Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
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Ablation of the Sam68 RNA binding protein protects mice from age-related bone lossC-terminal Src kinase associates with ligand-stimulated insulin-like growth factor-I receptorCbl associates with Pyk2 and Src to regulate Src kinase activity, alpha(v)beta(3) integrin-mediated signaling, cell adhesion, and osteoclast motilityNovel p47(phox)-related organizers regulate localized NADPH oxidase 1 (Nox1) activityThe novel adaptor protein Tks4 (SH3PXD2B) is required for functional podosome formationParathyroid hormone-related protein is required for tooth eruptionPhysical and functional association of c-Src and adhesion and degranulation promoting adaptor protein (ADAP) in osteoclastogenesis in vitroTargeted disruption of leucine-rich repeat kinase 1 but not leucine-rich repeat kinase 2 in mice causes severe osteopetrosisSuppression of arthritic bone destruction by adenovirus-mediated csk gene transfer to synoviocytes and osteoclastsMechanical loading in osteocytes induces formation of a Src/Pyk2/MBD2 complex that suppresses anabolic gene expressionDishevelled-2 docks and activates Src in a Wnt-dependent manner3BP2-deficient mice are osteoporotic with impaired osteoblast and osteoclast functionsGenetic evidence for a role for Src family kinases in TNF family receptor signaling and cell survival.Suppression of c-Src activity by C-terminal Src kinase involves the c-Src SH2 and SH3 domains: analysis with Saccharomyces cerevisiae.Disruption of Src Is Associated with Phenotypes Related to Williams-Beuren Syndrome and Altered Cellular Localization of TFII-I(1,2).Regulation of osteoclast structure and function by FAK family kinasesHck contributes to bone homeostasis by controlling the recruitment of osteoclast precursors.A novel and specific NADPH oxidase-1 (Nox1) small-molecule inhibitor blocks the formation of functional invadopodia in human colon cancer cellsBone is not essential for osteoclast activationSRC: a century of science brought to the clinic.Src family kinase/abl inhibitor dasatinib suppresses proliferation and enhances differentiation of osteoblasts.Development of inhibitors for protein tyrosine kinases.Osteoclasts and odontoclasts: signaling pathways to development and disease.GPCR kinase 2 interacting protein 1 (GIT1) regulates osteoclast function and bone massc-Src-mediated phosphorylation of NoxA1 and Tks4 induces the reactive oxygen species (ROS)-dependent formation of functional invadopodia in human colon cancer cells.Differential requirement for Src family tyrosine kinases in the initiation, progression, and metastasis of prostate cancerSrc inhibitors: genomics to therapeutics.Tyrosine phosphatase epsilon is a positive regulator of osteoclast function in vitro and in vivo.c-Jun N-terminal Kinase 2 Regulates Multiple Receptor Tyrosine Kinase Pathways in Mouse Mammary Tumor Growth and Metastasis.Parathyroid hormone-related protein induces spontaneous osteoclast formation via a paracrine cascadeIntracellular membrane trafficking in bone resorbing osteoclasts.Rescue of osteoclast function by transgenic expression of kinase-deficient Src in src-/- mutant mice.Requirement for NF-kappaB in osteoclast and B-cell developmentDrosophila C-terminal Src kinase negatively regulates organ growth and cell proliferation through inhibition of the Src, Jun N-terminal kinase, and STAT pathways.Mammary epithelial-specific disruption of c-Src impairs cell cycle progression and tumorigenesis.Onset and dynamics of osteosclerosis in mice induced by Reilly-Finkel-Biskis (RFB) murine leukemia virus. Increase in bone mass precedes lymphomagenesis.Rescue of odontogenesis in Dmp1-deficient mice by targeted re-expression of DMP1 reveals roles for DMP1 in early odontogenesis and dentin apposition in vivoSubstrate recognition by osteoclast precursors induces C-src/microtubule association.Decreased c-Src expression enhances osteoblast differentiation and bone formationReview of the effects of anti-angiogenic compounds on the epiphyseal growth plate.
P2860
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P2860
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
description
1993 nî lūn-bûn
@nan
1993年の論文
@ja
1993年学术文章
@wuu
1993年学术文章
@zh-cn
1993年学术文章
@zh-hans
1993年学术文章
@zh-my
1993年学术文章
@zh-sg
1993年學術文章
@yue
1993年學術文章
@zh
1993年學術文章
@zh-hant
name
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@ast
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@en
type
label
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@ast
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@en
prefLabel
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@ast
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts.
@en
P2093
P2860
P356
P1476
Osteopetrosis in Src-deficient mice is due to an autonomous defect of osteoclasts
@en
P2093
P2860
P304
P356
10.1073/PNAS.90.10.4485
P407
P577
1993-05-01T00:00:00Z