Browse our anti-ATF5 (ATF5) Antibodies

Human Activating Transcription Factor 5 (ATF5) interaction partners

1. 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 Antibodies), a transcriptional target of ATF5. Also provides evidence of decreased ATF5 being deleterious by rendering neurons more vulnerable to polyQ-induced apoptosis.

2. 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.

3. Our results suggest that ATF5 promotes invasion by inducing the expression of integrin-alpha2 and integrin-beta1 in several human cancer cell lines.

4. This study provides the first evidence that the methylation level of ATF5 decreased, and its mRNA expression was evidently up-regulated in glioma.

5. These results suggest that the hepatic functions of the human iPS (show SLC27A4 Antibodies)-HLCs (show HLCS Antibodies) could be enhanced by ATF5, c/EBPalpha (show CEBPA Antibodies), and PROX1 (show PROX1 Antibodies) transduction.

6. Activating transcription factor 5 enhances radioresistance and malignancy in cancer.

7. Data show that ATF5 is an essential structural protein that is required for the interaction between the mother centriole and the pericentriolar material.

8. Low expression level of ATF5 in hepatocellular carcinoma indicated aggressive tumor behavior and predicted a worse clinical outcome.

9. Report a global loss of 5hmC identified three new genes (ECM1 (show ECM1 Antibodies), ATF5, and EOMES (show EOMES Antibodies)) with potential anti-cancer functions that may promote the understanding of the molecular mechanisms of hepatocellular carcinoma development and progression.

10. the TAK1 (show MAP3K7 Antibodies)-NLK (show NLK Antibodies) pathway is a novel regulator of basal or IL-1beta (show IL1B Antibodies)-triggered C/EBP (show CEBPA Antibodies) activation though stabilization of ATF5

Mouse (Murine) Activating Transcription Factor 5 (ATF5) interaction partners

1. 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 Antibodies), a transcriptional target of ATF5. Also provides evidence of decreased ATF5 being deleterious by rendering neurons more vulnerable to polyQ-induced apoptosis.

2. Data indicate activating transcription factor 5 (ATF5) as a member of the transcriptional network governing pancreatic beta-cell survival during stress.

3. ATF5 is one of the transcription factors crucial for the vomeronasal sensory formation.

4. Atf5 is required for mouse olfactory bulb development via interneuron.

5. Data indicate that downregulation of ATF5 inhibits adipogenesis through C/EBPalpha (show CEBPA Antibodies) by impairing the interaction with p300 (show NOTCH1 Antibodies)-C/EBPbeta (show CEBPB Antibodies).

6. Both ATF5 and CHOP (show DDIT3 Antibodies) have proapoptotic functions in mouse embryonic fibroblasts.

7. Adult neurons express ATF5; its levels increase upon endoplasmic reticulum stress as a neuroprotective mechanism.

8. ATF5 is required for terminal differentiation and survival of olfactory sensory neurons.

9. BBF2H7 (show CREB3L2 Antibodies)-ATF5-MCL1 (show MCL1 Antibodies) pathway specifically suppressed ER stress-induced apoptosis in chondrocytes.

10. These findings indicate a reciprocal interaction between ATF5 and Shh (show SHH Antibodies) in which Shh (show SHH Antibodies) stimulates ATF5 expression and in which ATF5 contributes to Shh (show SHH Antibodies)-stimulated cerebellar granule neuron progenitor cell expansion.