ArticleDevelopmental cell2021
SH3BP4 promotes neuropilin-1 and α5-integrin endocytosis and is inhibited by Akt.
Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
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- Making gene editing accessible in resource limited environments: recommendations to guide a first-time user.Frontiers in genome editing · 2024Review
- TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.Cell death discovery · 2023Article
- Novel Alzheimer's disease genes and epistasis identified using machine learning GWAS platform.Scientific reports · 2023Article
- Organization, dynamics and mechanoregulation of integrin-mediated cell-ECM adhesions.Nature reviews. Molecular cell biology · 2023Review
- Induced nanoscale membrane curvature bypasses the essential endocytic function of clathrin.The Journal of cell biology · 2022Article
- Co-immunoprecipitation and semi-quantitative immunoblotting for the analysis of protein-protein interactions.STAR protocols · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cells probe their surrounding matrix for attachment sites via integrins that are internalized by endocytosis. We find that SH3BP4 regulates integrin surface expression in a signaling-dependent manner via clathrin-coated pits (CCPs). Dephosphorylated SH3BP4 at S246 is efficiently recruited to CCPs, while upon Akt phosphorylation, SH3BP4 is sequestered by 14-3-3 adaptors and excluded from CCPs. In the absence of Akt activity, SH3BP4 binds GIPC1 and targets neuropilin-1 and α5/β1-integrin for endocytosis, leading to inhibition of cell spreading. Similarly, chemorepellent semaphorin-3a binds neuropilin-1 to activate PTEN, which antagonizes Akt and thus recruits SH3BP4 to CCPs to internalize both receptors and induce cell contraction. In PTEN mutant non-small cell lung cancer cells with high Akt activity, expression of non-phosphorylatable active SH3BP4-S246A restores semaphorin-3a induced cell contraction. Thus, SH3BP4 links Akt signaling to endocytosis of NRP1 and α5/β1-integrins to modulate cell-matrix interactions in response to intrinsic and extrinsic cues.
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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.