Parathyroid-Specific Double Knockout of Gq and G11 α-Subunits Leads to a Phenotype Resembling Germline Knockout of the Extracellular Ca2+-Sensing Receptor | Zendy

Nina Wettschureck | Zendy; EunAh Lee | Zendy; Steven K. Libutti | Zendy; Stefan Offermanns | Zendy; Pamela Gehron Robey | Zendy; Allen M. Spiegel | Zendy

Open Access

Parathyroid-Specific Double Knockout of Gq and G11 α-Subunits Leads to a Phenotype Resembling Germline Knockout of the Extracellular Ca2+-Sensing Receptor

Author(s) -

Nina Wettschureck,

EunAh Lee,

Steven K. Libutti,

Stefan Offermanns,

Pamela Gehron Robey,

Allen M. Spiegel

Publication year - 2006

Publication title -

molecular endocrinology

Language(s) - English

Resource type - Journals

eISSN - 1944-9917

pISSN - 0888-8809

DOI - 10.1210/me.2006-0110

Subject(s) - heterotrimeric g protein , biology , germline , knockout mouse , extracellular , calcium sensing receptor , gene knockout , phenotype , receptor , calcimimetic , protein subunit , microbiology and biotechnology , endocrinology , medicine , signal transduction , parathyroid hormone , g protein , genetics , calcium , gene

Germline knockout of the extracellular Ca2+-sensing receptor (CaR) leads to a phenotype that includes severe hypercalcemia, hyperparathyroidism, relative hypocalciuria, skeletal abnormalities, retarded growth, and early postnatal death. To investigate the role of heterotrimeric G proteins in CaR signaling, we used cre/lox technology to delete the respective α-subunits of Gq and G11 selectively in parathyroid cells. Mice that were PTH-Cre+/−; Gnaqflox/flox; Gna11−/− (PTH-Gαq/Gα11-double knockouts) were viable, but showed all the features of germline knockout of the CaR except hypocalcuria. Our results demonstrate the critical role of both Gq and G11 in mediating inhibition of PTH secretion by extracellular Ca2+.

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