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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.
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 (zeige SLC27A4 ELISA Kits)-HLCs (zeige HLCS ELISA Kits) could be enhanced by ATF5, c/EBPalpha (zeige CEBPA ELISA Kits), and PROX1 (zeige PROX1 ELISA Kits) 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 (zeige ECM1 ELISA Kits), ATF5, and EOMES (zeige EOMES ELISA Kits)) with potential anti-cancer functions that may promote the understanding of the molecular mechanisms of hepatocellular carcinoma development and progression.
the TAK1 (zeige MAP3K7 ELISA Kits)-NLK (zeige NLK ELISA Kits) pathway is a novel regulator of basal or IL-1beta (zeige IL1B ELISA Kits)-triggered C/EBP (zeige CEBPA ELISA Kits) activation though stabilization of ATF5
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
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 (zeige CEBPA ELISA Kits) by impairing the interaction with p300 (zeige NOTCH1 ELISA Kits)-C/EBPbeta (zeige CEBPB ELISA Kits).
Both ATF5 and CHOP (zeige DDIT3 ELISA Kits) 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 (zeige CREB3L2 ELISA Kits)-ATF5-MCL1 (zeige MCL1 ELISA Kits) pathway specifically suppressed ER stress-induced apoptosis in chondrocytes.
These findings indicate a reciprocal interaction between ATF5 and Shh (zeige SHH ELISA Kits) in which Shh (zeige SHH ELISA Kits) stimulates ATF5 expression and in which ATF5 contributes to Shh (zeige SHH ELISA Kits)-stimulated cerebellar granule neuron progenitor cell expansion.
Data show that transcription factor ATF5 is expressed in the postnatal brain.
essential in malignant glioma genesis and ATF5-mediated survival pathway identified
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