Developmental expression and possible role of perinuclear theca proteins in mammalian spermatozoa

1995 ◽  
Vol 7 (4) ◽  
pp. 777 ◽  
Author(s):  
RJ Oko
2008 ◽  
Vol 20 (9) ◽  
pp. 116
Author(s):  
L. A. Mitchell ◽  
B. Nixon ◽  
M. A. Baker ◽  
R. J. Aitken

Capacitation is a pre-requisite for mammalian spermatozoa allowing them to gain the ability to fertilise an oocyte. A fundamental part of this mechanism is a dramatic increase in tyrosine phosphorylation. Implicated in this process in the mouse is a unique cAMP/PKA-mediated pathway involving a PKA-activated tyrosine kinase suggested to be pp60c-src (SRC). The Src kinases examined were predominantly expressed in the human sperm tail, a site compatible with a role in mediating the capacitation-associated tyrosine phosphorylation cascade. Co-immunoprecipitation revealed that PKA-c could be isolated from sperm and this interaction was restricted to capacitated cells, suggesting PKA-mediated activation of SRC forms an integral part of the signalling cascade assembled during capacitation. Upon activation, SRC undergoes autophosphorylation of Y416 and thus phosphorylation of this residue indicates the presence of active SRC kinase. The phosphorylation status of SRC was compared using both 2D-immunoblotting and immunocytochemical studies, both revealing a significant increase in SRC activation during capacitation. Furthermore, suppression of PKA and SRC through application of SU6656, or H89, a PKA inhibitor, led to a dramatic decrease in tyrosine phosphorylation and SRC activity. In conclusion, this study has provided evidence for the involvement of non-receptor tyrosine kinase, SRC, in regulating tyrosine phosphorylation associated with capacitation. Inhibition of SRC did not completely suppress tyrosine phosphorylation suggesting this complex signal transduction pathway exhibits a degree of functional redundancy.


Cell Research ◽  
2007 ◽  
Vol 17 (2) ◽  
pp. 163-173 ◽  
Author(s):  
Qing Yun Liu ◽  
Zhi Li Wu ◽  
Wen Jian Lv ◽  
Yuan Chang Yan ◽  
Yi Ping Li

Author(s):  
Y. Lax ◽  
S. Grossman ◽  
S. Rubinstein ◽  
N. Magid ◽  
H. Breitbart

PLoS ONE ◽  
2012 ◽  
Vol 7 (2) ◽  
pp. e32354 ◽  
Author(s):  
Dorke Meyer ◽  
Anja Voigt ◽  
Patricia Widmayer ◽  
Heike Borth ◽  
Sandra Huebner ◽  
...  

1995 ◽  
Vol 7 (4) ◽  
pp. 659 ◽  
Author(s):  
RJ Aitken

The cellular generation of reactive oxygen species was first observed in mammalian spermatozoa in the late 1940s. The field then remained dormant for 30 years until Thaddeus Mann and Roy Jones published a series of landmark papers in the 1970s in which the importance of lipid peroxidation as a mechanism for damaging mammalian spermatozoa was first intimated. The subsequent demonstration that human spermatozoa produce reactive oxygen species and are susceptible to peroxidative damage has triggered intense interest in the role of oxidative stress in the aetiology of male infertility. Moreover, data have recently been obtained to indicate that, although excessive exposure to reactive oxygen species may be harmful to spermatozoa, in physiological amounts these molecules are of importance in the control of normal sperm function. This review considers the dualistic role of reactive oxygen species and sets out the current understanding of the importance of oxidative processes in both the physiology and the pathology of the human spermatozoon. Extra keywords: human spermatozoa, reactive oxygen species.


Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 448 ◽  
Author(s):  
Pavel A. Kipnis ◽  
Brennan J. Sullivan ◽  
Shilpa D. Kadam

Seizure incidence, severity, and antiseizure medication (ASM) efficacy varies between males and females. Differences in sex-dependent signaling pathways that determine network excitability may be responsible. The identification and validation of sex-dependent molecular mechanisms that influence seizure susceptibility is an emerging focus of neuroscience research. The electroneutral cation-chloride cotransporters (CCCs) of the SLC12A gene family utilize Na+-K+-ATPase generated electrochemical gradients to transport chloride into or out of neurons. CCCs regulate neuronal chloride gradients, cell volume, and have a strong influence over the electrical response to the inhibitory neurotransmitter GABA. Acquired or genetic causes of CCCs dysfunction have been linked to seizures during early postnatal development, epileptogenesis, and refractoriness to ASMs. A growing number of studies suggest that the developmental expression of CCCs, such as KCC2, is sex-dependent. This review will summarize the reports of sexual dimorphism in epileptology while focusing on the role of chloride cotransporters and their associated modulators that can influence seizure susceptibility.


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