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The results demonstrated that high expression of activated ATF6 aggravates ER stressinduced VEC (show CDH5 Proteins) apoptosis through the mitochondrial apoptotic pathway. Furthermore, in response to ER stress, ATF6 upregulates the expression of caspase3, caspase9, CHOP (show DDIT3 Proteins), cytochrome c (show CYCS Proteins) and Bax (show BAX Proteins)/Bcl2 (show BCL2 Proteins).
Reporters constructed to monitor each mechanism show that phenobarbital-induced endoplasmic reticulum membrane expansion depends on transmembrane domain-induced ATF6
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.
Three branches of the Unfolded Protein Response (UPR) have been described, including the activation of the inositol-requiring enzyme 1 (IRE1 (show ERN1 Proteins)), the pancreatic ER kinase (PKR (show PKLR Proteins))-like ER kinase (PERK (show EIF2AK3 Proteins)), and the activating transcription factor 6 (ATF6).
The expression of ASNS (show ASNS Proteins) was significantly elevated when ATF6 was over expressed. The expressions of these 2 genes were both decreased in hepatocellular carcinoma (HCC (show FAM126A Proteins))patients, and it was more significantly with ASNS (show ASNS Proteins). The mRNA levels of ASNS (show ASNS Proteins) and ATF6 were positively correlated with each other. rs34050735 was associated with HCC (show FAM126A Proteins) in the case-control study and also an independent predictor of overall survival of HCC (show FAM126A Proteins) patients.
Human ATF6 mutations interrupt distinct sequential steps of the ATF6 activation mechanism.
Findings indicate a central role for activating transcription factor 6 (ATF6alpha) in the establishment of morphological features of senescence in normal primary fibroblasts.
A novel homozygous c.1691A>G (p.(Asp564Gly)) ATF6 mutation was identified in two siblings with autosomal recessive cone-rod dystrophy.
This review shown that the achromatopsia arising from genetic mutations in Activating Transcription Factor 6 (ATF6).
In summary, our study revealed a negative regulation of the UPR transducer ATF6 through post-translational SUMOylation. The information from this study will not only increase our understanding of the fine-tuning regulation of the UPR signaling but will also be informative to the modulation of the UPR for therapeutic benefits.
DREAM inhibition markedly improves ATF6 processing in the hippocampus and that it might contribute to a delay in memory decline in Huntington (show HTT Proteins) mice.
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 (show THBS4 Proteins), which however is a sensitive indicator of obstruction.
ATF6 is essential for ER stress-mediated SESN2 (show SESN2 Proteins) induction.
Forced activation of the ATF6 UPR branch reduced infarct volume and improved functional outcome at 24 h after stroke
However, depletion of XBP1 (show XBP1 Proteins) and ATF6, alone or in combination, prevented autophagy induction and significantly enhanced Japanese encephalitis virus-induced cell death.
Deletion of Atf6alpha suppressed inflammation, and ameliorated demyelination after experimental autoimmune encephalomyelitis.
we show that overexpression of the dominant-negative form of ATF6 (dnATF6) increases susceptibility to develop hepatic steatosis in diet-induced insulin (show INS Proteins)-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 (show INS Proteins)-resistant mice.
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.
ATF6 serves as an important role between ER stress and oxidative stress, by decreasing myocardial ischemia/reperfusion damage.
ATF6alpha mRNA and protein levels were higher in the uterus near the implantation site following embryo implantation.
Exposure of endothelial cells to VEGF (show VEGFA Proteins), high glucose, or hydrogen peroxide up-regulated the XBP1 (show XBP1 Proteins)/IRE1 alpha (show ERN1 Proteins) and ATF6 arms of the unfolded protein response compared with untreated cells.
This gene encodes a transcription factor that activates target genes for the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress. Although it is a transcription factor, this protein is unusual in that it is synthesized as a transmembrane protein that is embedded in the ER. It functions as an ER stress sensor/transducer, and following ER stress-induced proteolysis, it functions as a nuclear transcription factor via a cis-acting ER stress response element (ERSE) that is present in the promoters of genes encoding ER chaperones. This protein has been identified as a survival factor for quiescent but not proliferative squamous carcinoma cells. There have been conflicting reports about the association of polymorphisms in this gene with diabetes in different populations, but another polymorphism has been associated with increased plasma cholesterol levels. This gene is also thought to be a potential therapeutic target for cystic fibrosis.
activating transcription factor 6
, cyclic AMP-dependent transcription factor ATF-6 alpha-like
, cAMP-dependent transcription factor ATF-6 alpha
, cyclic AMP-dependent transcription factor ATF-6 alpha