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M phase-promoting factor

Borgne, A, Ostvold, A. C., Flament, S., Meijer, L. (1999). Intra-M phase-promoting factor phosphorylation of cyclin B at the prophase/ metaphase transition. The Journal of Biological Chemistry, 274, 11977-11986. [Pg.442]

These toxins can influence the cell cycle by a complex series of direct and indirect actions on a variety of molecular targets by inhibiting protein phosphatases, hence altering the phosphorylation state of proteins involved in the control of the cell cycle. Exposine of mammalian cells to OA leads to hyperphosphorylation and activation of cyclin-dependent kinase 1-cyclin B complex (CDKl-cyc-lin B, called also M-phase-promoting factor, MPF or Cdc2-cyclin B), which leads the cells to G2/M transition and to a mitosis-like state, characterized by a premature chromosome condensation and break of the nuclear lamina. This event seems to depend mainly on the inhibition of protein phosphatase 2A, which is necessary to maintain the complex CDKl-cydin B in its inactive form. Nevertheless, inhibition of other phosphatases, such as protein phosphatases 4 and 5, could mediate. [Pg.235]

Grieco D, Porcellini A, Avvedimento EV, Gottesman ME. 1996. Requirement for cAMP-PKA pathway activation by M phase-promoting factor in the transition from mitosis to interphase. Science 271(5256) 1718-1723. [Pg.477]

Yu BZ, Zheng J, Yu AM, Shi XY, Liu Y, Wu DD, Fu W, Yang J. 2004. Effects of protein kinase C on M-phase promoting factor in early development of fertilized mouse eggs. Cell Biochem Funct 22(5) 291-298. [Pg.497]

Santella L, Ercolano E, Lim D, Nusco GA, Moccia F. 2003. Activated M-phase-promoting factor (MPF) is exported from the nucleus of starfish oocytes to increase the sensitivity of the Ins(l,4,5)P3 receptors. Biochem Soc Trans 31(Pt l) 79-82. [Pg.546]

Entry of animal cells into mitosis is based on the mitosis-promoting factor (MPF). MPF consists of CDK1 (cdc2) and cyclin B. The intracellular concentration of cyclin B increases constantly until mitosis starts, and then declines again rapidly (top left). MPF is initially inactive, because CDKl is phosphorylated and cyclin B is dephosphorylated (top center). The M phase is triggered when a protein phosphatase [1] dephosphorylates the CDK while cyclin B is phosphorylated by a kinase [2]. in its active form, MPF phosphorylates various proteins that have functions in mitosis—e.g., histone HI (see p. 238), components of the cytoskeleton such as the laminins in the nuclear membrane, transcription factors, mitotic spindle proteins, and various enzymes. [Pg.394]

Entry into and the course of mitosis are primarily determined by the activity of the CDC2 kinase. The CDC2 kinase in the active form exists as a complex with cychn B and, together with the cyclin, forms the mitosis promoting factor, MPF. The activity of MPF oscillates in the cell cycle and is the triggering factor for entry of the cell into M phase. [Pg.415]

Entry into M phase is primarily determined by the activity of the cyclin B-CDC2 kinase complex, which is also called the mitosis-promoting factor, MPF. [Pg.463]

Hunt T. 1989. Maturation promoting factor, cyclin and the control of M-phase. Curr Opin Cell Biol l(2) 268-274. [Pg.534]

This is the Wigner-Eckart theorem, a very important result which underpins most applications of angular momentum theory to quantum mechanics. It states that the required matrix element can be written as the product of a 3- j symbol and a phase factor, which expresses all the angular dependence, and the reduced matrix element (rj, j T/ (d) if. j ) which is independent of component quantum numbers and hence of orientation. Thus one quantity is sufficient to determine all (2j + 1) x (2k + 1) x (2/ + 1) possible matrix elements (rj, j, mfIkq(A) rj, jf m ). The phase factor arises because the bra (rj, j, m transforms in the same way as the ket (— y m rj, j, —m). The definition of the reduced matrix element in equation (5.123), which is due to Edmonds [1] and also favoured by Zare [4], is the one we shall use throughout this book. The alternative definition, promoted by Brink and Satchler [3],... [Pg.163]


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