ArticleMolecular and cellular biochemistry2012
Phosphorylation of GIT1 tyrosine 321 is required for association with FAK at focal adhesions and for PDGF-activated migration of osteoblasts.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- Fluorinated Porcine Bone-Derived Hydroxyapatite Promotes Vascularized Osteogenesis by Coordinating Human Bone Marrow Mesenchymal Stem Cell/Human Umbilical Vein Endothelial Cell Complexes.Bioengineering (Basel, Switzerland) · 2024Article
- UBTF facilitates melanoma progression via modulating MEK1/2-ERK1/2 signalling pathways by promoting GIT1 transcription.Cancer cell international · 2021Article
- An antibacterial and injectable calcium phosphate scaffold delivering human periodontal ligament stem cells for bone tissue engineering.RSC advances · 2020Article
- GIT1 regulates angiogenic factor secretion in bone marrow mesenchymal stem cells via NF-κB/Notch signalling to promote angiogenesis.Cell proliferation · 2019Article
- SRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis.The Journal of biological chemistry · 2019Article
- Review
- Osteoblast migration in vertebrate bone.Biological reviews of the Cambridge Philosophical Society · 2018Review
- MeCP2, a target of miR-638, facilitates gastric cancer cell proliferation through activation of the MEK1/2-ERK1/2 signaling pathway by upregulating GIT1.Oncogenesis · 2017Article
- GIT1 gene deletion delays chondrocyte differentiation and healing of tibial plateau fracture through suppressing proliferation and apoptosis of chondrocyte.BMC musculoskeletal disorders · 2017Article
- Osteopontin inhibits osteoblast responsiveness through the down-regulation of focal adhesion kinase mediated by the induction of low-molecular weight protein tyrosine phosphatase.Molecular biology of the cell · 2017Article
- miR-125a-3p targetedly regulates GIT1 expression to inhibit osteoblastic proliferation and differentiation.Experimental and therapeutic medicine · 2016Article
- Role of Osteogenic Growth Peptide (OGP) and OGP(10-14) in Bone Regeneration: A Review.International journal of molecular sciences · 2016Review
- Decreased BMP2 signal in GIT1 knockout mice slows bone healing.Molecular and cellular biochemistry · 2014Article
- GIT1 phosphorylation on serine 46 by PKD3 regulates paxillin trafficking and cellular protrusive activity.The Journal of biological chemistry · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoblast migration and proliferation are fundamental processes in bone healing. We demonstrated that the G-protein-coupled receptor kinase interacting protein 1(GIT1) is a key regulator of bone mass and osteoblast cell migration, but little is known about GIT1 regulation by upstream signaling systems or the impact of GIT1 on downstream effectors. We found that platelet-derived growth factor (PDGF) stimulated the GIT1 tyrosine phosphorylation in osteoblast cells and increased the association of GIT1 with focal adhesion kinase (FAK) at osteoblast focal adhesions. The Src inhibitor PP2 and FAK siRNA inhibited GIT1 tyrosine phosphorylation and the increased association between GIT1 and FAK following stimulation with PDGF. The spa2 homology domain (SHD) of GIT1 was required for association with FAK. Furthermore, phosphorylation of tyrosine 321 of GIT1, which is localized within the SHD, was critical for association with FAK. Mutagenesis analysis revealed that GIT1Y321F inhibited the increased association between GIT1 and FAK. Immunofluorescent staining revealed that GIT1Y321F inhibited FAK activation in focal adhesions after PGDF stimulation. A cell spreading assay demonstrated that GIT1Y321F also inhibited osteoblast cell motility, while the Boyden chamber assay demonstrated that the GIT1Y321F mutation inhibited PDGF-induced osteoblastic cell migration. Phosphorylation of tyrosine 321 of GIT1 is necessary for PDGF-induced association with FAK, FAK activation in focal adhesions, and for osteoblastic cell migration.
Indexed as
Identifiers
What OpenQuestion holds
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.