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Knockout of TRPV6 Causes Osteopenia in Mice by Increasing Osteoclastic Differentiation and Activity
Author(s) -
Fangjing Chen,
Bin Ni,
Yueping Ou Yang,
Tianwen Ye,
Aimin Chen
Publication year - 2014
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000358653
Subject(s) - trpv6 , bone resorption , osteoclast , endocrinology , medicine , bone remodeling , rankl , chemistry , osteoporosis , calcium metabolism , calcium , resorption , homeostasis , activator (genetics) , biology , receptor
Calcium ion (Ca(2+)) signals are required for osteoclast differentiation. Previous study showed that transient receptor potential vanilloid 5 (TRPV5) is an essential Ca(2+) transporter in osteoclastogenesis and bone resorption. TRPV5 and TRPV6 represent two highly homologous members within the transient receptor potential (TRP) superfamily. However, the role of TRPV6 in bone metabolism is still controversial and little is known about the involvement of TRPV6 in receptor activator of nuclear factor κ-B ligand (RANKL)-induced osteoclastogenesis.

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