ArticleThe Journal of biological chemistry2010
The 19-amino acid insertion in the tumor-associated splice isoform Rac1b confers specific binding to p120 catenin.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Deconvoluting the multi-faceted roles of alternative splicing events in cancer: From underlying mechanisms to innovative therapeutics.Acta pharmaceutica Sinica. B · 2026Review
- The Roles of RAC1 and RAC1B in Colorectal Cancer and Their Potential Contribution to Cetuximab Resistance.Cancers · 2024Review
- Alternative splicing in EMT and TGF-β signaling during cancer progression.Seminars in cancer biology · 2024Review
- Protein music of enhanced musicality by music style guided exploration of diverse amino acid properties.Heliyon · 2021Article
- The Small GTPase RAC1B: A Potent Negative Regulator of-and Useful Tool to Study-TGFβ Signaling.Cancers · 2020Review
- Review
- RAC1B: A Rho GTPase with Versatile Functions in Malignant Transformation and Tumor Progression.Cells · 2019Review
- Activated Rho GTPases in Cancer-The Beginning of a New Paradigm.International journal of molecular sciences · 2018Review
- The Rac1 splice form Rac1b favors mouse colonic mucosa regeneration and contributes to intestinal cancer progression.Oncogene · 2018Article
- Review
- Cadherins function during the collective cell migration of Xenopus Cranial Neural Crest cells: revisiting the role of E-cadherin.Mechanisms of development · 2017Review
- Therapeutic Potential of Matrix Metalloproteinase Inhibition in Breast Cancer.Journal of cellular biochemistry · 2017Review
- EMT and stemness: flexible processes tuned by alternative splicing in development and cancer progression.Molecular cancer · 2017Review
- Rac1b enhances cell survival through activation of the JNK2/c-JUN/Cyclin-D1 and AKT2/MCL1 pathways.Oncotarget · 2016Article
- Tumor cell expression of MMP3 as a prognostic factor for poor survival in pancreatic, pulmonary, and mammary carcinoma.Genes & cancer · 2015Article
- Matrix metalloproteinases as breast cancer drivers and therapeutic targets.Frontiers in bioscience (Landmark edition) · 2015Review
- Regulation of epithelial-mesenchymal transition in breast cancer cells by cell contact and adhesion.Cancer informatics · 2015Article
- Tumor cell-derived MMP3 orchestrates Rac1b and tissue alterations that promote pancreatic adenocarcinoma.Molecular cancer research : MCR · 2014Article
- PTP-PEST targets a novel tyrosine site in p120 catenin to control epithelial cell motility and Rho GTPase activity.Journal of cell science · 2014Article
- Rac1b negatively regulates TGF-β1-induced cell motility in pancreatic ductal epithelial cells by suppressing Smad signalling.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The Rac1b splice isoform contains a 19-amino acid insertion not found in Rac1; this insertion leads to decreased GTPase activity and reduced affinity for GDP, resulting in the intracellular predominance of GTP-bound Rac1b. Here, using co-precipitation and proteomic methods, we find that Rac1b does not bind to many common regulators of Rho family GTPases but that it does display enhanced binding to SmgGDS, RACK1, and p120 catenin (p120(ctn)), proteins involved in cell-cell adhesion, motility, and transcriptional regulation. We use molecular modeling and structure analysis approaches to determine that the interaction between Rac1b and p120(ctn) is dependent upon protein regions that are predicted to be unstructured in the absence of molecular complex formation, suggesting that the interaction between these two proteins involves coupled folding and binding. We also find that directed cell movement initiated by Rac1b is dependent upon p120. These results define a distinct binding functionality of Rac1b and provide insight into how the distinct phenotypic program activated by this protein may be implemented through molecular recognition of effectors distinct from those of Rac1.
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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.