QuickView for CACNA1H;jsessionid=D4884D264F989B51601A1791B109E9B9;jsessionid=97768875D1A852069DFFB01DE8231909;jsessionid=5AF62B14C366251FF1F3720EE484FCAB;jsessionid=C7EC49B8ECE4B7644082EF287D22E79C;jsessionid=616FD67E83BB7B09C979F0D3BB15249B;jsessionid=A4D12E3F251A8D0823422513387091A9;jsessionid=DC439AD6A81DD181BD030BB2F40C80E8;jsessionid=43A4B2B68F479ECBB3BD85C8C5369598;jsessionid=733F53B118E1CEEF9E950A587EBB0726;jsessionid=FA071BA5240200CB1DAA56C7F7A2696A (gene)

1. CaV3.2 (CACNA1H) in Primary Aldosteronism.
2. Structural basis for human Cav3.2 inhibition by selective antagonists.
3. Involvement of interaction of Cav3.2 and nociceptive TRPA1 in pathological pain transmission.
4. A Novel Somatic Mutation of CACNA1H p.V1937M in Unilateral Primary Hyperaldosteronism.
5. Novel Scorpion Toxin ω-Buthitoxin-Hf1a Selectively Inhibits Calcium Influx via CaV3.3 and CaV3.2 and…

There were no clinical trials for CACNA1H;jsessionid=D4884D264F989B51601A1791B109E9B9;jsessionid=97768875D1A852069DFFB01DE8231909;jsessionid=5AF62B14C366251FF1F3720EE484FCAB;jsessionid=C7EC49B8ECE4B7644082EF287D22E79C;jsessionid=616FD67E83BB7B09C979F0D3BB15249B;jsessionid=A4D12E3F251A8D0823422513387091A9;jsessionid=DC439AD6A81DD181BD030BB2F40C80E8;jsessionid=43A4B2B68F479ECBB3BD85C8C5369598;jsessionid=733F53B118E1CEEF9E950A587EBB0726;jsessionid=FA071BA5240200CB1DAA56C7F7A2696A