We are analyzing https://link.springer.com/article/10.1007/s11010-013-1663-1.

Title:
Transcriptional and post-translational regulation of mouse cation transport regulator homolog 1 | Molecular and Cellular Biochemistry
Description:
Recently, cation transport regulator homolog 1 (Chac1) has been identified as a novel pro-apoptotic factor in cells under endoplasmic reticulum (ER) stress. Of the three major ER stress sensors, it is suggested that ATF4 participates in the transcriptional regulation of Chac1 gene expression. The precise characterization of the Chac1 promoter, however, has not yet been elucidated. In this study, we detected the induction of Chac1 mRNA expression using DNA array analysis and RT-PCR of thapsigargin (Tg)-inducible genes in Neuro2a cells. Chac1 mRNA expression was also induced immediately following treatment with tunicamycin (Tm) and brefeldin A. Characterization of the mouse Chac1 promoter activity using a luciferase reporter assay revealed that the CREB/ATF element and amino acid response element in the mouse Chac1 promoter are functional and respond to Tm stimulation and ATF4 overexpression. Mutations in either element in the Chac1 promoter did not inhibit the responsiveness of this promoter to Tm and ATF4; however, mutations in both of these elements dramatically decreased the basal activity and response to ER stress stimuli. In addition to the transcriptional regulation, we found that Chac1 protein expression was only detected in the presence of MG132, a proteasome inhibitor, even though mouse Chac1 gene was transiently overexpressed in Neuro2a cells. Taken together, we are the first to demonstrate the transcriptional and post-translational regulation of Chac1 expression in a neuronal cell line.
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Keywords {🔍}

pubmed, article, cas, google, scholar, protein, cell, response, central, factor, atf, chac, stress, transcription, gene, biol, endoplasmic, reticulum, mammalian, element, regulation, promoter, unfolded, ohhashi, cells, kinase, mol, biochem, transcriptional, expression, activating, mouse, homolog, mrna, human, chem, privacy, cookies, content, information, regulator, hirata, kiuchi, induction, induced, access, gadd, nature, xbp, yoshida,

Topics {✒️}

heme-regulated eif-2α kinase month download article/chapter er stress-inducible gene time-dependent phase shift endoplasmic-reticulum-resident kinase elements dramatically decreased nutrient-sensing response pathway transcription factors eukaryotic initiation factor-2 mouse chac1 gene atf4-atf3-chop cascade full article pdf hamster gadd153 gene asparagine synthetase gene prodeath transcription factor chac1 gene expression endoplasmic reticulum kinase unfolded protein response nrf2-interacting protein post-translational regulation fornace aj jr endoplasmic reticulum stress privacy choices/manage cookies conditions privacy policy chac1 protein expression er stress stimuli serum response factor harding hp integrated stress response amino acid responsiveness stress-dependent induction cellular redox state protein translation oxidative stress-inducible creb/atf element erse-ii element chac1 mrna expression pro-apoptotic factor elevated mrna expression mouse chac1 promoter dna array analysis related subjects medical information sciences /ebp homology protein transcriptional regulation cellular biochemistry aims reduces protein synthesis regulatory hubs article molecular atf4-chop pathway

Questions {❓}

Johannessen M, Delghandi MP, Moens U (2004) What turns CREB on?

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         headline:Transcriptional and post-translational regulation of mouse cation transport regulator homolog 1
         description:Recently, cation transport regulator homolog 1 (Chac1) has been identified as a novel pro-apoptotic factor in cells under endoplasmic reticulum (ER) stress. Of the three major ER stress sensors, it is suggested that ATF4 participates in the transcriptional regulation of Chac1 gene expression. The precise characterization of the Chac1 promoter, however, has not yet been elucidated. In this study, we detected the induction of Chac1 mRNA expression using DNA array analysis and RT-PCR of thapsigargin (Tg)-inducible genes in Neuro2a cells. Chac1 mRNA expression was also induced immediately following treatment with tunicamycin (Tm) and brefeldin A. Characterization of the mouse Chac1 promoter activity using a luciferase reporter assay revealed that the CREB/ATF element and amino acid response element in the mouse Chac1 promoter are functional and respond to Tm stimulation and ATF4 overexpression. Mutations in either element in the Chac1 promoter did not inhibit the responsiveness of this promoter to Tm and ATF4; however, mutations in both of these elements dramatically decreased the basal activity and response to ER stress stimuli. In addition to the transcriptional regulation, we found that Chac1 protein expression was only detected in the presence of MG132, a proteasome inhibitor, even though mouse Chac1 gene was transiently overexpressed in Neuro2a cells. Taken together, we are the first to demonstrate the transcriptional and post-translational regulation of Chac1 expression in a neuronal cell line.
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      headline:Transcriptional and post-translational regulation of mouse cation transport regulator homolog 1
      description:Recently, cation transport regulator homolog 1 (Chac1) has been identified as a novel pro-apoptotic factor in cells under endoplasmic reticulum (ER) stress. Of the three major ER stress sensors, it is suggested that ATF4 participates in the transcriptional regulation of Chac1 gene expression. The precise characterization of the Chac1 promoter, however, has not yet been elucidated. In this study, we detected the induction of Chac1 mRNA expression using DNA array analysis and RT-PCR of thapsigargin (Tg)-inducible genes in Neuro2a cells. Chac1 mRNA expression was also induced immediately following treatment with tunicamycin (Tm) and brefeldin A. Characterization of the mouse Chac1 promoter activity using a luciferase reporter assay revealed that the CREB/ATF element and amino acid response element in the mouse Chac1 promoter are functional and respond to Tm stimulation and ATF4 overexpression. Mutations in either element in the Chac1 promoter did not inhibit the responsiveness of this promoter to Tm and ATF4; however, mutations in both of these elements dramatically decreased the basal activity and response to ER stress stimuli. In addition to the transcriptional regulation, we found that Chac1 protein expression was only detected in the presence of MG132, a proteasome inhibitor, even though mouse Chac1 gene was transiently overexpressed in Neuro2a cells. Taken together, we are the first to demonstrate the transcriptional and post-translational regulation of Chac1 expression in a neuronal cell line.
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