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Identification of Novel ras Family Genes in A Human Teratocarcinoma Cell Line by Oligonucleotide Screening
Published in Juan Carlos Lacal, Frank McCormick, The ras Superfamily of GTPases, 2017
George T. Drivas, Mark G. Rush, Peter D’Eustachio
Ran/TC4 interacts with a second protein, RCC1 (regulator of chromosome condensation-1).48,50 RCC1 is a chromatin-associated DNA binding protein, mutations in which result in premature initiation of mitosis in both fission yeast50 and mammals.51 Specifically, in the absence of wild-type RCC1 function, the cell cycle checkpoint that prevents the onset of mitosis until the completion of DNA synthesis fails to operate. Such cells enter mitosis even in the presence of DNA synthesis inhibitors due to the premature activation of mitosis promoting factor (MPF).
Disruption of Nongenomic Steroid Actions on Gametes and Serotonergic Pathways Controlling Reproductive Neuroendocrine Function by Environmental Chemicals
Published in Rajesh K. Naz, Endocrine Disruptors, 2004
Moreover, inhibitors of transcription did not prevent 17,20β-P-induced final OM in teleosts, which supports the concept that the action of the MIS is nongenomic [77]. The finding that increases in cyclic AMP levels by pharmacological agents block MIS stimulation of OM in vitro also suggests that the action of the MIS is nongenomic and instead involves a second messenger signal transduction pathway [77]. A decrease in cyclic AMP is required for MIS induction of final oocyte maturation in rainbow trout and spotted seatrout, which is mediated by activation of a pertussis toxin-sensitive inhibitory G-protein in the signal transduction pathway across the oocyte plasma membrane to the cytoplasm [77, 83]. A cytoplasmic factor, named maturation-promoting factor, composed of cdc 2 kinase and cyclin B, is formed and is the intracellular mediator of OM [77].
The Cell and Cell Division
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
This process is tightly controlled at certain critical points of the cell cycle, which are known as cell cycle checkpoints, at which certain brakes can be applied to stop the process if conditions are unfavorable (Fig. 20). Checkpoints are found at the G1/S transition (the start checkpoint); another is found at G2/M. Most studies have concentrated on the G2/M transition (the mitosis checkpoint). This cell cycle control mechanism is based on two series of proteins: the cyclin-dependent protein kinases (CDKs), which phosphorylate a series of downstream proteins on serine and threonine residues, and the cyclins, which along with other regulatory proteins bind to CDKs to alter their activity. Different cyclins are synthesized during different parts of the cell cycle (mitotic cyclins and G1 cyclins) (Fig. 21). In mammalian cells, there are at least six types of cyclin (A, B, C, D, E, and F). Entry into mitosis is stimulated by activation of a CDK by mitotic cyclin; in amphibians, this is known as maturation promotion factor (MPF) and consists of a cyclin and a cyclin-dependent kinase called cdc2—another is known as cdc4. Repetitive synthesis and degradation of cyclins is associated with the cell cycle. Activation of MPF drives mitosis, and degradation of cyclin then allows the cell to enter the S phase. As we shall see later, there is a set of proteins that can inhibit CDK known as cyclin-dependent kinase inhibitors (or inhibitors of cyclin-dependent kinases—INKs). The activity of the CDK can therefore be abruptly switched on and off during different parts of the cell cycle.
Human oocyte cryopreservation: revised evidence for practice
Published in Human Fertility, 2023
Virginia N. Bolton, Catherine Hayden, Michele Robinson, Dima Abdo, Angela Pericleous-Smith
It has been suggested that warmed oocytes should be incubated in culture medium to allow repolymerisation of the meiotic spindle (ACE and BFS, Cutting et al., 2009) before insemination using ICSI. With respect to the timing of ICSI following warming, it has been suggested that ICSI should be carried out within 1 hour of warming to avoid any potentially deleterious effects of in vitro aging (Iussig et al., 2019). Thawed slow frozen oocytes allowed to age in vitro show reduced levels of maturation-promoting factor (MPF) after 1 hour in culture (Bromfield et al., 2009). Since MPF is critical in the preservation of spindle integrity, it has been suggested that as for slow frozen oocytes, the duration of culture of vitrified oocytes between warming and ICSI should be limited to 1h to prevent potential loss in the organisation of the meiotic spindle (Iussig et al., 2019).
Clinical exome sequencing identifies novel compound heterozygous mutations of the WEE2 gene in primary infertile women with fertilization failure
Published in Gynecological Endocrinology, 2021
Ancong Wang, Shan Huang, Min Liu, Baosong Wang, Fengxia Wu, Dongyi Zhu, Xiangyu Zhao
The mature oocyte is arrested at the second meiotic metaphase (MII) and must undergo MII exit in order to be fertilized. Fertilization results in a series of rapid and transient increases in intracellular calcium concentration. These Ca2+ signals drive cell cycle recovery by inactivating the maturation promoting factor (MPF), which is regulated by the inhibitory phosphorylation of cdc2. Cdc2 is a kinase family catalyzed by WEE2 protein [7]. It is found that WEE2 protein encoded by WEE2 gene belongs to WEE kinase protein family, which comes from maternal origin and preserved among different species. Studies on some oocytes of mammals have shown that WEE2 is involved in GV phase quiescence, MII, and prokaryote formation [8–11]. Recently, studies reported that primary infertility in several women with fertilization failure was caused by mutations of the WEE2 gene [12–18].
Role of granulosa cell mitogen-activated protein kinase 3/1 in gonadotropin-mediated meiotic resumption from diplotene arrest of mammalian oocytes
Published in Growth Factors, 2018
Kankshi Sahu, Anumegha Gupta, Alka Sharma, Meenakshi Tiwari, Ashutosh N. Pandey, Shilpa Prasad, Pramod K. Yadav, Ajai K. Pandey, Tulsidas G. Shrivastav, Shail K. Chaube
A transient decrease of cAMP level may induce maturation promoting factor (MPF) destabilization (Gupta et al., 2017; Pandey et al., 2010; Tiwari & Chaube, 2017a,b). MPF is composed of an enzymatic subunit cyclin-dependent kinase 1 (Cdk1) and regulatory subunit cyclin B1 (Gupta et al., 2017; Pandey et al., 2010; Tripathi et al., 2010). The phosphorylation at Thr14/Tyr15 and dephosphorylation at Thr161 amino acid residues of Cdk1 as well as dissociation and degradation of cyclin B1 result in MPF destabilization (Gupta et al., 2017; Prasad et al., 2015, 2016, 2017; Tiwari & Chaube, 2017a,b,c). The destabilized MPF triggers meiotic resumption from diplotene arrest in follicular oocytes (Prasad et al., 2015; Tiwari & Chaube, 2016; Tripathi et al., 2010).