Dataset Information

Cell-autonomous hepatocyte-specific GP130 signalling alone is sufficient to trigger robust innate immune response in mice

ABSTRACT: Members of the IL-6 cytokine family contribute to inflammatory and regenerative processes. Engagement of the signalling receptor subunit gp130 is common to almost all members of the family. In the liver, all major cell types respond to IL-6, making it difficult to delineate cell type-specific effects of IL-6 type cytokines. We therefore generated mouse models for liver cell type-specific analysis of IL-6 signalling.

INSTRUMENT(S): Orbitrap Fusion, Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Blood Plasma, Liver

SUBMITTER: Christoph Krisp

LAB HEAD: Dirk Schmidt-Arras

PROVIDER: PXD020744 | Pride | 2021-08-20

REPOSITORIES: Pride

ACCESS DATA

Publications

Cell-autonomous hepatocyte-specific GP130 signaling is sufficient to trigger a robust innate immune response in mice.

Schumacher Neele N Yan Karsten K Gandraß Monja M Müller Miryam M Krisp Christoph C Häsler Robert R Carambia Antonella A Nofer Jerzy-Roch JR Bernardes Joanna P JP Khouja Mouhamad M Thomsen Ilka I Chalupsky Karel K Bolik Julia J Hölscher Christoph C Wunderlich Thomas T Herkel Johannes J Rosenstiel Philip P Schramm Christoph C Schlüter Hartmut H Renné Thomas T Mittrücker Hans-Willi HW Rose-John Stefan S Schmidt-Arras Dirk D

Journal of hepatology 20200925 2

<h4>Background & aims</h4>Interleukin (IL)-6 cytokine family members contribute to inflammatory and regenerative processes. Engagement of the signaling receptor subunit gp130 is common to almost all members of the family. In the liver, all major cell types respond to IL-6-type cytokines, making it difficult to delineate cell type-specific effects. We therefore generated mouse models for liver cell type-specific analysis of IL-6 signaling.<h4>Methods</h4>We produced mice with a Cre-inducible expr ...[more]

PMID: 32987028

Similar Datasets

Project description:Here we exploit the essential process of X-chromosome dosage compensation to elucidate basic mechanisms that control the assembly, genome-wide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription. ChIP-chip experiments using antibodies against DPY-27, SDC-3, DPY-30, DPY-26, MIX-1, SMC-4, ASH-2 in wild-type embryos. ChIP-chip experiments using antibodies against SDC-3, DPY-27, DPY-30, ASH-2, and IgG in different DCC mutants. ChIP-chip experiments using antibodies against RNA Pol II (hypophosphorylated and S2 and S5) in wild type and sdc-2 partial loss of function mutants.

Dataset Information

Cell-autonomous hepatocyte-specific GP130 signalling alone is sufficient to trigger robust innate immune response in mice

Publications

Cell-autonomous hepatocyte-specific GP130 signaling is sufficient to trigger a robust innate immune response in mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure