Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
about
Cbl-b is a novel physiologic regulator of glycoprotein VI-dependent platelet activation.Loss of Cbl-PI3K interaction in mice prevents significant bone loss following ovariectomyThe loss of Cbl-phosphatidylinositol 3-kinase interaction perturbs RANKL-mediated signaling, inhibiting bone resorption and promoting osteoclast survival.Functional osteoclast attachment requires inositol-1,4,5-trisphosphate receptor-associated cGMP-dependent kinase substrate.Abrogation of Cbl-PI3K interaction increases bone formation and osteoblast proliferation.Sustained release of adiponectin improves osteogenesis around hydroxyapatite implants by suppressing osteoclast activity in ovariectomized rabbitsNur77 prevents excessive osteoclastogenesis by inducing ubiquitin ligase Cbl-b to mediate NFATc1 self-limitation.Loss of Cbl-PI3K interaction enhances osteoclast survival due to p21-Ras mediated PI3K activation independent of Cbl-bThe E3 ubiquitin ligase Cbl-b improves the prognosis of RANK positive breast cancer patients by inhibiting RANKL-induced cell migration and metastasis.c-Cbl and Cbl-b act redundantly to protect osteoclasts from apoptosis and to displace HDAC6 from beta-tubulin, stabilizing microtubules and podosomesRegulation of osteoclast function.The many faces of p38 mitogen-activated protein kinase in progenitor/stem cell differentiation.E3 ubiquitin ligase-mediated regulation of bone formation and tumorigenesis.Cbl-family proteins as regulators of cytoskeleton-dependent phenomena.Modulation of Immune Cell Functions by the E3 Ligase Cbl-b.FRK suppresses the proliferation of human glioma cells by inhibiting cyclin D1 nuclear accumulation.Cbl-b enhances Runx2 protein stability and augments osteocalcin promoter activity in osteoblastic cell lines.Adenoviral vector-mediated overexpression of osteoprotegerin accelerates osteointegration of titanium implants in ovariectomized rats.Ubiquitin ligase Cbl-b acts as a negative regulator in discoidin domain receptor 2 signaling via modulation of its stability.The actin-binding protein PPP1r18 regulates maturation, actin organization, and bone resorption activity of osteoclasts.[Implication of the ubiquitin ligase c-Cbl in bone formation and tumorigenesis].
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P2860
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
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article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on July 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@en
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@nl
type
label
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@en
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@nl
prefLabel
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@en
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@nl
P2093
P2860
P356
P1476
Loss of Cbl-b increases osteoclast bone-resorbing activity and induces osteopenia.
@en
P2093
Arata Nakajima
Archana Sanjay
Cecile Itzsteink
Naga Suresh Adapala
Riccardo Chiusaroli
Roland Baron
William C Horne
P2860
P304
P356
10.1359/JBMR.090205
P577
2009-07-01T00:00:00Z