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Study reports that reduced levels of ATF5 in brain of Huntington's disease patients, probably due to its sequestration into the characteristic PolyQ containing neuronal inclusion bodies, correlates with decreased levels of the antiapoptotic protein MCL1 (显示 MCL1 蛋白), a transcriptional target of ATF5. Also provides evidence of decreased ATF5 being deleterious by rendering neurons more vulnerable to polyQ-induced apoptosis.
ATF5 expression can rescue UPR(mt) signaling in atfs-1-deficient worms requiring the same UPR(mt) promoter element identified in C. elegans. Furthermore, mammalian cells require ATF5 to maintain mitochondrial activity during mitochondrial stress and promote organelle recovery. Combined, these data suggest that regulation of the UPR(mt) is conserved from worms to mammals.
Our results suggest that ATF5 promotes invasion by inducing the expression of integrin-alpha2 and integrin-beta1 in several human cancer cell lines.
This study provides the first evidence that the methylation level of ATF5 decreased, and its mRNA expression was evidently up-regulated in glioma.
These results suggest that the hepatic functions of the human iPS (显示 SLC27A4 蛋白)-HLCs (显示 HLCS 蛋白) could be enhanced by ATF5, c/EBPalpha (显示 CEBPA 蛋白), and PROX1 (显示 PROX1 蛋白) transduction.
Activating transcription factor 5 enhances radioresistance and malignancy in cancer.
Data show that ATF5 is an essential structural protein that is required for the interaction between the mother centriole and the pericentriolar material.
Low expression level of ATF5 in hepatocellular carcinoma indicated aggressive tumor behavior and predicted a worse clinical outcome.
Report a global loss of 5hmC identified three new genes (ECM1 (显示 ECM1 蛋白), ATF5, and EOMES (显示 EOMES 蛋白)) with potential anti-cancer functions that may promote the understanding of the molecular mechanisms of hepatocellular carcinoma development and progression.
the TAK1 (显示 MAP3K7 蛋白)-NLK (显示 NLK 蛋白) pathway is a novel regulator of basal or IL-1beta (显示 IL1B 蛋白)-triggered C/EBP (显示 CEBPA 蛋白) activation though stabilization of ATF5
Data indicate activating transcription factor 5 (ATF5) as a member of the transcriptional network governing pancreatic beta-cell survival during stress.
ATF5 is one of the transcription factors crucial for the vomeronasal sensory formation.
Atf5 is required for mouse olfactory bulb development via interneuron.
Data indicate that downregulation of ATF5 inhibits adipogenesis through C/EBPalpha (显示 CEBPA 蛋白) by impairing the interaction with p300 (显示 NOTCH1 蛋白)-C/EBPbeta (显示 CEBPB 蛋白).
Both ATF5 and CHOP (显示 DDIT3 蛋白) have proapoptotic functions in mouse embryonic fibroblasts.
Adult neurons express ATF5; its levels increase upon endoplasmic reticulum stress as a neuroprotective mechanism.
ATF5 is required for terminal differentiation and survival of olfactory sensory neurons.
BBF2H7 (显示 CREB3L2 蛋白)-ATF5-MCL1 (显示 MCL1 蛋白) pathway specifically suppressed ER stress-induced apoptosis in chondrocytes.
These findings indicate a reciprocal interaction between ATF5 and Shh (显示 SHH 蛋白) in which Shh (显示 SHH 蛋白) stimulates ATF5 expression and in which ATF5 contributes to Shh (显示 SHH 蛋白)-stimulated cerebellar granule neuron progenitor cell expansion.
plays a role in inhibition of nerve growth factor-induced neuronal outgrowth and regulation of neurogenesis
activating transcription factor 5
, cAMP-dependent transcription factor ATF-5
, cyclic AMP-dependent transcription factor ATF-5
, transcription factor ATFx
, BZIP protein ATF7
, NRIF3-associated protein
, activating transcription factor 5-alpha/beta
, activating transcription factor 7
, activating transcription factor X
, transcription factor-like protein ODA-10