Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The epididymal maturation of spermatozoa is regulated by changes in the luminal ion concentration and the processing of the sperm surface membrane by several glycosidases and proteases. In the present study, we identified five novel protease inhibitors that are highly expressed in the mouse epididymis. Four of the proteins were found to belong to the Kazal protease inhibitor family and were named SPINK8, SPINK10, SPINK11, and SPINK12, whereas one of the proteins, WFDC10, contained the WAP four-disulfide core domain structure. The novel genes showed very specific segmental expression patterns. The expression of all the five genes was regulated by testis-derived factors and decreased after gonadectomy. With the exception of Spink11, mRNA levels could be restored by testosterone replacement. We hypothesize that the protease inhibitors discovered represent a group of epididymal genes that contribute to the regulation of sperm maturation by regulating the proteolytic processing of the sperm membrane during epididymal transit.
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PMID:Novel epididymal protease inhibitors with Kazal or WAP family domain. 1693 May 50

Epididymal maturation is critical for acquisition of motility and fertilizing capacity by sperm. During epididymal transit, the surface of sperm undergoes prominent sequential changes through interactions with secreted proteins, including protease inhibitors. In the present study, we characterized three epididymis-specific SPINKs (serine protease inhibitors, Kazal-type): SPINK8, SPINK11, and SPINK12. We found that these epididymal SPINKs are expressed in an epididymal region-specific manner and their expression is developmentally regulated. Remarkably, cellular analyses revealed that SPINK8 and SPINK12 are transferred to the sperm. To investigate the in vivo properties of SPINK12, we analyzed knockout mice generated by CRISPR/Cas9-mediated genome editing. Loss of SPINK12 did not alter epididymal tubule structure or sperm phenotypes. Spink12 mutant mice exhibited normal fertility, suggesting that SPINK12 is functionally redundant in the epididymis.
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PMID:Expressional and functional analyses of epididymal SPINKs in mice. 3059 Jan 35