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Thapsigargin
Thapsigargin—From Traditional Medicine to Anticancer Drug
Robust Sampling of Altered Pathways for Drug Repositioning Reveals
Dg265thesispdf.Pdf
Thapsia Garganica Carmen Quiñonero López1,2, Patricia Corral3, Bénédicte Lorrain‑Lorrette3, Karen Martinez‑Swatson4, Franck Michoux3 and Henrik Toft Simonsen1*
Presenilin-1 Established ER-Ca2+ Leak: a Follow up on Its Importance for the Initial Insulin Secretion in Pancreatic Islets and Β-Cells Upon Elevated Glucose
Calpain Mobilizes Atg9/Bif-1 Vesicles from Golgi Stacks Upon Autophagy
Thapsigargin, Origin, Chemistry, Structure-Activity Relationships and Prodrug Development
Diplomarbeit / Diploma Thesis
Inactivation of Cys674 in SERCA2 Increases BP by Inducing Endoplasmic Reticulum Stress and Soluble Epoxide Hydrolase
Mitochondria Associations Mroj Alassaf1,2,3, Mary C Halloran1,2,3*
Large-Scale Phenotypic Drug Screen Identifies Neuroprotectants in Zebrafish and Mouse Models of Retinitis Pigmentosa Liyun Zhan
Multiplexed High-Throughput Screenings for Immune Modulators of Cytotoxic T Lymphocyte Ziyan Zhao University of Connecticut - Storrs,
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Endoplasmic Reticulum Ca2+ Signaling and Calpains Mediate Renal Cell Death
The Concise Guide to PHARMACOLOGY 2015/16: Transporters
Cardiovascular Research Product Guide | Edition 2 | USD
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Α-Mangostin Reduced ER Stress-Mediated Tumor Growth Through Autophagy Activation
The Concise Guide to PHARMACOLOGY 2015/16
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Intermedin Protects Thapsigargin‑Induced Endoplasmic Reticulum Stress in Cardiomyocytes by Modulating Protein Kinase a and Sarco/Endoplasmic Reticulum Ca2+‑Atpase
Endoplasmic Reticulum Stress Signaling in Cancer and Neurodegenerative Disorders: Tools and Strategies to Understand Its Complexity T
Voltage Dependence and Activation Mechanisms of The
Regulation of Type-2 Diabetes Through IP3R and Mtrs Along with SERCA and CRAC Channels by Agomelatine, Luzindol, 2-APB and Thaps
Honokiol and Muscarinic Signaling Wang Et Al
Critical Examination of Selected Aspects of the Toxtracker® in Vitro Genotoxicity Assay
Thapsigargin at Non-Cytotoxic Levels Induces a Potent Host Antiviral Response That Blocks Influenza a Virus Replication
Cell Death Induced by the ER Stressor
Pharmacologic Agents Targeting Autophagy