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• W2188792318 endingPage "67" @default.
• W2188792318 startingPage "58" @default.
• W2188792318 abstract "The development of a mammalian embryo is initiated by a sequence of molecular events collectively referred to as ‘oocyte activation’ and regulated by the release of intracellular calcium in the ooplasm. Over the last decade, phospholipase C zeta (PLCζ), a sperm protein introduced into the oocyte upon gamete fusion, has gained almost universal acceptance as the protein factor responsible for initiating oocyte activation. A large body of consistent and reproducible evidence, from both biochemical and clinical settings, confers support for the role of PLCζ in this fundamental biological context, which has significant ramifications for the management of human male infertility. Oocyte activation deficiency (OAD) and total fertilisation failure (TFF) are known causes of infertility and have both been linked to abnormalities in the structure, expression, and localisation pattern of PLCζ in human sperm. Assisted oocyte activators (AOAs) represent the only therapeutic option available for OAD at present, although these agents have been the source of much debate recently, particularly with regard to their potential epigenetic effects upon the embryo. Consequently, there is much interest in the deployment of sensitive PLCζ assays as prognostic/diagnostic tests and human recombinant PLCζ protein as an alternative form of therapy. Although PLCζ deficiency has been directly linked to a cohort of infertile cases, we have yet to identify the specific causal mechanisms involved. While two genetic mutations have been identified which link defective PLCζ protein to an infertile phenotype, both were observed in the same patient, and have yet to be described in other patients. Consequently, some researchers are investigating the possibility that genetic variations in the form of single nucleotide polymorphisms (SNPs) could provide some explanation, especially since >6000 SNPs have been identified in the PLCζ gene. As yet, however, there is no consistent data to suggest that any of these SNPs influence the functional ability of PLCζ. Other laboratories appear to be focussing upon the PLCζ promoter, which is bi-directional and shared with the actin filament capping muscle Z-line alpha 3 gene (CAPZA3), or seeking to identify interacting proteins within the ooplasm. The aim of this review is to provide a synopsis of recent progress in the application of PLCζ in diagnostic and therapeutic medicine, to discuss our current understanding of how the functional ability of PLCζ might be controlled, and thus how PLCζ deficiency might arise, and finally, to consider the potential implications of alternative sperm protein candidates, such as post-acrosomal WW-domain binding protein (PAWP), which has caused much debate and confusion in the field over the last few years." @default.
• W2188792318 created "2016-06-24" @default.
• W2188792318 creator A5023848591 @default.
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• W2188792318 creator A5081433587 @default.
• W2188792318 date "2016-05-01" @default.
• W2188792318 modified "2023-10-03" @default.
• W2188792318 title "Phospholipase C zeta (PLCζ) and male infertility: Clinical update and topical developments" @default.
• W2188792318 cites W1512332775 @default.
• W2188792318 cites W1597024492 @default.
• W2188792318 cites W1731057385 @default.
• W2188792318 cites W1801532055 @default.
• W2188792318 cites W1876415227 @default.
• W2188792318 cites W1895234960 @default.
• W2188792318 cites W1966607834 @default.
• W2188792318 cites W1967202041 @default.
• W2188792318 cites W1967876375 @default.
• W2188792318 cites W1969127101 @default.
• W2188792318 cites W1982784931 @default.
• W2188792318 cites W1983924599 @default.
• W2188792318 cites W1984128131 @default.
• W2188792318 cites W1989520345 @default.
• W2188792318 cites W199111168 @default.
• W2188792318 cites W2005308362 @default.
• W2188792318 cites W2006693497 @default.
• W2188792318 cites W2007490029 @default.
• W2188792318 cites W2012709143 @default.
• W2188792318 cites W2018361301 @default.
• W2188792318 cites W2020544415 @default.
• W2188792318 cites W2027043598 @default.
• W2188792318 cites W2027690388 @default.
• W2188792318 cites W2035843184 @default.
• W2188792318 cites W2042834905 @default.
• W2188792318 cites W2043025459 @default.
• W2188792318 cites W2046665167 @default.
• W2188792318 cites W2050247347 @default.
• W2188792318 cites W2054073262 @default.
• W2188792318 cites W2061098698 @default.
• W2188792318 cites W2061282090 @default.
• W2188792318 cites W2064541275 @default.
• W2188792318 cites W2065715357 @default.
• W2188792318 cites W2069346368 @default.
• W2188792318 cites W2071020879 @default.
• W2188792318 cites W2072881208 @default.
• W2188792318 cites W2073329661 @default.
• W2188792318 cites W2080289922 @default.
• W2188792318 cites W2083420802 @default.
• W2188792318 cites W2086974151 @default.
• W2188792318 cites W2087840656 @default.
• W2188792318 cites W2088769561 @default.
• W2188792318 cites W2090103674 @default.
• W2188792318 cites W2097228907 @default.
• W2188792318 cites W2097939257 @default.
• W2188792318 cites W2098620041 @default.
• W2188792318 cites W2098824600 @default.
• W2188792318 cites W2103080851 @default.
• W2188792318 cites W2106466510 @default.
• W2188792318 cites W2107265844 @default.
• W2188792318 cites W2108632460 @default.
• W2188792318 cites W2108702954 @default.
• W2188792318 cites W2109341213 @default.
• W2188792318 cites W2113458225 @default.
• W2188792318 cites W2117711260 @default.
• W2188792318 cites W2120181657 @default.
• W2188792318 cites W2121641375 @default.
• W2188792318 cites W2123921145 @default.
• W2188792318 cites W2128480501 @default.
• W2188792318 cites W2134305003 @default.
• W2188792318 cites W2134341806 @default.
• W2188792318 cites W2140958036 @default.
• W2188792318 cites W2141981489 @default.
• W2188792318 cites W2145025925 @default.
• W2188792318 cites W2153849534 @default.
• W2188792318 cites W2156164053 @default.
• W2188792318 cites W2156255933 @default.
• W2188792318 cites W2160581079 @default.
• W2188792318 cites W2163193992 @default.
• W2188792318 cites W2165525635 @default.
• W2188792318 cites W2167278688 @default.
• W2188792318 cites W2169240955 @default.
• W2188792318 cites W2169389485 @default.
• W2188792318 cites W2182606439 @default.
• W2188792318 cites W2185447678 @default.
• W2188792318 cites W309129877 @default.
• W2188792318 cites W4232377443 @default.
• W2188792318 cites W4234730888 @default.
• W2188792318 cites W4248189705 @default.
• W2188792318 cites W909688392 @default.
• W2188792318 doi "https://doi.org/10.1016/j.jbior.2015.11.009" @default.
• W2188792318 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26700242" @default.
• W2188792318 hasPublicationYear "2016" @default.
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