PI3K activation increases SDF-1 production and number of osteoclast precursors, and enhances SDF-1-mediated osteoclast precursor migration-Reference-Cited by-同舟云学术

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PI3K activation increases SDF-1 production and number of osteoclast precursors, and enhances SDF-1-mediated osteoclast precursor migration

Published:2019-06 Issue: Volume:10 Page:100203
ISSN:2352-1872
Container-title:Bone Reports
language:en
Short-container-title:Bone Reports

Author:

Adapala Naga Suresh,Root Sierra,Lorenzo Joseph,Aguila Hector,Sanjay Archana

Funder

National Institute of Health

Publisher

Elsevier BV

Subject

Orthopedics and Sports Medicine,Endocrinology, Diabetes and Metabolism

Reference57 articles.

1. The loss of Cbl-phosphatidylinositol 3-kinase interaction perturbs RANKL-mediated signaling, inhibiting bone resorption and promoting osteoclast survival;Adapala;J. Biol. Chem.,2010

2. Cbl-phosphatidylinositol 3 kinase interaction differentially regulates macrophage colony-stimulating factor-mediated osteoclast survival and cytoskeletal reorganization;Adapala;Ann. N. Y. Acad. Sci.,2010

3. Loss of Cbl-PI3K interaction enhances osteoclast survival due to p21-Ras mediated PI3K activation independent of Cbl-b;Adapala;J. Cell. Biochem.,2014

4. Loss of Cbl-PI3K interaction in mice prevents significant bone loss following ovariectomy;Adapala;Bone,2014

5. Commitment and differentiation of osteoclast precursor cells by the sequential expression of c-Fms and receptor activator of nuclear factor kappaB (RANK) receptors;Arai;J. Exp. Med.,1999

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