ArticleJournal of cellular physiology2010
GPCR kinase 2 interacting protein 1 (GIT1) regulates osteoclast function and bone mass.
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Dendronized chitosan hydrogel with GIT1 to accelerate bone defect repair through increasing local neovascular amount.Bone reports · 2023Article
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- Microcephaly with altered cortical layering in GIT1 deficiency revealed by quantitative neuroimaging.Magnetic resonance imaging · 2021Article
- Macrophage GIT1 Contributes to Bone Regeneration by Regulating Inflammatory Responses in an ERK/NRF2-Dependent Way.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- The Role of Autophagy in Osteoclast Differentiation and Bone Resorption Function.Biomolecules · 2020Review
- Associations of Serum MicroRNA with Bone Mineral Density in Community-Dwelling Subjects: The Yakumo Study.BioMed research international · 2020Article
- GIT1 regulates angiogenic factor secretion in bone marrow mesenchymal stem cells via NF-κB/Notch signalling to promote angiogenesis.Cell proliferation · 2019Article
- Arf GAPs as Regulators of the Actin Cytoskeleton-An Update.International journal of molecular sciences · 2019Review
- GIT1 contributes to autophagy in osteoclast through disruption of the binding of Beclin1 and Bcl2 under starvation condition.Cell death & disease · 2018Article
- Lack of endogenous parathyroid hormone delays fracture healing by inhibiting vascular endothelial growth factor‑mediated angiogenesis.International journal of molecular medicine · 2018Article
- PGC1β Organizes the Osteoclast Cytoskeleton by Mitochondrial Biogenesis and Activation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- Inhibiting GIT1 reduces the growth, invasion, and angiogenesis of osteosarcoma.Cancer management and research · 2018Article
- V-ATPases and osteoclasts: ambiguous future of V-ATPases inhibitors in osteoporosis.Theranostics · 2018Review
- GIT1 gene deletion delays chondrocyte differentiation and healing of tibial plateau fracture through suppressing proliferation and apoptosis of chondrocyte.BMC musculoskeletal disorders · 2017Article
- miR-125a-3p targetedly regulates GIT1 expression to inhibit osteoblastic proliferation and differentiation.Experimental and therapeutic medicine · 2016Article
- Expanding functions of GIT Arf GTPase-activating proteins, PIX Rho guanine nucleotide exchange factors and GIT-PIX complexes.Journal of cell science · 2016Review
- Decreased BMP2 signal in GIT1 knockout mice slows bone healing.Molecular and cellular biochemistry · 2014Article
- Endothelial nitric-oxide synthase (eNOS) is activated through G-protein-coupled receptor kinase-interacting protein 1 (GIT1) tyrosine phosphorylation and Src protein.The Journal of biological chemistry · 2014Article
- Impaired angiogenesis during fracture healing in GPCR kinase 2 interacting protein-1 (GIT1) knock out mice.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
G-protein-coupled receptor (GPCR) kinase 2 interacting protein-1 (GIT1) is a scaffold protein expressed in various cell types including neurons, endothelial, and vascular smooth muscle cells. The GIT1 knockout (KO) mouse has a pulmonary phenotype due to impaired endothelial function. Because GIT1 is tyrosine phosphorylated by Src kinase, we anticipated that GIT1 KO should have a bone phenotype similar to Src KO. Microcomputed tomography of the long bones revealed that GIT1 KO mice have a 2.3-fold increase in bone mass compared to wild-type controls. Histomorphometry showed increased trabecular number and connectivity suggesting impaired bone remodeling. Immunoblot analysis of GIT1 expression showed that it was expressed in both osteoclasts and osteoblasts. Osteoblast activity and function assayed by alkaline phosphatase, mineral nodule formation, and in vivo calcein labeling were normal in GIT1 KO mice suggesting that the observed increase in bone mass was due to an osteoclast defect. GIT1 KO bone marrow cells differentiated into multinucleated osteoclasts, but had defective bone resorbing function on dentin slices. This defect was likely caused by loss of podosome belt based on immunofluorescence analysis and previous studies showing that GIT1 is required for podosome formation. Furthermore, we found that GIT1 was a regulator of receptor activator of NFκB (RANK) signaling since it was tyrosine phosphorylated in a Src-dependent manner and was required for phospholipase C-γ2 phosphorylation. These data show that GIT1 is a key regulator of bone mass in vivo by regulating osteoclast function and suggest GIT1 as a potential target for osteoporosis therapy.
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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.