Protein kinases regulate hyperactivated motility of human sperm.
Protein kinases regulate hyperactivated motility of human sperm.
复制标题
蛋白激酶调节人类精子的过度活跃运动。
DOI:
10.1097/cm9.0000000000001551
复制
发表时间:
2021-10-20
影响因子:
6.1
通讯作者:
Ni Y
中科院分区:
文献类型:
--
作者:
Wang YY;Sun PB;Li K;Gao T;Zheng DW;Wu FP;Liu AJ;Ni Y
Once the sperm enters into the female reproductive tract, they undergo an important process called capacitation, which involves a series of physiological and biochemical changes that ensure fertilization. During capacitation, calcium ions (Ca2+) increase the bending amplitude of a sperm’s flagellum. This causes hyperactivation, which is manifested as the asymmetrical beating of the flagellum. Tyrosine phosphorylation is also a cause for human sperm hyperactivation; asthenospermia—that is, reduced sperm motility—occurs when the sperm are incapable of hyperactivation owing to impaired tyrosine phosphorylation.[1] Hyperactivated motility enables the sperm to migrate and penetrate the cumulus cells and zona pellucida surrounding the oocyte, leading to fertilization. Therefore, the hyperactivated motility of sperm is critical for male reproductive ability, and the molecular mechanism underlying human sperm hyperactivation requires discussion.Transcription and translation do not occur in sperm because they have highly compacted DNA and lack endoplasmic reticulum. Therefore, hyperactivated motility is primarily regulated by post-translational modifications, such as protein phosphorylation, which can activate or inhibit specific signaling pathways. Multiple protein kinases have been found in human sperm. These include protein kinase A (PKA), protein kinase B (also called AKT), protein kinase G (PKG), and mitogen-activated protein kinases (MAPKs), which play important roles in sperm motility.