ArticleJournal of cell science2012
A crucial role for Ras suppressor-1 (RSU-1) revealed when PINCH and ILK binding is disrupted.
Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Parvin is essential for indirect flight muscle (IFM) performance and Zasp52 localisation to the Z-disc in Drosophila melanogaster.Cell and tissue research · 2025Article
- The ILK-PINCH-parvin complex: a conserved primary adhesome regulating biological processes.Histochemistry and cell biology · 2025Review
- Genetic analyses in mouse fibroblast and melanoma cells demonstrate novel roles for PDGF-AB ligand and PDGF receptor alpha.Scientific reports · 2020Article
- Integrin-linked kinase (ILK) regulates KRAS, IPP complex and Ras suppressor-1 (RSU1) promoting lung adenocarcinoma progression and poor survival.Journal of molecular histology · 2020Article
- RSU-1 Maintains Integrity ofG3 (Bethesda, Md.) · 2020Article
- Ras Suppressor-1 (RSU1) in Cancer Cell Metastasis: A Tale of a Tumor Suppressor.International journal of molecular sciences · 2020Review
- Identification of a Multiplex Biomarker Panel for Hypertrophic Cardiomyopathy Using Quantitative Proteomics and Machine Learning.Molecular & cellular proteomics : MCP · 2020Observational
- Novel functions for integrin-associated proteins revealed by analysis of myofibril attachment ineLife · 2018Article
- Rsu1 contributes to cell adhesion and spreading in MCF10A cells via effects on P38 map kinase signaling.Cell adhesion & migration · 2015Article
- Rsu1 contributes to regulation of cell adhesion and spreading by PINCH1-dependent and - independent mechanisms.Journal of cell communication and signaling · 2013Article
- Interactions by 2D Gel Electrophoresis Overlap (iGEO): a novel high fidelity approach to identify constituents of protein complexes.Proteome science · 2013Article
- Elevated expression of the integrin-associated protein PINCH suppresses the defects of Drosophila melanogaster muscle hypercontraction mutants.PLoS genetics · 2013Article
- Cell adhesion in Drosophila: versatility of cadherin and integrin complexes during development.Current opinion in cell biology · 2012Review
- Parvin-ILK: An intimate relationship.Bioarchitecture · 2012Article
- Molecular basis for Ras suppressor-1 binding to PINCH-1 in focal adhesion assembly.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
PINCH, integrin-linked kinase (ILK) and Ras suppressor-1 (RSU-1) are molecular scaffolding proteins that form a physical complex downstream of integrins, and have overlapping roles in cellular adhesion. In Drosophila, PINCH and ILK colocalize in cells and have indistinguishable functions in maintaining wing adhesion and integrin to actin linkage in the muscle. We sought to determine whether the direct physical interaction between PINCH and ILK was essential for their functions using transgenic flies expressing a version of PINCH with a point mutation that disrupts ILK binding (PINCH(Q38A)). We demonstrate that the PINCH-ILK interaction is not required for viability, for integrin-mediated adhesion of the wing or muscle, or for maintaining appropriate localization or levels of either PINCH or ILK. These results suggest alternative modes for PINCH localization, stabilization and linkage to the actin cytoskeleton that are independent of a direct interaction with ILK. Furthermore, we identified a synthetic lethality in flies carrying both the PINCH(Q38A) mutation and a null mutation in the gene encoding RSU-1. This lethality does not result from PINCH mislocalization or destabilization, and illustrates a novel compensatory role for RSU-1 in maintaining viability in flies with compromised PINCH-ILK binding. Taken together, this work highlights the existence of redundant mechanisms in adhesion complex assembly that support integrin function in vivo.
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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 OpenQuestion graph.