scholarly journals Indirect semiquantitative determination of p34cdc2 levels in G1 and G2 cells of the carbohydrate-starved root meristems in Vicia faba var. minor

2014 ◽  
Vol 68 (4) ◽  
pp. 255-259 ◽  
Author(s):  
Justyna Polit
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Vicia Faba ◽  
Absolute Level ◽  
Cycle Enzyme ◽  
Meristematic Cells ◽  
Semiquantitative Determination ◽  
M Phase ◽  
Cell Cycle Block

In eukaryotes, the 34kDa kinase (p34) encoded by the <em>cdc2</em> gene is a key regulator of both the onset of DNA synthesis (G<sub>1</sub> to S phase transition) and the onset of mitosis (G<sub>1</sub> to M phase transition). Using mouse anti-human PSTAIRE and FITClabelled goat antibodies, indirect semiquantitative determination of p34<sup><em>cdc2</em></sup> levels was performed in meristematic cells from the control (intact) and excised, carbohydrate-starved main roots of Vicia faba var. minor. No evident differences in the intensity of fluorescence was found either between the G<sub>1</sub> and G<sub>2</sub> cells or between the control cells and the cells arrested at both Principal Control Points by carbohydrate starvation. It seems thus, that the cell cycle block induced in meristematic cells of <em>V. faba</em> var. <em>minor</em> is not correlated with the absolute level of the key cell cycle enzyme responsible for phosphory-lution of cellular proteins, but primarily with the altered activity of p34<sup><em>cdc2</em></sup>.

The Polo-like kinase Plx1 is a component of the MPF amplification loop at the G2/M-phase transition of the cell cycle in Xenopus eggs

1998 ◽  
Vol 111 (12) ◽  
pp. 1751-1757 ◽  
Author(s):  
A. Abrieu ◽  
T. Brassac ◽  
S. Galas ◽  
D. Fisher ◽  
J.C. Labbe ◽  
...  
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Cyclin A ◽  
Cyclin B ◽  
Cdc2 Kinase ◽  
C Terminus ◽  
M Phase ◽  
Egg Extracts ◽  
Amplification Loop

We have investigated whether Plx1, a kinase recently shown to phosphorylate cdc25c in vitro, is required for activation of cdc25c at the G2/M-phase transition of the cell cycle in Xenopus. Using immunodepletion or the mere addition of an antibody against the C terminus of Plx1, which suppressed its activation (not its activity) at G2/M, we show that Plx1 activity is required for activation of cyclin B-cdc2 kinase in both interphase egg extracts receiving recombinant cyclin B, and cycling extracts that spontaneously oscillate between interphase and mitosis. Furthermore, a positive feedback loop allows cyclin B-cdc2 kinase to activate Plx1 at the G2/M-phase transition. In contrast, activation of cyclin A-cdc2 kinase does not require Plx1 activity, and cyclin A-cdc2 kinase fails to activate Plx1 and its consequence, cdc25c activation in cycling extracts.

Targeted Modulation of FAK/PI3K/PDK1/AKT and FAK/p53 Pathways by Cucurbitacin B for the Antiproliferation Effect Against Human Cholangiocarcinoma Cells

2020 ◽  
Vol 48 (06) ◽  
pp. 1475-1489
Author(s):  
Sirinapha Klungsaeng ◽  
Veerapol Kukongviriyapan ◽  
Auemduan Prawan ◽  
Sarinya Kongpetch ◽  
Laddawan Senggunprai
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tyrosine Kinases ◽  
Molecular Mechanisms ◽  
Inhibitory Effect ◽  
Chemotherapeutic Agents ◽  
Cucurbitacin B ◽  
M Phase ◽  
Cell Cycle Disruption

