Transcriptomics

Dataset Information

0

Integrin b1 acetylation-induced transcriptomic reprograming of mouse embryonic endothelial cells and functions


ABSTRACT: Reciprocal regulation of integrin-dependent cell-matrix adhesions and cell-cell junctions is critical for controlling endothelial permeability and proliferation in cancer and inflammatory diseases, but remain poorly understood. Here, we investigated how acetylation of the distal NPKY-motif of b1-integrin influences endothelial cell physiology and barrier function. Expression of an acetylation-mimetic B1A-K794Q-GFP mutant induced transcriptomic reprograming of embryonic endothelial cells particularly in genes responsible for cell adhesion, proliferation, polarity and barrier function. B1A-K794Q-GFP induced a constitutive activation of MAPK signaling, an impairment of junctions, increased proliferation and an altered contact inhibition at confluency. Structural analysis of integrin b1 interaction with KINDLIN-2, biochemical pulldown assay and molecular dynamic analysis showed that acetylation of K794 increases KINDLIN-2 binding to the integrin b1 cytoplasmic tail. Accordingly, altering KINDLIN-2 levels modified Claudin-5 expression and endothelial barrier function. Revealing how integrin b1 acetylation regulates endothelial cell junctions offers new therapeutic possibilities for controlling vascular permeability.

ORGANISM(S): Mus musculus

PROVIDER: GSE238019 | GEO | 2024/01/01

REPOSITORIES: GEO

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1

Similar Datasets

2015-12-16 | E-GEOD-76020 | biostudies-arrayexpress
2023-06-10 | GSE205882 | GEO
2015-12-16 | GSE76020 | GEO
2020-06-08 | PXD019110 | Pride
| PRJNA997375 | ENA
2016-04-20 | GSE78184 | GEO
2023-03-13 | GSE213099 | GEO
2021-11-25 | PXD026711 | Pride
2020-07-20 | PXD017088 | Pride
2014-04-06 | E-GEOD-48443 | biostudies-arrayexpress