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Time series XBP1s ChIP-Seq in wild-type mice and XBP1 liver-specific knockout mice

ABSTRACT: We reported the liver XBP1s cistrome (taken at 4h interval for a total of 48 hrs) in the liver of wild-type mice and XBP1 liver-specific knockout mice

ORGANISM(S): Mus musculus

PROVIDER: GSE130760 | GEO | 2019/11/26

REPOSITORIES: GEO

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Time course XBP1s ChIP-Seq in Xbp1 flx/flx (WT, wild-type) mice and AlbCre;Xbp1 flx/flx (XBP1 LKO, liver-specific knockout) mice

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Time series XBP1s ChIP-Seq in wild-type mice and XBP1 liver-specific knockout mice

Project description:Time series XBP1s ChIP-Seq in wild-type mice and XBP1 liver-specific knockout mice

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Time course XBP1s ChIP-Seq in Xbp1 flx/flx (WT, wild-type) mice and AlbCre Xbp1 flx/flx (XBP1 LKO, liver-specific knockout) mice

Project description:Time course XBP1s ChIP-Seq in Xbp1 flx/flx (WT, wild-type) mice and AlbCre Xbp1 flx/flx (XBP1 LKO, liver-specific knockout) mice

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Profiling gene expression in 32Dcl3 cells following Xbp1 retrovirus vector transfection

Project description:The significant changes of hematopoietic cells induced by Xbp1S expression indicate that there is global alteration in gene expression. UPR induces transcription of Xbp1, and phosphorylation of the ER transmembrane kinase IRE1 initiates UPR-mediated mRNA splicing of Xbp1, resulting in the production of Xbp1S, an active form of a basic leucine zipper transcription factor. In the present study, Xbp1S retrovirus vector infected 32cl3 cells show cell cycle arrest and myeloid differentiation. Xbp1S may modulate important genes of differentiation and the cell cycle. RNA samples extracted from 32Dcl3 cells with pMIG (empty vector), pMY-Xbp1U (unspliced form) and pMY-Xbp1S (spliced form) retroviral vector transfected cells were subjected to expression profiling using the Affymetrix GeneChip microarray system.

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Adipocyte XBP1s regulates systemic insulin sensitivity by modulating adiponectin multimerization

Project description:The physiological role of the spliced form of X-box-binding protein 1 (XBP1s), a key transcription factor of the endoplasmic reticulum (ER) stress response, in adipose tissue remains largely unknown. Here we show that overexpression of XBP1s promotes adiponectin multimerization in adipocytes, thereby regulating systemic glucose homeostasis. Ectopic expression of XBP1s in adipocytes improves glucose tolerance and insulin sensitivity in both lean and obese (ob/ob) mice. The beneficial effect of adipocyte XBP1s on glucose homeostasis is associated with elevated serum levels of HMW adiponectin and indeed, is adiponectin dependent. Mechanistically, XBP1s promotes adiponectin multimerization rather than activating its transcription likely through a direct regulation of the expression of several ER-chaperones involved in adiponectin maturation, including Grp78, Pdia6, ERp44 and DsbA-L. Thus, we conclude that XBP1s is an important regulator of adiponectin multimerization, which may lead to a new therapeutic approach for the treatment of type 2 diabetes and hypoadiponectinemia. Epididymal adipose tissue from wild type and XBP1-overexpressing mice was subjected to gene expression profiling.

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