CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis. - Wikidata - awgldk - TriplyDB

CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis.

CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis.

http://www.wikidata.org/entity/Q37056644

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Anticancer drugs for the modulation of endoplasmic reticulum stress and oxidative stress Limited ATF4 Expression in Degenerating Retinas with Ongoing ER Stress Promotes Photoreceptor Survival in a Mouse Model of Autosomal Dominant Retinitis Pigmentosa mtDNA, Metastasis, and the Mitochondrial Unfolded Protein Response (UPRmt).Selective mRNA translation during eIF2 phosphorylation induces expression of IBTKα.Dermal wound transcriptomic responses to Infection with Pseudomonas aeruginosa versus Klebsiella pneumoniae in a rabbit ear wound model.Integrated analyses of DNA methylation and hydroxymethylation reveal tumor suppressive roles of ECM1, ATF5, and EOMES in human hepatocellular carcinoma The Protective Effect of Lacidipine on Myocardial Remodeling Is Mediated by the Suppression in Expression of GPR78 and CHOP in Rats.Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element Translational Repression Protects Human Keratinocytes from UVB-Induced Apoptosis through a Discordant eIF2 Kinase Stress Response Ribosome Reinitiation Directs Gene-specific Translation and Regulates the Integrated Stress Response.Ribosome Elongation Stall Directs Gene-specific Translation in the Integrated Stress Response.Transcription factor ATF4 directs basal and stress-induced gene expression in the unfolded protein response and cholesterol metabolism in the liver.Translation Regulation of the Glutamyl-prolyl-tRNA Synthetase Gene EPRS through Bypass of Upstream Open Reading Frames with Noncanonical Initiation Codons Loss of CLPP alleviates mitochondrial cardiomyopathy without affecting the mammalian UPRmt.Regulation of PERK-eIF2α signalling by tuberous sclerosis complex-1 controls homoeostasis and survival of myelinating oligodendrocytes Regulation of the transcriptome by ER stress: non-canonical mechanisms and physiological consequences.ER-stress in Alzheimer's disease: turning the scale?Regulatory crosstalk within the mammalian unfolded protein response.Comparison of reprogramming genes in induced pluripotent stem cells and nuclear transfer cloned embryos.Stress management by autophagy: Implications for chemoresistance.Upstream Open Reading Frames Differentially Regulate Gene-specific Translation in the Integrated Stress Response The integrated stress response.The integrated stress response and proteotoxicity in cancer therapy.Integrating the UPRmt into the mitochondrial maintenance network.Mitochondrial dysfunction in cancer: Potential roles of ATF5 and the mitochondrial UPR.The Transcription Factor ATF5 Mediates a Mammalian Mitochondrial UPR The Mitochondrial Unfolded Protein Response as a Non-Oncogene Addiction to Support Adaptation to Stress during Transformation in Cancer and Beyond.Schlafen2 mutation unravels a role for chronic ER stress in the loss of T cell quiescence.ATF5 regulates β-cell survival during stress.The transcription factor ATF5: role in cellular differentiation, stress responses, and cancer.The mitochondrial UPR: mechanisms, physiological functions and implications in ageing.Mitochondrial targeted HSP90 inhibitor Gamitrinib-TPP (G-TPP) induces PINK1/Parkin-dependent mitophagy.Transcription Factor C/EBP Homologous Protein in Health and Diseases.Blood-brain barrier transport and neuroprotective potential of blackberry-digested polyphenols: an in vitro study.Recent insights into PERK-dependent signaling from the stressed endoplasmic reticulum.Translational control of a human CDKN1A mRNA splice variant regulates the fate of UVB-irradiated human keratinocytes.The eIF2-alpha kinase HRI: a potential target beyond the red blood cell.Modulation of Navitoclax Sensitivity by Dihydroartemisinin-Mediated MCL-1 Repression in BCR-ABL+ B-Lineage Acute Lymphoblastic Leukemia.UPRmt regulation and output: a stress response mediated by mitochondrial-nuclear communication.The mitochondrial unfolded protein response: Signaling from the powerhouse.

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CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis.

http://www.wikidata.org/entity/Q37056644

description

article científic

@ca

article scientifique

@fr

articolo scientifico

@it

artigo científico

@pt

bilimsel makale

@tr

scientific article published on 12 June 2013

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

CHOP induces activating transc ...... ations in protein homeostasis.

@en

CHOP induces activating transcription factor 5

@nl

type

label

CHOP induces activating transc ...... ations in protein homeostasis.

@en

CHOP induces activating transcription factor 5

@nl

prefLabel

CHOP induces activating transc ...... ations in protein homeostasis.

@en

CHOP induces activating transcription factor 5

@nl

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MBC.E13-01-0067

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Molecular Biology of the Cell

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CHOP induces activating transc ...... ations in protein homeostasis.

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Brian F Teske

http://www.w3.org/2001/XMLSchema#string

Donghui Zhou

http://www.w3.org/2001/XMLSchema#string

Jixiu Shan

http://www.w3.org/2001/XMLSchema#string

Michael E Fusakio

http://www.w3.org/2001/XMLSchema#string

Michael S Kilberg

http://www.w3.org/2001/XMLSchema#string

Ronald C Wek

http://www.w3.org/2001/XMLSchema#string

P2860

Nucleophosmin (NPM1/B23) interacts with activating transcription factor 5 (ATF5) protein and promotes proteasome- and caspase-dependent ATF5 degradation in hepatocellular carcinoma cells

ERAD inhibitors integrate ER stress with an epigenetic mechanism to activate BH3-only protein NOXA in cancer cells

Regulated translation initiation controls stress-induced gene expression in mammalian cells

CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

Feedback inhibition of the unfolded protein response by GADD34-mediated dephosphorylation of eIF2alpha

CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

Gadd153 sensitizes cells to endoplasmic reticulum stress by down-regulating Bcl2 and perturbing the cellular redox state

Downregulation of activating transcription factor 5 is required for differentiation of neural progenitor cells into astrocytes

The BCL-2 protein family: opposing activities that mediate cell death

The unfolded protein response: from stress pathway to homeostatic regulation

P304

2477-2490

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scholarly article

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10.1091/MBC.E13-01-0067

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15

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24

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Jeanette N. McClintick

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2013-06-12T00:00:00Z

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23761072

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3727939

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