ArticleProceedings of the National Academy of Sciences of the United States of America2011
Full activity of the deleted in liver cancer 1 (DLC1) tumor suppressor depends on an LD-like motif that binds talin and focal adhesion kinase (FAK).
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 105 citations in OpenAlex.
- Article
- Filamin a binds deleted in liver cancer 1 (DLC1) to promote its tumor suppressor activity and inhibit the SRF coactivator MRTF-A.Neoplasia (New York, N.Y.) · 2026Article
- Mechanosensitive biochemical imprinting of the talin interaction with DLC1 regulates RhoA activity and cardiomyocyte remodeling.Science advances · 2025Article
- Focal adhesion in the tumour metastasis: from molecular mechanisms to therapeutic targets.Biomarker research · 2025Review
- The pro-oncogenic noncanonical activity of a RAS•GTP:RanGAP1 complex facilitates nuclear protein export.Nature cancer · 2024Article
- DLC1 promotes mechanotransductive feedback for YAP via RhoGAP-mediated focal adhesion turnover.Journal of cell science · 2024Article
- The focal adhesion protein talin is a mechanically gated A-kinase anchoring protein.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- CDK5: an oncogene or an anti-oncogene: location location location.Molecular cancer · 2023Review
- The molecular and clinical role of Tensin 1/2/3 in cancer.Journal of cellular and molecular medicine · 2023Review
- The role of single protein elasticity in mechanobiology.Nature reviews. Materials · 2023Article
- SH3 domain regulation of RhoGAP activity: Crosstalk between p120RasGAP and DLC1 RhoGAP.Nature communications · 2022Article
- Talin‑1 interaction network in cellular mechanotransduction (Review).International journal of molecular medicine · 2022Review
- Proteasomal turnover of the RhoGAP tumor suppressor DLC1 is regulated by HECTD1 and USP7.Scientific reports · 2022Article
- DLC1 inhibits colon adenocarcinoma cell migration by promoting secretion of the neurotrophic factor MANF.Frontiers in oncology · 2022Article
- Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein.Nature communications · 2021Article
- The tumor suppressor activity of DLC1 requires the interaction of its START domain with Phosphatidylserine, PLCD1, and Caveolin-1.Molecular cancer · 2021Article
- Talin rod domain-containing protein 1 (TLNRD1) is a novel actin-bundling protein which promotes filopodia formation.The Journal of cell biology · 2021Article
- Initiation of focal adhesion assembly by talin and kindlin: A dynamic view.Protein science : a publication of the Protein Society · 2021Review
- Mechanical Unfolding of Proteins-A Comparative Nonequilibrium Molecular Dynamics Study.Biophysical journal · 2020Article
- Cancer-Associated Point Mutations in theCancer research · 2020Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The deleted in liver cancer 1 (DLC1) tumor suppressor gene, which is frequently inactivated in cancer, encodes a Rho-GAP (GTPase activating protein) focal adhesion protein whose negative regulation of Rho-GTPases is necessary but not sufficient for its full tumor suppressor activity. Here, we report that DLC1 forms a complex with two prooncogenic focal adhesion proteins, talin and the focal adhesion kinase (FAK). We identified an 8-aa sequence (residues 469LDDILYHV476) in DLC1 and designated it an LD-like motif, because it shares homology with the LD motifs of paxillin. This motif was necessary for DLC1 binding to talin and FAK, because a DLC1 mutant, from which six of the residues have been deleted, and another mutant carrying amino acid substitutions in three of the residues are deficient for binding both proteins and localization of DLC1 to focal adhesions. FAK binding was independent of talin and vice versa. In bioassays, both DLC1 mutants were less active than wild-type (WT) DLC1, although the ability of the mutants to negatively regulate overall Rho-GTP was not impaired. We conclude that the LD-like motif, which binds talin and FAK, is required for the full tumor suppressor activity of DLC1 and contributes to the association of DLC1 with focal adhesions.
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