Inadequate responses to traditional chemotherapeutic agents in cholangiocarcinoma (CCA) emphasize a requirement for new effective compounds for the treatment of this malignancy. This study aimed to investigate the antiproliferative property of cucurbitacin B on KKU-100 CCA cells. The determination of underlying molecular mechanisms was also carried out. The results revealed that cucurbitacin B suppressed growth and replicative ability to form colonies of CCA cells, suggesting the antiproliferative effect of this compound against the cells. Flow cytometry analysis demonstrated that the interfering effect of cucurbitacin B on the CCA cell cycle at the G2/M phase was accountable for its antiproliferation property. Accompanied with cell cycle disruption, cucurbitacin B altered the expression of proteins involved in the G2/M phase transition including downregulation of cyclin A, cyclin D1, and cdc25A, and upregulation of p21. Additional molecular studies demonstrated that cucurbitacin B suppressed the activation of focal adhesion kinase (FAK) which consequently resulted in inhibition of its kinase-dependent and kinase-independent downstream targets contributing to the regulation of cell proliferation including PI3K/PDK1/AKT and p53 proteins. In this study, the transient knockdown of FAK using siRNA was employed to ascertain the role of FAK in CCA cell proliferation. Finally, the effect of cucurbitacin B on upstream receptor tyrosine kinases regulating FAK activation was elucidated. The results showed that the inhibitory effect of cucurbitacin B on FAK activation in CCA cells is mediated via interference of EGFR and HER2 expression. Collectively, cucurbitacin B might be a promising drug for CCA treatment by targeting FAK protein.

Crystal structure of the catalytic subunit of Cdc25B required for G 2 /M phase transition of the cell cycle 1 1Edited by I. A. Wilson

1999 ◽  
Vol 293 (3) ◽  
pp. 559-568 ◽  
Author(s):  
Ross A Reynolds ◽  
Anthony W Yem ◽  
Cindy L Wolfe ◽  
Martin R Deibel ◽  
Constance G Chidester ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Phase Transition ◽  
Cell Cycle ◽  
Catalytic Subunit ◽  
M Phase

scholarly journals Nuclear Accumulation of p21Cip1 at the Onset of Mitosis: a Role at the G2/M-Phase Transition

1998 ◽  
Vol 18 (1) ◽  
pp. 546-557 ◽  
Author(s):  
Vjekoslav Dulić ◽  
Gretchen H. Stein ◽  
Dariush Farahi Far ◽  
Steven I. Reed
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Nuclear Translocation ◽  
Cyclin A ◽  
Cyclin B1 ◽  
Negative Control ◽  
Cell Cycle Checkpoint ◽  
Nuclear Accumulation ◽  
E6 Oncoprotein ◽  
M Phase

ABSTRACT Cell cycle arrest in G1 in response to ionizing radiation or senescence is believed to be provoked by inactivation of G1 cyclin-cyclin-dependent kinases (Cdks) by the Cdk inhibitor p21Cip1/Waf1/Sdi1. We provide evidence that in addition to exerting negative control of the G1/S phase transition, p21 may play a role at the onset of mitosis. In nontransformed fibroblasts, p21 transiently reaccumulates in the nucleus near the G2/M-phase boundary, concomitant with cyclin B1 nuclear translocation, and associates with a fraction of cyclin A-Cdk and cyclin B1-Cdk complexes. Premitotic nuclear accumulation of cyclin B1 is not detectable in cells with low p21 levels, such as fibroblasts expressing the viral human papillomavirus type 16 E6 oncoprotein, which functionally inactivates p53, or in tumor-derived cells. Moreover, synchronized E6-expressing fibroblasts show accelerated entry into mitosis compared to wild-type cells and exhibit higher cyclin A- and cyclin B1-associated kinase activities. Finally, primary embryonic fibroblasts derived from p21−/− mice have significantly reduced numbers of premitotic cells with nuclear cyclin B1. These data suggest that p21 promotes a transient pause late in G2 that may contribute to the implementation of late cell cycle checkpoint controls.

p21WAF1/CIP1 Inhibits Cell Cycle Progression but Not G2/M-Phase Transition Following Methylmercury Exposure

2002 ◽  
Vol 178 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Ma Aileen C. Mendoza ◽  
Rafael A. Ponce ◽  
Ying C. Ou ◽  
Elaine M. Faustman
Keyword(s):  
Phase Transition ◽  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Methylmercury Exposure ◽  
M Phase
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