QuickView for CACNA1H;jsessionid=D4884D264F989B51601A1791B109E9B9;jsessionid=97768875D1A852069DFFB01DE8231909;jsessionid=5AF62B14C366251FF1F3720EE484FCAB;jsessionid=C7EC49B8ECE4B7644082EF287D22E79C;jsessionid=B70F3FFAE8D6F540BD46126DF0554200;jsessionid=7F169CD363B166A7D741785242D26ABE;jsessionid=3C0392A83BCFFEA7777740A722252896;jsessionid=2AC2E9DD49C5C87CEFB16CAAD9DABE2D;jsessionid=6D522B79ED47DDFE9CC15054EC27AD93;jsessionid=4A90E2B135712ACA8A621829E9D041B1;jsessionid=C878AFC5CD5CD2899914AF9840FE7007 (gene)

1. CaV3.2 (CACNA1H) in Primary Aldosteronism.
2. A Novel Somatic Mutation of CACNA1H p.V1937M in Unilateral Primary Hyperaldosteronism.
3. Targeting T-type/CaV3.2 channels for chronic pain.
4. Adiponectin receptor 1-mediated stimulation of Cav3.2 channels in trigeminal ganglion neurons induce…
5. The T-type calcium channel CaV3.2 regulates insulin secretion in the pancreatic β-cell.

There were no clinical trials for CACNA1H;jsessionid=D4884D264F989B51601A1791B109E9B9;jsessionid=97768875D1A852069DFFB01DE8231909;jsessionid=5AF62B14C366251FF1F3720EE484FCAB;jsessionid=C7EC49B8ECE4B7644082EF287D22E79C;jsessionid=B70F3FFAE8D6F540BD46126DF0554200;jsessionid=7F169CD363B166A7D741785242D26ABE;jsessionid=3C0392A83BCFFEA7777740A722252896;jsessionid=2AC2E9DD49C5C87CEFB16CAAD9DABE2D;jsessionid=6D522B79ED47DDFE9CC15054EC27AD93;jsessionid=4A90E2B135712ACA8A621829E9D041B1;jsessionid=C878AFC5CD5CD2899914AF9840FE7007