Our findings show that in the kidney GPR37L1 participates in renal proximal tubule luminal sodium transport and regulation of blood pressure by increasing the renal expression and function of NHE3 by decreasing cAMP production.
Gpr37l1 genetic ablation in Ptch1(+/-) model animals results in marked deferment of medulloblastoma occurrence and decreased incidence of aggressive tumor types.
Despite its absence in the heart and kidney GPR37L1 regulates baseline blood pressure in female mice and is crucial for cardiovascular compensatory responses in males. The expression of GPR37L1 in the brain yet absence from peripheral cardiovascular tissues suggests this orphan receptor is a hitherto unknown contributor to central cardiovascular control.
This study demonstrated that GPR37L1 protects neurons during ischemia presumably by modulating extracellular glutamate concentration and NMDAR activation.
K349N substitution in Gpr37L1 did not grossly alter receptor expression surface trafficking or constitutive signaling in transfected cells. In vivo studies revealed that a complete loss of Gpr37L1 function in mice results in increased seizure susceptibility. Mice lacking the related receptor Gpr37 also exhibited an increase in seizure susceptibility while genetic deletion of both receptors resulted greater vulnerability
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