ArticleMolecular biology of the cell2005
GLUT1CBP(TIP2/GIPC1) interactions with GLUT1 and myosin VI: evidence supporting an adapter function for GLUT1CBP.
Article in Molecular biology of the cell, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- The Actin Motor Protein Myosin 6 Contributes to Cell Migration and Expression of GIPC1 and Septins in Breast Cancer Cells.Cancer management and research · 2024Article
- GIPC3 couples to MYO6 and PDZ domain proteins, and shapes the hair cell apical region.Journal of cell science · 2023Article
- GIPC3 couples to MYO6 and PDZ domain proteins and shapes the hair cell apical region.bioRxiv : the preprint server for biology · 2023Article
- GIPC1 promotes tumor growth and migration in gastric cancer via activating PDGFR/PI3K/AKT signaling.Oncology research · 2023Article
- G-alpha interacting protein interacting protein, C terminus 1 regulates epileptogenesis by increasing the expression of metabotropic glutamate receptor 7.CNS neuroscience & therapeutics · 2022Article
- Neural tube closure requires the endocytic receptor Lrp2 and its functional interaction with intracellular scaffolds.Development (Cambridge, England) · 2021Article
- Whole exome sequencing identified mutations causing hearing loss in five consanguineous Pakistani families.BMC medical genetics · 2020Article
- Myosin VI maintains the actin-dependent organization of the tubulobulbar complexes required for endocytosis during mouse spermiogenesis†‡.Biology of reproduction · 2020Article
- Article
- Distinct roles of two myosins in C. elegans spermatid differentiation.PLoS biology · 2019Article
- Engaging myosin VI tunes motility, morphology and identity in endocytosis.Traffic (Copenhagen, Denmark) · 2018Article
- Molecular Pharmacology of VEGF-A Isoforms: Binding and Signalling at VEGFR2.International journal of molecular sciences · 2018Review
- Structure analyses reveal a regulated oligomerization mechanism of the PlexinD1/GIPC/myosin VI complex.eLife · 2017Article
- Filopodia formation and endosome clustering induced by mutant plus-end-directed myosin VI.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Determination of GLUT1 Oligomerization Parameters using Bioluminescent Förster Resonance Energy Transfer.Scientific reports · 2016Article
- Neuropilin Functions as an Essential Cell Surface Receptor.The Journal of biological chemistry · 2015Review
- Signaling through the Phosphatidylinositol 3-Kinase (PI3K)/Mammalian Target of Rapamycin (mTOR) Axis Is Responsible for Aerobic Glycolysis mediated by Glucose Transporter in Epidermal Growth Factor Receptor (EGFR)-mutated Lung Adenocarcinoma.The Journal of biological chemistry · 2015Article
- PKCs Sweeten Cell Metabolism by Phosphorylation of Glut1.Molecular cell · 2015Article
- Receptor tyrosine kinases endocytosis in endothelium: biology and signaling.Arteriosclerosis, thrombosis, and vascular biology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We identified a novel interaction between myosin VI and the GLUT1 transporter binding protein GLUT1CBP(GIPC1) and first proposed that as an adapter molecule it might function to couple vesicle-bound proteins to myosin VI movement. This study refines the model by identifying two myosin VI binding domains in the GIPC1 C terminus, assigning respective oligomerization and myosin VI binding functions to separate N- and C-terminal domains, and defining a central region in the myosin VI tail that binds GIPC1. Data further supporting the model demonstrate that 1) myosin VI and GIPC1 interactions do not require a mediating protein; 2) the myosin VI binding domain in GIPC1 is necessary for intracellular interactions of GIPC1 with myosin VI and recruitment of overexpressed myosin VI to membrane structures, but not for the association of GIPC1 with such structures; 3) GIPC1/myosin VI complexes coordinately move within cellular extensions of the cell in an actin-dependent and microtubule-independent manner; and 4) blocking either GIPC1 interactions with myosin VI or GLUT1 interactions with GIPC1 disrupts normal GLUT1 trafficking in polarized epithelial cells, leading to a reduction in the level of GLUT1 in the plasma membrane and concomitant accumulation in internal membrane structures.
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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.