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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 (show MCL1 Proteins), 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 (show SLC27A4 Proteins)-HLCs (show HLCS Proteins) could be enhanced by ATF5, c/EBPalpha (show CEBPA Proteins), and PROX1 (show PROX1 Proteins) 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 (show ECM1 Proteins), ATF5, and EOMES (show EOMES Proteins)) with potential anti-cancer functions that may promote the understanding of the molecular mechanisms of hepatocellular carcinoma development and progression.
the TAK1 (show MAP3K7 Proteins)-NLK (show NLK Proteins) pathway is a novel regulator of basal or IL-1beta (show IL1B Proteins)-triggered C/EBP (show CEBPA Proteins) 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 (show CEBPA Proteins) by impairing the interaction with p300 (show NOTCH1 Proteins)-C/EBPbeta (show CEBPB Proteins).
Both ATF5 and CHOP (show DDIT3 Proteins) 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 (show CREB3L2 Proteins)-ATF5-MCL1 (show MCL1 Proteins) pathway specifically suppressed ER stress-induced apoptosis in chondrocytes.
These findings indicate a reciprocal interaction between ATF5 and Shh (show SHH Proteins) in which Shh (show SHH Proteins) stimulates ATF5 expression and in which ATF5 contributes to Shh (show SHH Proteins)-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