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Comment :

Type  MGI:General Description  mutant sperm exhibited normal capacitation events, but failed to exhibit the expected intracellular [Ca2+]i mobilization in response to ZP progesterone, another physiological inducer of the acrosome reaction, failed to induce sustained [Ca2+]i increases in mutant sperm, also resulting in partial inhibition of the acrosome reaction finally, assessment of store-operated channel (SOC) function using thapsigargin indicated that capacitative Ca2+ entry through SOC channels was severely impaired in mutant sperm