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Data suggest that ATF5 is modified by SUMO2/3 at a conserved SUMO-targeting consensus site; this SUMOylation of ATF5 appears to be required for transport of ATF5 to centrosome. (ATF5 = activating transcription factor-5; SUMO = small ubiquitin-like modifier)
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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, a transcriptional target of ATF5. Also provides evidence of decreased ATF5 being deleterious by rendering neurons more vulnerable to polyQ-induced apoptosis.
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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.
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Our results suggest that ATF5 promotes invasion by inducing the expression of integrin-alpha2 and integrin-beta1 in several human cancer cell lines.
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This study provides the first evidence that the methylation level of ATF5 decreased, and its mRNA expression was evidently up-regulated in glioma.
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These results suggest that the hepatic functions of the human iPS-HLCs could be enhanced by ATF5, c/EBPalpha, and PROX1 transduction.
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Activating transcription factor 5 enhances radioresistance and malignancy in cancer.
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Data show that ATF5 is an essential structural protein that is required for the interaction between the mother centriole and the pericentriolar material.
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Low expression level of ATF5 in hepatocellular carcinoma indicated aggressive tumor behavior and predicted a worse clinical outcome.
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Report a global loss of 5hmC identified three new genes (ECM1, ATF5, and EOMES) with potential anti-cancer functions that may promote the understanding of the molecular mechanisms of hepatocellular carcinoma development and progression.
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the TAK1-NLK pathway is a novel regulator of basal or IL-1beta-triggered C/EBP activation though stabilization of ATF5
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ATF5 promotes the proliferation of HSV-1 via a potential mechanism by which ATF5 enhances the transcription of viral genes during the course of an HSV-1 infection
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N-terminal hydrophobic amino acids play an important role in the regulation of ATF5 protein expression in IL-1beta-mediated immune response and that ATF5 is a negative regulator for IL-1beta-induced expression of SAA1 and SAA2 in HepG2 cells.
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The 5'-untranslated region regulates ATF5 mRNA stability via nonsense-mediated mRNA decay in response to environmental stress.
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demonstrated that interference with the function of ATF5 could markedly increase the apoptosis of ovarian cancer cells and identified B-cell leukemia lymphoma-2 as an ATF5-targeted apoptosis-related gene
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The evidence suggests a role for ATF5 in the regulation of osteogenic differentiation in adipose-derived stem cells.
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a mechanistic link between elevated NPM1 expression and depressed ATF5 in HCC and suggests that regulation of ATF5 by NPM1 plays an important role in the proliferation and survival of HCC.
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ATF5 polymorphisms influence ATF function and response to treatment in children with childhood acute lymphoblastic leukemia.
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coordinated actions by ATF5, p300, Elk-1, and ERK/mitogen-activated protein kinase are essential for ATF5-dependent Egr-1 activation and cell proliferation and survival
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an essential role for HSP70 in maintaining high levels of ATF5 expression in glioma cells and support the conclusion that ATF5 is an important substrate protein of HSP70 that mediates HSP70-promoted cell survival in glioma cells.
