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  Indian J Med Microbiol
 

Figure 4: A model describing the biochemical cascade in sperm capacitation: intracellular HCO3− activates sAC to generate cAMP leading to PKA activation and cholesterol efflux from the sperm plasma membrane which further stimulate the HCO3−/sAC/cAMP/PKA cascade. PKA activates Src to phosphorylate/inactivate PIP2-bound gelsolin. PIP2 is a cofactor for PLD activation and this activation is stimulated by PKCα, leading to phosphatidylcholine hydrolysis and production of phosphatidic acid (PA) which mediates the conversion of G-actin to F-actin. Thus, activation of PLD and prevention of F-actin dispersion by inhibiting gelsolin, allows F-actin formation. F-actin in the head prevents immature acrosome reaction and in the tail F-actin regulates sperm motility including HA motility.

Figure 4: A model describing the biochemical cascade in sperm capacitation: intracellular HCO<sub>3</sub>− activates sAC to generate cAMP leading to PKA activation and cholesterol efflux from the sperm plasma membrane which further stimulate the HCO<sub>3</sub>−/sAC/cAMP/PKA cascade. PKA activates Src to phosphorylate/inactivate PIP<sub>2</sub>-bound gelsolin. PIP2 is a cofactor for PLD activation and this activation is stimulated by PKCα, leading to phosphatidylcholine hydrolysis and production of phosphatidic acid (PA) which mediates the conversion of G-actin to F-actin. Thus, activation of PLD and prevention of F-actin dispersion by inhibiting gelsolin, allows F-actin formation. F-actin in the head prevents immature acrosome reaction and in the tail F-actin regulates sperm motility including HA motility.