropropionic acid (3-NP) is an inhibitor of mitochondrial rESpiratory complex II. Intrastriatal administration of 3-NP producES neuropathology rESemble to Huntington disease. 3-NP-induced neuronal death was involved in autophagy and apoptosis. In vitro studiES with 3-NP in TP53 wt and null cells, 3-NP or CCCP increased the protein levels of DRAM1 in a TP53-dependent or independent manner. DRAM1 induction contributed to 3-NP-induced autophagy activation. Knock-down of DRAM1 with siRNA inhibited the activity of V-ATPase, acidification of lysosomES and activation of lysosomal proteasES. Knock-down of DRAM1 reduced the clearance of autophagososmES.
3-NP also induced a transcription independent upregulation of BAX protein levels. Knock-down of DRAM1 supprESsed the increase in BAX levels. Co-immunoprecipitation and pull-down studiES revealed an interaction of DRAM1 and BAX protein. Stably exprESsion of exogenous DRAM1 increased the half-life of BAX. Upregulation of DRAM1 recruited BAX to lysosomES and induced cathepsin B-dependent cleavage of Bid and cytochrome c release. Knockdown of DRAM1, BAX or inhibition of lysosomal enzymES reduced 3-NP-induced cytochrome c release and cell death.
ThESe data suggESt that DRAM1 plays important rolES in regulating autophagy flux and apoptosis. DRAM1 promotES autophagy flux through a mechanism involvES activation of V-ATPase and enhancES the acidification of lysosomES. DRAM1 promotES apoptosis via a mechanism involving recruitment of BAX to lysosomES to trigger cathepsin B-mediated Bid cleavage.
Generating B-lymphoblastoid cell linES using Epstein Barr virus transformation.
Generating immortalized B-lymphoblastoid cell linES via Epstein Barr virus transformation using the B95-8 EBV-infected and producing marmoset cell line.
WEStern Blot Using The invitrogen NuPAGE Novex Bis-Tris MiniGel System(Aubin Penna.Ph.D)
WEStern Blot Using The invitrogen NuPAGE Novex Bis-Tris MiniGel System(Aubin Penna.Ph.D)
我是如何成为一名科学家的 - Alfredo QuinonES-Hinojosa
本视频由科普中国和生物医学大讲堂出品
Alfredo QuinonES-Hinojosa（Q博士）（霍普金斯达大学）：我是如何成为一名科学家
出生于墨西哥的Q博士，19岁时翻越美国边界的栅栏，成为加利福尼亚的一名农场工人。由于他自己的决心，努力工作和自律，以及来自家庭和朋友的大量支持，他离开了农场工作，完成了大学和医学院的学业，最终成为一位非常成功的医生、科学家和脑外科医生。
关于讲师：Alfredo QuinonES-Hinojosa是约翰霍普金斯大学，神经外科学和肿瘤学，神经系统的细胞与分子医学的副教授，脑肿瘤外科手术的主任。Q博士作为一个专家外科医生，他致力于干细胞，在脑肿瘤的病因和治疗领域的研究。
Alfredo QuinonES-Hinojosa (Dr. Q) (Johns Hopkins): How I Became a Scientist
At age 19, QuiñonES-Hinojosa jumped the fence from Mexico to become a farm worker in California. Thanks to his own determination, hard work and discipline and a lot of support from family and friends, he left farm work, completed university and medical school, and ultimately became a highly succESsful physician-scientist and brain surgeon.
About the speaker: Alfredo QuiñonES-Hinojosa is an Associate ProfESsor of Neurosurgery and Oncology, Neuroscience and Cellular and Molecular Medicine and Director of the Brain Tumor Surgery Program at Johns Hopkins University. As well as being an expert surgeon, he rESearchES the role of stem cells both in causing brain tumors and potentially in fighting them.
This talk was first released in iBioMagazine Issue 5.
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Controlling the Cell Cycle: Cdk SubstratES - David O. Morgan
本视频由科普中国和生物医学大讲堂出品
David O. Morgan (UCSF) Part 2: Controlling the Cell Cycle: Cdk SubstratES
Cyclin-dependent kinasES (Cdks) are the central components of the control system that initiatES the events of the cell cycle. In the second part of this lecture, I discuss my laboratory's efforts to addrESs the problem of how the Cdks trigger cell-cycle events. I dEScribe our methods for identifying the protein substratES of the Cdks, and I discuss how thESe studiES have led to important cluES about how Cdks find their correct targets in the cell and how phosphorylation of those targets governs their function.
Photoreceptors and Image ProcESsing Part 1A - Jeremy Nathans
本视频由科普中国和生物医学大讲堂出品
Jeremy Nathans (Johns Hopkins) Part 1A: Photoreceptors and Image ProcESsing
In this set of lecturES, Jeremy Nathans explorES the molecular mechanisms within the retina that mediate the first steps in vision. The first lecture focusES on the structure of the light sensing receptors, the intracellular signals that are triggered by light absorption, and the ways in which the retina extracts information from a complex scene. See more at http://www.ibioseminars.org