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Cation channel, sperm associated 2

Calcium ions play a primary role in the regulation of sperm motility. This gene belongs to a family of putative cation channels that are specific to spermatozoa and localize to the flagellum. The protein family features a single repeat with six membrane-spanning segments and a predicted calcium-selective pore region. This gene is part of a tandem repeat on chromosome 15q15; the second copy of this gene is thought to be a pseudogene. Additional splice variants have been described but their full-length nature has not been determined. [provided by RefSeq, Aug 2008] (from NCBI)
Top mentioned proteins: CAN, DIS, HAD, IL-8, Adenylate Cyclase
Papers on CatSper2
In vivo influence of sodium fluoride on sperm chemotaxis in male mice.
Wang et al., China. In Arch Toxicol, 28 Feb 2014
Ca(2+) concentration, adenylate cyclase (AC) content and mRNA expression of mACIII, mACVIII, Golf alpha, CatSper1, CatSper2 were measured to elucidate the possible molecular mechanisms.
Effects of Vitamin-E treatment on CatSper genes expression and sperm quality in the testis of the aging mouse.
Sankian et al., Mashhad, Iran. In Iran J Reprod Med, Dec 2013
Also, intensity of signal for CatSper1 and CatSper2 increased in the head and middle piece of sperm in experimental group as compared to those of control ones.
Disruption of the principal, progesterone-activated sperm Ca2+ channel in a CatSper2-deficient infertile patient.
Lishko et al., San Francisco, United States. In Proc Natl Acad Sci U S A, May 2013
The female steroid hormone progesterone regulates ovulation and supports pregnancy, but also controls human sperm function within the female reproductive tract.
Genetic testing for hearing loss in the United States should include deletion/duplication analysis for the deafness/infertility locus at 15q15.3.
Babovic-Vuksanovic et al., Rochester, United States. In Mol Cytogenet, 2012
Sensorineural hearing loss and male infertility (Deafness-Infertility Syndrome; DIS) is a contiguous gene deletion syndrome resulting from homozygous deletion of the CATSPER2 and STRC genes on chromosome 15q15.3.
Regulation of fertilization in male rats by CatSper2 knockdown.
Zhou et al., Nanjing, China. In Asian J Androl, 2012
In this study, in vivo electroporation (EP) and rete testis microinjection-mediated plasmid DNA were adopted to silence CatSper2 expression, which is essential in sperm hyperactivation.
A comprehensive gene mutation screen in men with asthenozoospermia.
Repping et al., Amsterdam, Netherlands. In Fertil Steril, 2011
INTERVENTION(S): Screening nine candidate genes for mutations: ADCY10, AKAP4, CATSPER1, CATSPER2, CATSPER3, CATSPER4, GAPDHS, PLA2G6, and SLC9A10.
Molecular cloning, spatial and temporal expression analysis of CatSper genes in the Chinese Meishan pigs.
Mao et al., Yangzhou, China. In Reprod Biol Endocrinol, 2010
BACKGROUND: Sperm ion channel proteins (CatSpers) are essential for sperm hyperactivated motility, and then penetration through the zona pellucida.
Genetic male infertility and mutation of CATSPER ion channels.
Smith et al., Iowa City, United States. In Eur J Hum Genet, 2010
Previously, contiguous gene deletions including the CATSPER2 gene implicated the sperm-specific CATSPER channel in syndromic male infertility (SMI).
Effects of sodium fluoride on hyperactivation and Ca2+ signaling pathway in sperm from mice: an in vivo study.
Wang et al., China. In Arch Toxicol, 2010
The purpose of this study was to investigate the effect of sodium fluoride (NaF) on sperm hyperactivation, Ca2+/CALM-CAMK2 signaling, and CatSper1 and CatSper2 mRNA expression in mice sperm.
CATSPER-Related Male Infertility
Smith et al., Seattle, United States. In Unknown Journal, 2010
including CATSPER2 and STRC.
CatSper genes expression, semen characteristics and histology of testes in the contusive spinal cord-injured mice model.
Mowla et al., Tehrān, Iran. In Spinal Cord, 2009
Data show that there is a significant downregulation of CatSpers 2 following spinal cord injury.
Pharmacological targeting of native CatSper channels reveals a required role in maintenance of sperm hyperactivation.
Babcock et al., Seattle, United States. In Plos One, 2008
Removal of external Ca(2+) increases SBFI signals in wild-type but not CatSper2-null sperm.
CatSper-null mutant spermatozoa are unable to ascend beyond the oviductal reservoir.
Suarez et al., Ithaca, United States. In Reprod Fertil Dev, 2008
CatSper-null mutant spermatozoa are unable to ascend beyond the oviductal reservoir.
Sensorineural deafness and male infertility: a contiguous gene deletion syndrome.
Smith et al., Iowa City, United States. In Bmj Case Rep, 2008
The deleted region is about 100 kb long and involves four genes (KIAA0377, CKMT1B, STRC and CATSPER2), each of which has a telomeric duplicate.
Expression of CatSper family transcripts in the mouse testis during post-natal development and human ejaculated spermatozoa: relationship to sperm motility.
Xiong et al., Wuhan, China. In Mol Hum Reprod, 2007
The CatSper2 transcript was present in the testis of the 8-day-old mice, and was repressed in the adult testis after two sharp up-regulations at day 18 and 35.
Different regulatory systems operate in the midpiece and principal piece of the mammalian sperm flagellum.
Schimenti et al., Ithaca, United States. In Soc Reprod Fertil Suppl, 2006
For example, the soluble adenylyl cyclase (sAC), which is required for activation of motility, is restricted to the midpiece, while the plasma membrane calcium channels CatSper1 and CatSper2, which are required for hyperactivation of motility, are restricted to the principal piece.
Association of Catsper1 or -2 with Ca(v)3.3 leads to suppression of T-type calcium channel activity.
Gopalakrishnan et al., United States. In J Biol Chem, 2006
CatSper1 and CatSper2 can associate with and modulate the function of the Ca(v)3.3 channel, which might be important in the regulation of sperm function.
Insights into sperm cell motility signaling through sNHE and the CatSpers.
Garbers et al., Dallas, United States. In Mol Cell Endocrinol, 2006
Using a signal peptide trapping strategy, we identified two new genes, a putative sperm Na+/H+ exchanger (sNHE) and the putative cation channel CatSper2, with unique and essential roles in sperm motility.
Identical phenotypes of CatSper1 and CatSper2 null sperm.
Babcock et al., Seattle, United States. In J Biol Chem, 2005
CatSper1 and CatSper2 null sperm show identical phenotypes in mice
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