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Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [H3K27ac ChIP-seq]

ABSTRACT: To examined the epigenetic alteration in male Nkx6.1 control and cKO spinal cord astrocytes

ORGANISM(S): Mus musculus

PROVIDER: GSE282688 | GEO | 2024/12/05

REPOSITORIES: GEO

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Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [Nkx6.1 ChIP-seq]

Project description:To profile gene expression expresion in astrocytes between control and Nkx6.1 conditional knockout astrocytes in the mouse spinal cord. Furthermore, we sought to profile DNA binding patterns regulated by Nkx6.1 in spinal cord astrocyte.

2024-12-05 | GSE282687 | GEO

Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [RNA-seq]

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2024-12-05 | GSE282689 | GEO

Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [Nkx6.1 ChIP-seq]

Project description:Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [Nkx6.1 ChIP-seq]

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Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [H3K27ac ChIP-seq]

Project description:Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [H3K27ac ChIP-seq]

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Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [RNA-seq]

Project description:Sex-Specific Astrocyte Regulation of Spinal Motor Circuits by Nkx6.1 [RNA-seq]

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In vivo analysis of astrocyte ribosome-associated mRNA after traumatic spinal cord injury

Project description:Analysis of gene expression by astrocytes or non-astrocyte cells in spinal cord injury (SCI) lesions may lead to the identification of molecules that impact on axon regrowth. We conducted genome-wide RNA sequencing of (i) immunoprecipitated astrocyte-specific ribosome-associated RNA (ramRNA) from WT or STAT3-CKO astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples 14 days following SCI. DOI: 10.1038/nature17623 Young adult female mGFAP-Cre-RiboTag or mGFAP-Cre-RiboTag-STAT3-LoxP mice underwent severe crush SCI at thoracic level 10. 14 days following SCI, the central 3mm of the SCI lesion was extracted, homogenized and (i) astrocyte-specific ribosome-associated RNA (ramRNA) precipitated via a hemagglutinin (HA) tag targeted to either WT (n=4) or STAT3-CKO (n=3) astrocytes, and (ii) the non-precipitated (flow-through) RNA deriving from non-astrocyte cells in the same tissue samples. Sex and age-matched mGFAP-Cre-RiboTag mice served as uninjured controls (n=4).

2016-03-30 | E-GEOD-76097 | biostudies-arrayexpress

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2016-03-30 | GSE76097 | GEO

Identification of Nkx6.1 regulated genes in mature pancreatic islets.

2013-09-12 | GSE40470 | GEO

Identification of Nkx6.1 regulated genes in mature pancreatic islets.

Project description:Nkx6.1 target genes were identified in mature pancreatic islets by comparing gene expression in conditional Nkx6.1-ablated islets versus control islets using microarray analysis. Nkx6.1 was conditionally ablated in mature pancreatic islets by recombination of a Nkx6.1-flox allele using the tamoxifen-inducible Pdx1-CreERTM allele (Gu et al 2002). Mice were injected with 2 mg/25 g tamoxifen in corn oil four times between 4 and 6 weeks of age. Islets were isolated after the final tamoxifen injection. Total RNA was isolated and pooled from pancreata of 6 week old Nkx6.1fl/-;Pdx1-CreERTM (mutant) versus Nkx6.1fl/+;Pdx1-CreERTM (control) littermates for 3 biological replicates.

2013-09-12 | E-GEOD-40470 | biostudies-arrayexpress

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Project description:Loss of functional beta-cell mass is a hallmark of Type 1 and Type 2 diabetes, and methods for restoring these cells are needed. We have previously reported that overexpression of the homeodomain transcription factor Nkx6.1 in rat pancreatic islets induces beta-cell proliferation and enhances glucose-stimulated insulin secretion, but the pathway by which Nkx6.1 activates beta-cell expansion has not been defined. Here we demonstrate that Nkx6.1 induces expression of the Nr4a1 and Nr4a3 orphan nuclear receptors, and that these factors are both necessary and sufficient for Nkx6.1-mediated beta-cell proliferation. Consistent with this finding, global knockout of Nr4a1 results in a decrease in beta-cell area in neonatal and young mice. Overexpression of Nkx6.1 and the Nr4a receptors results in increased expression of key cell cycle inducers E2F1 and cyclin E1. Furthermore, Nkx6.1 and Nr4a receptors induce components of the anaphase-promoting complex, including Ube2c, resulting in degradation of the cell cycle inhibitor p21CIP1. These studies identify a new bipartite pathway for activation of beta-cell proliferation, suggesting several new targets for expansion of functional beta-cell mass. We set up a microarray using primary rat islets that were left untreated or transduced with adenoviruses overexpressing betagal or Nkx6.1 for 48 h.

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