Home

Konflikt Ägypten Fragebogen thapsigargin mechanism stark Es ist ein Glück, dass ich möchte

Frontiers | STING, the Endoplasmic Reticulum, and Mitochondria: Is Three a  Crowd or a Conversation?
Frontiers | STING, the Endoplasmic Reticulum, and Mitochondria: Is Three a Crowd or a Conversation?

Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial  Cells | PLOS ONE
Diabetes Alters Intracellular Calcium Transients in Cardiac Endothelial Cells | PLOS ONE

Promising therapeutic effect of thapsigargin nanoparticles on chronic  kidney disease through the activation of Nrf2 and FoxO1 | Aging
Promising therapeutic effect of thapsigargin nanoparticles on chronic kidney disease through the activation of Nrf2 and FoxO1 | Aging

IJMS | Free Full-Text | Thapsigargin—From Traditional Medicine to  Anticancer Drug
IJMS | Free Full-Text | Thapsigargin—From Traditional Medicine to Anticancer Drug

Cells | Free Full-Text | Calcium Pathways in Human Neutrophils—The Extended  Effects of Thapsigargin and ML-9
Cells | Free Full-Text | Calcium Pathways in Human Neutrophils—The Extended Effects of Thapsigargin and ML-9

Molecules | Free Full-Text | Mipsagargin: The Beginning—Not the  End—of Thapsigargin Prodrug-Based Cancer Therapeutics
Molecules | Free Full-Text | Mipsagargin: The Beginning—Not the End—of Thapsigargin Prodrug-Based Cancer Therapeutics

Thapsigargin: key to new host-directed coronavirus antivirals?: Trends in  Pharmacological Sciences
Thapsigargin: key to new host-directed coronavirus antivirals?: Trends in Pharmacological Sciences

HRC promotes anoikis resistance and metastasis by suppressing endoplasmic  reticulum stress in hepatocellular carcinoma
HRC promotes anoikis resistance and metastasis by suppressing endoplasmic reticulum stress in hepatocellular carcinoma

Silybin regulates P450s activity by attenuating endoplasmic reticulum  stress in mouse nonalcoholic fatty liver disease | Acta Pharmacologica  Sinica
Silybin regulates P450s activity by attenuating endoplasmic reticulum stress in mouse nonalcoholic fatty liver disease | Acta Pharmacologica Sinica

Frontiers | Mechanism of Endoplasmic Reticulum Stress in Cerebral Ischemia
Frontiers | Mechanism of Endoplasmic Reticulum Stress in Cerebral Ischemia

Tunicamycin specifically aggravates ER stress and overcomes chemoresistance  in multidrug-resistant gastric cancer cells by inhibiting N-glycosylation |  Journal of Experimental & Clinical Cancer Research | Full Text
Tunicamycin specifically aggravates ER stress and overcomes chemoresistance in multidrug-resistant gastric cancer cells by inhibiting N-glycosylation | Journal of Experimental & Clinical Cancer Research | Full Text

Calcium Influx Caused by ER Stress Inducers Enhances Oncolytic Adenovirus  Enadenotucirev Replication and Killing through PKCα Activation: Molecular  Therapy - Oncolytics
Calcium Influx Caused by ER Stress Inducers Enhances Oncolytic Adenovirus Enadenotucirev Replication and Killing through PKCα Activation: Molecular Therapy - Oncolytics

Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum  stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2  induction - ScienceDirect
Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2 induction - ScienceDirect

Molecular mechanism of ER stress‐induced gene expression of tumor necrosis  factor‐related apoptosis‐inducing ligand (TRAIL) in macrophages - Huang -  2015 - The FEBS Journal - Wiley Online Library
Molecular mechanism of ER stress‐induced gene expression of tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) in macrophages - Huang - 2015 - The FEBS Journal - Wiley Online Library

Differential impact of imipramine on thapsigargin- and tunicamycin-induced  endoplasmic reticulum stress and mitochondrial dysfunction in neuroblastoma  SH-SY5Y cells - ScienceDirect
Differential impact of imipramine on thapsigargin- and tunicamycin-induced endoplasmic reticulum stress and mitochondrial dysfunction in neuroblastoma SH-SY5Y cells - ScienceDirect

Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells  and both processes are regulated by ROS-dependent pathway - ScienceDirect
Thapsigargin induces apoptosis when autophagy is inhibited in HepG2 cells and both processes are regulated by ROS-dependent pathway - ScienceDirect

IJMS | Free Full-Text | Valproate Attenuates Endoplasmic Reticulum  Stress-Induced Apoptosis in SH-SY5Y Cells via the AKT/GSK3β Signaling  Pathway
IJMS | Free Full-Text | Valproate Attenuates Endoplasmic Reticulum Stress-Induced Apoptosis in SH-SY5Y Cells via the AKT/GSK3β Signaling Pathway

Effect of endoplasmic reticulum calcium on paraquat‑induced apoptosis of  human lung type II alveolar epithelial A549 cells
Effect of endoplasmic reticulum calcium on paraquat‑induced apoptosis of human lung type II alveolar epithelial A549 cells

Cell death induced by the ER stressor thapsigargin involves death receptor  5, a non-autophagic function of MAP1LC3B, and distinct contributions from  unfolded protein response components | Cell Communication and Signaling |  Full Text
Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components | Cell Communication and Signaling | Full Text

Kinetics of Thapsigargin- Ca2+-ATPase (Sarcoplasmic Reticulum) Interaction  Reveals a Two-step Binding Mechanism and Picomolar Inhibition * - Journal  of Biological Chemistry
Kinetics of Thapsigargin- Ca2+-ATPase (Sarcoplasmic Reticulum) Interaction Reveals a Two-step Binding Mechanism and Picomolar Inhibition * - Journal of Biological Chemistry

Proteomic Signatures in Thapsigargin-Treated Hepatoma Cells | Chemical  Research in Toxicology
Proteomic Signatures in Thapsigargin-Treated Hepatoma Cells | Chemical Research in Toxicology

Cell death induced by the ER stressor thapsigargin involves death receptor  5, a non-autophagic function of MAP1LC3B, and distinct contributions from  unfolded protein response components | Cell Communication and Signaling |  Full Text
Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components | Cell Communication and Signaling | Full Text

Frontiers | The Cross-Links of Endoplasmic Reticulum Stress, Autophagy, and  Neurodegeneration in Parkinson's Disease
Frontiers | The Cross-Links of Endoplasmic Reticulum Stress, Autophagy, and Neurodegeneration in Parkinson's Disease

Endoplasmic reticulum stress signalling – from basic mechanisms to clinical  applications - Almanza - 2019 - The FEBS Journal - Wiley Online Library
Endoplasmic reticulum stress signalling – from basic mechanisms to clinical applications - Almanza - 2019 - The FEBS Journal - Wiley Online Library

MANF Ablation Causes Prolonged Activation of the UPR without  Neurodegeneration in the Mouse Midbrain Dopamine System | eNeuro
MANF Ablation Causes Prolonged Activation of the UPR without Neurodegeneration in the Mouse Midbrain Dopamine System | eNeuro

Thapsigargin promotes colorectal cancer cell migration through upregulation  of lncRNA MALAT1
Thapsigargin promotes colorectal cancer cell migration through upregulation of lncRNA MALAT1

Transient Receptor Potential Ankyrin-1 and Vanilloid-3 Differentially  Regulate Endoplasmic Reticulum Stress and Cytotoxicity in Human Lung  Epithelial Cells After Pneumotoxic Wood Smoke Particle Exposure | Molecular  Pharmacology
Transient Receptor Potential Ankyrin-1 and Vanilloid-3 Differentially Regulate Endoplasmic Reticulum Stress and Cytotoxicity in Human Lung Epithelial Cells After Pneumotoxic Wood Smoke Particle Exposure | Molecular Pharmacology

Molecules | Free Full-Text | Mipsagargin: The Beginning—Not the  End—of Thapsigargin Prodrug-Based Cancer Therapeutics
Molecules | Free Full-Text | Mipsagargin: The Beginning—Not the End—of Thapsigargin Prodrug-Based Cancer Therapeutics

SEC24A identified as an essential mediator of thapsigargin-induced cell  death in a genome-wide CRISPR/Cas9 screen | Cell Death Discovery
SEC24A identified as an essential mediator of thapsigargin-induced cell death in a genome-wide CRISPR/Cas9 screen | Cell Death Discovery