Browse our anti-ATF6 (ATF6) Antibodies

Human Activating Transcription Factor 6 (ATF6) interaction partners

1. Our data demonstrate a near absence of cone structure in subjects harboring ATF6 mutations. This implicates ATF6 as having a major role in cone development and suggests that at least a subset of subjects with ATF6-ACHM have markedly fewer cellular targets for cone-directed gene therapies than do subjects with CNGA3- or CNGB3-ACHM.

2. Pharmacologic inhibition or knock-down of downstream targets of ATF6a, protein disulfide isomerases (PDI) and ERO1b, a thiol oxidase that is involved in the re-oxidation of PDIs also independently induced pronounced killing of osteosarcoma (OS) cells following chemotherapy.

3. Findings indicate a role for activating transcription factor 6 (ATF6) during differentiation and identify a new strategy to generate mesodermal tissues through the modulation of the ATF6 arm of the unfolded protein response (UPR).

4. Endoplasmic reticulum stress-related ATF6 upregulates CIP2A and contributes to the prognosis of colon cancer.

5. we have demonstrated that ATF6alpha expression in mASM and hASM cells in vitro plays an important role in ASM proliferation and contractility, which are key features of asthma

6. miR-103/107-Wnt3a/beta-catenin-ATF6 pathway is critical to the progression of apoptosis in preadipocytes, which suggested that approaches to activate miR-103/107 could potentially be useful as new therapies for treating obesity and metabolic syndrome-related disorders

7. Overexpression of the transcriptionally active N-terminal domain of ATF6 reversed the increases in IRE1 levels.

8. Non-structural protein 2B of human rhinovirus16 induced an endoplasmic reticulum stress response through the PERK and ATF6 pathways rather than the IRE1 pathway.

9. ATF6 expression correlates with precancerous changes and low-grade dysplasia in ulcerative colitis-associated colorectal cancer

10. While PERK complexes shift to large complexes, ATF6alpha complexes are reduced to smaller complexes on endoplasmic reticulum (ER) stress. In contrast, IRE1alpha complexes were not significantly increased in size on ER stress, unless IRE1alpha is overexpressed.

11. 147 is a pro-drug that preferentially activates ATF6 signaling through a mechanism involving localized metabolic activation and selective covalent modification of endoplasmic reticulumresident proteins that regulate ATF6 activity.

12. sustained intestinal activation of ATF6 in the colon to promote dysbiosis and microbiota-dependent tumorigenesis.

13. results support a critical role of ATF6alpha in the establishment and maintenance of cellular senescence in normal human fibroblasts via the up-regulation of a COX2/PGE2 intracrine pathway.

14. The results demonstrated that high expression of activated ATF6 aggravates ER stressinduced VEC apoptosis through the mitochondrial apoptotic pathway. Furthermore, in response to ER stress, ATF6 upregulates the expression of caspase3, caspase9, CHOP, cytochrome c and Bax/Bcl2.

15. Reporters constructed to monitor each mechanism show that phenobarbital-induced endoplasmic reticulum membrane expansion depends on transmembrane domain-induced ATF6

16. ATF6 plays a distinct role in viral protein stability and the host uses different cleavage strategies, rather than conventional cleavage by generating p50ATF6, to combat viral infection.

17. Three branches of the Unfolded Protein Response (UPR) have been described, including the activation of the inositol-requiring enzyme 1 (IRE1), the pancreatic ER kinase (PKR)-like ER kinase (PERK), and the activating transcription factor 6 (ATF6).

18. The expression of ASNS was significantly elevated when ATF6 was over expressed. The expressions of these 2 genes were both decreased in hepatocellular carcinoma (HCC)patients, and it was more significantly with ASNS. The mRNA levels of ASNS and ATF6 were positively correlated with each other. rs34050735 was associated with HCC in the case-control study and also an independent predictor of overall survival of HCC patients.

19. Human ATF6 mutations interrupt distinct sequential steps of the ATF6 activation mechanism.

20. Findings indicate a central role for activating transcription factor 6 (ATF6alpha) in the establishment of morphological features of senescence in normal primary fibroblasts.

