← Search

Omics · study · 2026

OASL Regulates Endothelial Function via USP39-Mediated Deubiquitination of CDK1 to Promote Large Full-Thickness Skin Defect Healing

Listed in NCBI GEO

Large full-thickness skin defects (LFSDs) remain a major clinical challenge due to insufficient vascular regeneration and impaired tissue repair.

Description

Emerging evidence suggests that oligoadenylate synthase-like protein (OASL), an interferon-stimulated protein, contributes to endothelial homeostasis and vascular function; however, its role in endothelial regeneration and wound healing has not been elucidated. Here, we investigated the molecular mechanism by which OASL regulates endothelial regeneration and explored its therapeutic potential for LFSD repair.

Links

Where it is published

Documentation and papers

Topics

From keywords
Life Sciences
Provenance · 1 source records, 7 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE33762914 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[organism].NCBITaxon:9606source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title