ArticleCell communication and signaling : CCS2024
A non-catalytic role of IPMK is required for PLCγ1 activation in T cell receptor signaling by stabilizing the PLCγ1-Sam68 complex.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Structural insights into the development of inhibitors for inositol phosphate kinases.FEBS letters · 2026Review
- IPMK at the crossroads of cellular signaling in health and disease.FEBS letters · 2026Review
- Diagnostic and prognostic signatures of glomerular membrane dysregulation in immune nephropathies.Frontiers in immunology · 2026Article
- From Obscurity to Prominence: IPMK's Expanding Role in Cellular Signaling, Physiology, and Disease.Biomolecules · 2025Review
- Single-molecule analysis reveals that IPMK enhances the DNA-binding activity of the transcription factor SRF.Nucleic acids research · 2025Article
- Inositol Phosphate Kinase Architecture: Practical Approaches and Lessons Learned.Methods in molecular biology (Clifton, N.J.) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundPhospholipase C gamma 1 (PLCγ1) is an important mediator of the T cell receptor (TCR) and growth factor signaling. PLCγ1 is activated by Src family kinases (SFKs) and produces inositol 1,4,5-triphosphate (InsP
methodsConcanavalin A (ConA)-induced acute hepatitis model was established in CD4
resultsIPMK
conclusionsOur results demonstrate that IPMK non-catalytically promotes PLCγ1 phosphorylation by stabilizing the PLCγ1-Sam68 complex. Targeting IPMK in CD4
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Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.