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Thapsigargin-induced severe ER stress stimulates release of... | Download  Scientific Diagram
Thapsigargin-induced severe ER stress stimulates release of... | Download Scientific Diagram

Figure S2. Thapsigargin-induced ER Ca 2+ release is reduced in STIM1KO... |  Download Scientific Diagram
Figure S2. Thapsigargin-induced ER Ca 2+ release is reduced in STIM1KO... | Download Scientific Diagram

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

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

Unfolded Protein Response (UPR) and Endoplasmic Reticulum (ER) Stress FAQs
Unfolded Protein Response (UPR) and Endoplasmic Reticulum (ER) Stress FAQs

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

Thapsigargin - Wikipedia
Thapsigargin - Wikipedia

Effect of endoplasmic reticulum stress on metabolic and stress signaling  and kidney-specific functions in Madin-Darby bovine kid
Effect of endoplasmic reticulum stress on metabolic and stress signaling and kidney-specific functions in Madin-Darby bovine kid

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

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

Neuronal Apoptosis Induced by Endoplasmic Reticulum Stress Is Regulated by  ATF4–CHOP-Mediated Induction of the Bcl-2 Homology 3-Only Member PUMA |  Journal of Neuroscience
Neuronal Apoptosis Induced by Endoplasmic Reticulum Stress Is Regulated by ATF4–CHOP-Mediated Induction of the Bcl-2 Homology 3-Only Member PUMA | Journal of Neuroscience

Effects of endoplasmic reticulum stress on apoptosis induction in  radioresistant macrophages
Effects of endoplasmic reticulum stress on apoptosis induction in radioresistant macrophages

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

JNK activation by thapsigargin versus saturated free fatty acid (SFA).... |  Download Scientific Diagram
JNK activation by thapsigargin versus saturated free fatty acid (SFA).... | Download Scientific Diagram

IJMS | Free Full-Text | An Involvement of Oxidative Stress in Endoplasmic  Reticulum Stress and Its Associated Diseases
IJMS | Free Full-Text | An Involvement of Oxidative Stress in Endoplasmic Reticulum Stress and Its Associated Diseases

MITOL prevents ER stress‐induced apoptosis by IRE1α ubiquitylation at ER–mitochondria  contact sites | The EMBO Journal
MITOL prevents ER stress‐induced apoptosis by IRE1α ubiquitylation at ER–mitochondria contact sites | The EMBO Journal

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

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

Endoplasmic reticulum stress, the unfolded protein response and autophagy  in kidney diseases | Nature Reviews Nephrology
Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases | Nature Reviews Nephrology

Pancreatic INS-1 β-Cell Response to Thapsigargin and Rotenone: A  Comparative Proteomics Analysis Uncovers Key Pathways of β-Cell Dysfunction  | Chemical Research in Toxicology
Pancreatic INS-1 β-Cell Response to Thapsigargin and Rotenone: A Comparative Proteomics Analysis Uncovers Key Pathways of β-Cell Dysfunction | 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

Endoplasmic Reticulum Stress Mediates Vascular Smooth Muscle Cell  Calcification via Increased Release of Grp78 (Glucose-Regulated Protein, 78  kDa)-Loaded Extracellular Vesicles | Arteriosclerosis, Thrombosis, and  Vascular Biology
Endoplasmic Reticulum Stress Mediates Vascular Smooth Muscle Cell Calcification via Increased Release of Grp78 (Glucose-Regulated Protein, 78 kDa)-Loaded Extracellular Vesicles | Arteriosclerosis, Thrombosis, and Vascular Biology