ArticleMolecular cell2012
The signaling adaptor GAB1 regulates cell polarity by acting as a PAR protein scaffold.
Article in Molecular cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
The trial behind it
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
23 citing papers in PubMed, 38 citations in OpenAlex.
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- NDR1/2 kinases regulate cell polarization and cell motility through Cdc42 GTPase and Pard3 signaling in mammalian cells.bioRxiv : the preprint server for biology · 2025Article
- The Role of GAB1 in Cancer.Cancers · 2023Review
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- Polarized endosome dynamics engage cytoplasmic Par-3 that recruits dynein during asymmetric cell division.Science advances · 2021Article
- CagA-ASPP2 complex mediates loss of cell polarity and favorsProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Elevated expression of Gab1 promotes breast cancer metastasis by dissociating the PAR complex.Journal of experimental & clinical cancer research : CR · 2019Article
- Structural Basis for MARK1 Kinase Autoinhibition by Its KA1 Domain.Structure (London, England : 1993) · 2018Article
- Cholinergic Grb2-Associated-Binding Protein 1 Regulates Cognitive Function.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Intramolecular autoinhibition of checkpoint kinase 1 is mediated by conserved basic motifs of the C-terminal kinase-associated 1 domain.The Journal of biological chemistry · 2017Article
- Molecular determinants of KA1 domain-mediated autoinhibition and phospholipid activation of MARK1 kinase.The Biochemical journal · 2017Article
- Uniformity under in vitro conditions: Changes in the phenotype of cancer cell lines derived from different medulloblastoma subgroups.PloS one · 2017Article
- Regulation of Cell Polarity by PAR-1/MARK Kinase.Current topics in developmental biology · 2017Review
- Scaffolding protein Gab1 regulates myeloid dendritic cell migration in allergic asthma.Cell research · 2016Article
- Article
- Dual function of partitioning-defective 3 in the regulation of YAP phosphorylation and activation.Cell discovery · 2016Article
- Structural insight into the mechanism of synergistic autoinhibition of SAD kinases.Nature communications · 2015Article
- PARD3 induces TAZ activation and cell growth by promoting LATS1 and PP1 interaction.EMBO reports · 2015Article
- Rewiring cell polarity signaling in cancer.Oncogene · 2015Review
- Establishment of epithelial polarity--GEF who's minding the GAP?Journal of cell science · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Cell polarity plays a key role in development and is disrupted in tumors, yet the molecules and mechanisms that regulate polarity remain poorly defined. We found that the scaffolding adaptor GAB1 interacts with two polarity proteins, PAR1 and PAR3. GAB1 binds PAR1 and enhances its kinase activity. GAB1 brings PAR1 and PAR3 into a transient complex, stimulating PAR3 phosphorylation by PAR1. GAB1 and PAR6 bind the PAR3 PDZ1 domain and thereby compete for PAR3 binding. Consequently, GAB1 depletion causes PAR3 hypophosphorylation and increases PAR3/PAR6 complex formation, resulting in accelerated and enhanced tight junction formation, increased transepithelial resistance, and lateral domain shortening. Conversely, GAB1 overexpression, in a PAR1/PAR3-dependent manner, disrupts epithelial apical-basal polarity, promotes multilumen cyst formation, and enhances growth factor-induced epithelial cell scattering. Our results identify GAB1 as a negative regulator of epithelial cell polarity that functions as a scaffold for modulating PAR protein complexes on the lateral membrane.
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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.