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      The expression of cyclin-dependent kinase inhibitors p15, p16, p21, and p27 during ovarian follicle growth initiation in the mouse

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      1 , 2 , 1 , 2 , 3 ,
      Reproductive biology and endocrinology : RB&E
      BioMed Central

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          Abstract

          Background

          Cyclins regulate the cell cycle in association with cyclin dependent kinases (CDKs). CDKs are under inhibitory control of cyclin dependent kinase inhibitors (CDKIs).

          Method

          In this study we tested the expression of CDKIs p15, p16, p21 and p27 by immunohistochemistry to determine the role of CDKIs in the initiation of primordial follicle growth. Ovaries were collected from 60-day-old cycling B6D2F1/J mice (n = 16).

          Results

          Expression of p15, p16, p21 and p27 did not vary in granulosa and theca cells by the follicle stage. However, p16 staining was stronger (++) in the oocytes of all primordial, and 57.4 ± 3.1% of primary follicles compared to the remaining primary and more advanced follicles (+). Interestingly, primary follicles with weaker (+) oocyte staining for p16 had significantly larger mean follicle diameter compared to the primary and primordial follicles with stronger (++) oocyte staining (55.6 ± 2.1 vs. 32.0 ± 1.0 and 26.5 ± 0.7 μm, respectively, p < 0.0001). This difference in follicle diameter was mainly due to a larger mean oocyte diameter (primary follicles, stronger vs. weaker, 19.6 ± 0.6 vs. 31.5 ± 1.4 μm, p < 0.0001). Oocytes of atretic follicles showed stronger staining with all four CDKIs.

          Conclusions

          These preliminary findings suggest that the initiation of oocyte growth, which seems to lead follicle growth, is associated with diminished p16 expression in the mouse ovary. Further studies are needed to investigate the factors that regulate the expression of p16 in the oocyte, which might also govern the initiation of primordial follicle growth.

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          Most cited references17

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          Cell cycle control in mammalian cells: role of cyclins, cyclin dependent kinases (CDKs), growth suppressor genes and cyclin-dependent kinase inhibitors (CKIs).

          All eukaryotic cells possess similar mechanisms to regulate the progression of the cell cycle. However, higher eukaryotes have evolved to respond to a large array of positive and negative signals with an intracellular or extracellular origin. These signals are eventually integrated by a conserved protein engine consisting of holoenzymes with kinase activity, which trigger crucial transitions during the cell cycle. In this review, the mechanisms by which the mammalian cell cycle engine integrates intracellular and extracellular signals of different nature are discussed.
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            Identification and properties of an atypical catalytic subunit (p34PSK-J3/cdk4) for mammalian D type G1 cyclins.

            Murine D type cyclins associate with a catalytic subunit (p34PSK-J3) with properties distinct from known cyclin-dependent kinases (cdks). Mouse p34PSK-J3 shows less than 50% amino acid identity to p34cdc2, p33cdk2, and p36cdk3, lacks a PSTAIRE motif, and does not bind to p13suc1. Cyclin D1-p34PSK-J3 complexes accumulate in macrophages during G1 and decline in S phase, whereas complexes involving cyclins D2 and D3 form in proliferating T cells. Although histone H1 kinase activity is not detected in cyclin D or PSK-J3 immunoprecipitates, cyclin D-p34PSK-J3 complexes assembled in vitro stably bind and phosphorylate the retinoblastoma gene product (pRb) and an Rb-like protein (p107) but do not interact with pRb mutants that are functionally inactive. Thus, p34PSK-J3 is a cyclin D-regulated catalytic subunit that acts as an Rb (but not H1) kinase.
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              Formation and activation of a cyclin E-cdk2 complex during the G1 phase of the human cell cycle.

              Human cyclin E, originally identified on the basis of its ability to function as a G1 cyclin in budding yeast, associated with a cell cycle-regulated protein kinase in human cells. The cyclin E-associated kinase activity peaked during G1, before the appearance of cyclin A, and was diminished during exit from the cell cycle after differentiation or serum withdrawal. The major cyclin E-associated kinase in human cells was Cdk2 (cyclin-dependent kinase 2). The abundance of the cyclin E protein and the cyclin E-Cdk2 complex was maximal in G1 cells. These results provide further evidence that in all eukaryotes assembly of a cyclin-Cdk complex is an important step in the biochemical pathway that controls cell proliferation during G1.
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                Author and article information

                Journal
                Reprod Biol Endocrinol
                Reproductive biology and endocrinology : RB&E
                BioMed Central (London )
                1477-7827
                2003
                7 May 2003
                : 1
                : 41
                Affiliations
                [1 ]Department of Anatomy & Cell Biology, State University of New York Health Science Center, Brooklyn, NY, USA
                [2 ]Department of Obstetrics & Gynecology, New York Methodist Hospital, Brooklyn, NY, USA
                [3 ]Center for Reproductive Medicine & Infertility, Weill Medical College of Cornell University, New York, NY, USA
                Article
                1477-7827-1-41
                10.1186/1477-7827-1-41
                156659
                12777178
                914ececc-313c-4343-a01d-290022b2ce2f
                Copyright © 2003 Bayrak and Oktay; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
                History
                : 25 February 2003
                : 7 May 2003
                Categories
                Research

                Human biology
                Human biology

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