ArticleBiology of reproduction2011
Reduced fertility in vitro in mice lacking the cystatin CRES (cystatin-related epididymal spermatogenic): rescue by exposure of spermatozoa to dibutyryl cAMP and isobutylmethylxanthine.
Article in Biology of reproduction, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- PSMA8-Containing 20S Proteasome Regulates Spermiogenesis and Male Fertility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The single-cell atlas of the epididymis in mice reveals the changes in epididymis function before and after sexual maturity.Frontiers in cell and developmental biology · 2024Article
- Type 2 Cystatins and Their Roles in the Regulation of Human Immune Response and Cancer Progression.Cancers · 2023Review
- Article
- Evolution of a New Testis-Specific Functional Promoter Within the Highly ConservedFrontiers in genetics · 2021Article
- Proteostasis in the Male and Female Germline: A New Outlook on the Maintenance of Reproductive Health.Frontiers in cell and developmental biology · 2021Review
- Functional Mammalian Amyloids and Amyloid-Like Proteins.Life (Basel, Switzerland) · 2020Review
- Impact of semen-derived amyloid (SEVI) on sperm viability and motility: its implication in male reproductive fitness.European biophysics journal : EBJ · 2019Article
- Identification of multiple male reproductive tract-specific proteins that regulate sperm migration through the oviduct in mice.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- The epididymal amyloid matrix: structure and putative functions.Andrology · 2019Review
- Transcript profiling in the testes and prostates of postnatal day 30 Sprague-Dawley rats exposed prenatally and lactationally to 2-hydroxy-4-methoxybenzophenone.Reproductive toxicology (Elmsford, N.Y.) · 2018Article
- Why are Functional Amyloids Non-Toxic in Humans?Biomolecules · 2017Review
- Functional Amyloids in Reproduction.Biomolecules · 2017Review
- Male infertility-related molecules involved in sperm-oocyte fusion.The Journal of reproduction and development · 2017Review
- Cystatin-related epididymal spermatogenic subgroup members are part of an amyloid matrix and associated with extracellular vesicles in the mouse epididymal lumen.Molecular human reproduction · 2016Article
- Impact of glycosylation on the unimpaired functions of the sperm.Clinical and experimental reproductive medicine · 2015Review
- Fertility defects in mice expressing the L68Q variant of human cystatin C: a role for amyloid in male infertility.The Journal of biological chemistry · 2014Article
- Albumin is synthesized in epididymis and aggregates in a high molecular mass glycoprotein complex involved in sperm-egg fertilization.PloS one · 2014Article
- Alteration in the processing of the ACRBP/sp32 protein and sperm head/acrosome malformations in proprotein convertase 4 (PCSK4) null mice.Molecular human reproduction · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The cystatin CRES (cystatin-related epididymal spermatogenic; Cst8) is the defining member of a reproductive subgroup of family 2 cystatins of cysteine protease inhibitors and is present in the epididymis and spermatozoa, suggesting roles in sperm maturation and fertilization. To elucidate the role of CRES in reproduction, mice lacking the Cst8 gene were generated and their fertility examined. Although both male and female Cst8(-/-) mice generated offspring in vivo, spermatozoa from Cst8(-/-) mice exhibited a profound fertility defect in vitro. Compared to spermatozoa from Cst8(+/+) mice, spermatozoa from Cst8(-/-) mice were unable to undergo a progesterone-stimulated acrosome reaction and had decreased levels of protein tyrosine phosphorylation, suggesting a defect in the ability of Cst8(-/-) spermatozoa to capacitate. Incubation of Cst8(-/-) spermatozoa with dibutyryl cAMP and 3-isobutyl-1-methylxanthine rescued the fertility defect, including the capacity for sperm protein tyrosine phosphorylation. Both untreated Cst8(+/+) and Cst8(-/-) spermatozoa, however, exhibited similar increased total levels of cAMP and protein kinase A (PKA) activity throughout the capacitation time course compared to spermatozoa incubated under noncapacitating conditions. Taken together, these results suggest that mice lacking CRES may have altered local levels of cAMP/PKA activity, perhaps because of improper partitioning or tethering of these signaling molecules, or that the CRES defect does not directly involve cAMP/PKA but other signaling pathways that regulate protein tyrosine phosphorylation and capacitation.
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