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#hyperactivation

2 public questions tagged with this topic.

Fertilization in mammals-iv

Sperm hyperactivation depends on:

Hyperactivation is whiplash-like, high-amplitude flagellar beating enabling sperm to detach from oviductal epithelium, traverse viscous mucus and penetrate cumulus and zona matrix. It is initiated during capacitation in female tract by alkalinization and progesterone from cumulus cells opening CatSper, sperm-specific pH-sensitive calcium channel complex located in principal piece of flagellum. Calcium entry through CatSper raises intracellular calcium, alters dynein sliding, producing asymmetric bends. Knockout of CatSper subunits in mice abolishes hyperactivation and fertility despite normal motility, while potassium, chloride or sodium channels alone are insufficient to drive this capacitation-dependent motility switch.

Ref: Qi et al., eLife 2007 & Lishko et al., Cell 2012: CatSper calcium channels driving sperm hyperactivation and chemotaxis.

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Cancer

PTEN loss leads to hyperactivation of

PI3K–Akt pathway, is consistent with established principles of cell signaling, receptor pharmacology and cellular regulation. Experimental measurements of binding parameters, genetic loss-of-function studies and pharmacological interventions all converge on the same interpretation. Related options address neighboring concepts but do not satisfy the precise criterion stated in the question.

Ref: NCERT Biology Class 11–12 Alberts et al Molecular Biology of the Cell Lodish et al, Molecular Cell Biology Cooper & Hausman, The Cell Abbas et al., Cellular and Molecular Immunology (for immunology sections)

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