UNASSIGNED: The development of a @entity1 embryo is initiated by a sequence of molecular events collectively referred to as 'oocyte activation' and regulated by the release of intracellular @entity460 in the ooplasm. Over the last decade, phospholipase C zeta (PLC  ), 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 PLC   in this fundamental biological context, which has significant ramifications for the management of @entity1 @entity4810 . Oocyte activation deficiency (OAD) and total fertilisation failure (TFF) are known causes of @entity249 and have both been linked to abnormalities in the structure, expression, and localisation pattern of PLC   in @entity1 sperm. @entity3457 ( @entity3457 ) 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 PLC   assays as prognostic/diagnostic tests and @entity1 recombinant PLC   protein as an alternative form of therapy. Although @entity2195 has been directly linked to a cohort of @entity249 cases, we have yet to identify the specific causal mechanisms involved. While two genetic mutations have been identified which link defective PLC   protein to an @entity249 phenotype, both were observed in the same @entity1 , and have yet to be described in other @entity1 . 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 PLC   gene. As yet, however, there is no consistent data to suggest that any of these SNPs influence the functional ability of PLC  . Other laboratories appear to be focussing upon the PLC   promoter, which is bi-directional and shared with the actin filament capping muscle Z-line alpha 3 gene ( @entity19337 ), 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 PLC   in diagnostic and therapeutic medicine, to discuss our current understanding of how the functional ability of PLC   might be controlled, and thus how @entity2195 might arise, and finally, to consider the potential implications of alternative sperm protein candidates, such as post-acrosomal WW-domain binding protein ( @entity58573 ), which has caused much debate and @entity911 in the field over the last few years.

Phospholipase C zeta (PLC  ) and XXXX : Clinical update and topical developments.

@entity1 :: ('9606', 'Species') :: ['mammalian', 'human', 'patients', 'patient'] @entity249 :: ('MESH:D007246', 'Disease') :: ['infertility', 'infertile'] @entity19337 :: ('93661', 'Gene') :: ['CAPZA3'] @entity4810 :: ('MESH:D007248', 'Disease') :: ['male infertility'] @entity911 :: ('MESH:D003221', 'Disease') :: ['confusion'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity2195 :: ('OMIM:211750', 'Disease') :: ['PLC   deficiency'] @entity58573 :: ('164684', 'Gene') :: ['PAWP'] @entity3457 :: ('OMIM:612348', 'Disease') :: ['Assisted oocyte activators', 'AOAs']
@entity4810 :: (MESH:D007248,Disease) :: ['male infertility']
