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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.
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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.
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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).
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Endoplasmic reticulum stress-related ATF6 upregulates CIP2A and contributes to the prognosis of colon cancer.
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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
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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
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Overexpression of the transcriptionally active N-terminal domain of ATF6 reversed the increases in IRE1 levels.
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Non-structural protein 2B of human rhinovirus16 induced an endoplasmic reticulum stress response through the PERK and ATF6 pathways rather than the IRE1 pathway.
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ATF6 expression correlates with precancerous changes and low-grade dysplasia in ulcerative colitis-associated colorectal cancer
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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.
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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.
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sustained intestinal activation of ATF6 in the colon to promote dysbiosis and microbiota-dependent tumorigenesis.
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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.
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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.
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Reporters constructed to monitor each mechanism show that phenobarbital-induced endoplasmic reticulum membrane expansion depends on transmembrane domain-induced ATF6
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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.
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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).
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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.
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Human ATF6 mutations interrupt distinct sequential steps of the ATF6 activation mechanism.
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Findings indicate a central role for activating transcription factor 6 (ATF6alpha) in the establishment of morphological features of senescence in normal primary fibroblasts.