Mouse (Murine) Activating Transcription Factor 6 (ATF6) interaction partners

1. Compensatory cardiac hypertrophy activates ER stress and ATF6, which induces RHEB and activates mTORC1. Thus, ATF6 is a previously unrecognized link between growth stimuli and mTORC1-mediated cardiac growth.

2. we have demonstrated that ATF6alpha expression in mASM and hASM cells in vitro plays an important role in ASM proliferation and contractility, which are key features of asthma

3. deletion of ATF6alpha leads to modulated endoplasmic reticulum stress response and decreased survival in oligodendrocytes in response to ER stress and fails to improve locomotor deficits after spinal cord injury

4. Abolished activating transcription factor 6 (ATF6) exacerbated gluconeogenic metabolism by mechanistic target of rapamycin protein (MTOR) mediated down regulation of autophage.

5. Metaphyseal chondrodysplasia Schmid type disease severity in mice is increased by ATF6alpha ablation and decreased by ATF6beta ablation triggered by mutations in collagen X.

6. ATF6alpha deficiency renders myelinating oligodendrocytes sensitive to IFN-gamma-induced ER stress in the developing CNS; and renders oligodendrocytes vulnerable to inflammation during experimental autoimmune encephalomyelitis. The results presented in this study suggest that ATF6alpha deficiency increases the vulnerability of oligodendrocytes in immune-mediated demyelinating diseases.

7. DREAM inhibition markedly improves ATF6 processing in the hippocampus and that it might contribute to a delay in memory decline in Huntington mice.

8. The findings demonstrate reciprocal regulation of the unfolded protein response, including ATF6alpha activation and endoplasmic reticulum expansion, and reduced contractile differentiation in bladder outlet obstruction occurring independently of thrombospondin-4, which however is a sensitive indicator of obstruction.

9. ATF6 is essential for ER stress-mediated SESN2 induction.

10. Forced activation of the ATF6 UPR branch reduced infarct volume and improved functional outcome at 24 h after stroke

11. However, depletion of XBP1 and ATF6, alone or in combination, prevented autophagy induction and significantly enhanced Japanese encephalitis virus-induced cell death.

12. Deletion of Atf6alpha suppressed inflammation, and ameliorated demyelination after experimental autoimmune encephalomyelitis.

13. we show that overexpression of the dominant-negative form of ATF6 (dnATF6) increases susceptibility to develop hepatic steatosis in diet-induced insulin-resistant mice and fasted mice. Furthermore, hepatic overexpression of the active form of ATF6 promotes hepatic fatty acid oxidation and protects against hepatic steatosis in diet-induced insulin-resistant mice.

14. The present study extends our understanding and provides new insights into the physiological significance of ATF6, a key signal transducer of ER stress, in ovarian granulosa cells.

15. ATF6 serves as an important role between ER stress and oxidative stress, by decreasing myocardial ischemia/reperfusion damage.

16. ATF6alpha mRNA and protein levels were higher in the uterus near the implantation site following embryo implantation.

17. ATF6a favorably controls chondrogenesis and bone formation (1) by acting as a co-factor of Runx2 and enhancing Runx2-incited hypertrophic chondrocyte differentiation, and (2) by affecting IHH and PTHrP signaling.

18. Data show that EIF2AK3/PERK-mediated downregulation of miR-424(322)-503 cluster regulates optimal activation of IRE1 protein and activating transcription factor 6 (ATF6) during conditions of endoplasmic reticulum stress.

19. Our results suggest that ATF6alpha plays an important role in neuronal survival after KA-induced excitotoxicity through the regulation of Ca(2+) response and neuronal activity

20. results identify a role for DREAM silencing in the activation of ATF6 signaling, which promotes early neuroprotection in HD.

Cow (Bovine) Activating Transcription Factor 6 (ATF6) interaction partners

1. Exposure of endothelial cells to VEGF, high glucose, or hydrogen peroxide up-regulated the XBP1/IRE1 alpha and ATF6 arms of the unfolded protein response compared with untreated cells.