Protocadherin-7 (PCDH7)

Protocadherin-7 (PCDH7) is a member of the non-clustered protocadherin d1 subgroup within the cadherin superfamily, characterized by seven extracellular cadherin domains, a single transmembrane domain, and a cytoplasmic tail with multiple isoforms[1]. Primarily expressed in the nervous system and skeletal tissues, PCDH7 mediates cell-cell recognition and adhesion, with distinct roles depending on tissue type. In bone, PCDH7 is upregulated by RANKL and is essential for osteoclast multinucleation and bone resorption, directly impacting bone mass and homeostasis[1]. In the nervous system, PCDH7 localizes to synapses—interacting with the GluN1 NMDA receptor subunit—where it regulates dendritic spine morphology and synaptic function[5]. It also modulates cellular mechanics and intercellular structures, partly through inhibiting protein phosphatase 1α (PP1α), thereby increasing actomyosin contraction and altering cell adhesiveness[3]. Disruption or aberrant expression of PCDH7 has been linked to cancer progression, bone metabolic disease, and neurological disorders.

Other names

Protocadherin-7PCDH7BH-protocadherinBHPCDHPPP1R120Brain-heart protocadherinProtein phosphatase 1 regulatory subunit 120BH-Pcdh

No clinically validated drugs; experimental insights include modulation of cell adhesion, inhibition of PP1α, alteration of actomyosin contraction, and regulation of NMDA receptor function[3][5].