Universal control mechanism regulating onset of M-phase

Nurse, Paul

doi:10.1038/344503a0

Cited by 2,734 publications

(1,649 citation statements)

References 97 publications

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“…p93 Dis1 was thus overproduced under the Rep1 promoter in ts cdc25 mutant (Nurse 1990) which had been cultured at 36 The T-shaped cells were not present at 0 h but were plentiful after 4 h. Overproduction of p93 Dis1 in cdc25 cells was verified by immunoblotting (data not shown). Thus cell shape abnormality occurred without cell division in the presence of interphase microtubule arrays.…”

Section: Overproduction P93 Dis1 In G2-arrested Cellsmentioning

confidence: 85%

Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction

et al. 1996

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Background: Fission yeast microtubule associating protein (MAP) p93 Dis1 functions for sister chromatid separation: dis1 mutants fail to separate chromosomes, while the spindle elongates but without cyclin destruction. p93 Dis1 localizes along microtubules in interphase cytoplasm, but shifts to the spindle pole body (SPB) and spindle microtubules upon the entry into mitosis. In this study, regions of p93 Dis1 were dissected to examine their role.

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Section: Overproduction P93 Dis1 In G2-arrested Cellsmentioning

confidence: 85%

Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction

et al. 1996

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“…Differing from these results, our data revealed that IAP antagonists and cIAP1/2 siRNAs can slow cell proliferation by inducing G2/M phase arrest, alone or in combination with chemotherapeutic agents (Figures 2A, 3A and Figure S2). Among various cell cycle checkpoint proteins participating in the evolution of the cell cycle, cyclin A‐CDK1 complex and cyclin A‐CDK2 are required for passage into the late S/G2 phase while the cyclin B1‐CDK1 complex is involved in G2/M transition 42, 43, 44. Activity of these CDKs is regulated by inhibitor p21 45.…”

Section: Discussionmentioning

confidence: 99%

Targeting inhibitors of apoptosis proteins suppresses medulloblastoma cell proliferation via G2/M phase arrest and attenuated neddylation of p21

et al. 2018

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Medulloblastoma (MB) is the most common type of malignant childhood brain tumor. We previously showed that inhibitors of apoptosis proteins (IAP) small‐molecule inhibitors (LCL161 or LBW242) combined with chemotherapy have synergistic antiproliferative effects on MB cells. The synergistic antitumor effects of combination treatments happen through induction of autophagy and caspase‐3/7‐activated apoptosis. Here, we investigated the effects of IAP inhibitors or silencing IAP on cell cycle regulation. We discovered that treatment with IAP inhibitors or their combination with conventional chemotherapy (vincristine or cisplatin), as well as RNAi knockdown of cIAP1/2 or XIAP arrested MB cells in the G2/M phase through downregulation of cyclin B1‐CDK1 and cyclin A‐CDK1/2. Among these three IAPs, only silencing cIAP1 expression enhanced p21 dependent‐G2/M phase accumulation. IAP inhibitors reduced cIAP1 expression and increased p21 expression in time course experiments. Furthermore, cIAP1 can govern p21 proteasomal degradation via neddylation in lieu of ubiquitination. Inhibition of IAPs significantly abrogated cIAP1‐mediated p21 degradation. We also observed an inverse correlation between nuclear cIAP1 and nuclear p21 expressions in MB tumor tissues. These findings provide new mechanistic evidence of the influence of IAP inhibitors on MB cell proliferation through disruption of the cell cycle.

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“…The universal driver for the G 2 /M transition is the M-phase promoting factor MPF. MPF is a heterodimer composed of a regulatory cyclin subunit, cyclin B, and a catalytic subunit, Cdc2 kinase (Dunphy et al, 1988;Gautier et al, 1988;Nurse, 1990). Active Cdc2 drives entry into M-phase by phosphorylating substrates that lead to nuclear envelope breakdown (lamins A and B in vertebrates) and spindle formation (nucleolin; Belenguer et al, 1990;Heald and McKeon, 1990;Peter et al, 1990a,b).…”

Section: Cell Cycle Resumptionmentioning

confidence: 99%

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

Horner

Wolfner

2008

Developmental Dynamics

183

177

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The transition from mature oocyte to developing embryo requires a coordinated series of events, collectively known as egg activation. Egg activation includes changes to egg coverings to prevent polyspermy, release of oocyte meiotic arrest, generation of haploid female and male pronuclei, changes in maternal mRNAs and protein populations, and cytoskeletal rearrangements. In many animals, egg activation is triggered by fertilization, which increases intracellular calcium within the oocyte and thereby regulates molecular events of egg activation. In other animals, fertilization-independent external signals, including mechanical stimulation of eggs and/or changes in ionic milieu, trigger activation. Recent studies have clarified the upstream portion of pathways leading to eggshell changes and cell cycle resumption and have identified activation-induced changes in maternal mRNA and protein profiles that can identify molecular players in the downstream events of egg activation. We review signals that trigger activation and how they link to subsequent molecular events of egg activation. Developmental Dynamics 237:527-544, 2008.

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Universal control mechanism regulating onset of M-phase

Abstract: The onset of M-phase is regulated by a mechanism common to all eukaryotic cells. Entry into M-phase is determined by activation of the p34cdc2 protein kinase which requires p34cdc2 dephosphorylation and association with cyclin.

Cited by 2,734 publications

References 97 publications

Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction

Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction

Targeting inhibitors of apoptosis proteins suppresses medulloblastoma cell proliferation via G2/M phase arrest and attenuated neddylation of p21

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

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Universal control mechanism regulating onset of M-phase

Abstract: The onset of M-phase is regulated by a mechanism common to all eukaryotic cells. Entry into M-phase is determined by activation of the p34cdc2 protein kinase which requires p34cdc2 dephosphorylation and association with cyclin.

Cited by 2,734 publications

References 97 publications

Dissection of fission yeast microtubule associating protein p93Dis1: regions implicated in regulated localization and microtubule interaction

Dissection of fission yeast microtubule associating protein p93Dis1: regions implicated in regulated localization and microtubule interaction

Targeting inhibitors of apoptosis proteins suppresses medulloblastoma cell proliferation via G2/M phase arrest and attenuated neddylation of p21

Transitioning from egg to embryo: Triggers and mechanisms of egg activation

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Product

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Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction

Dissection of fission yeast microtubule associating protein p93^Dis1: regions implicated in regulated localization and microtubule interaction