scholarly journals An Intrinsic Cell Cycle Checkpoint Pathway Mediated by MEK and ERK in Drosophila

2006 ◽  
Vol 11 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Vladic Mogila ◽  
Fan Xia ◽  
Willis X. Li
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

scholarly journals Centrosome Dynamics and Its Role in Inflammatory Response and Metastatic Process

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 629
Author(s):  
Massimo Pancione ◽  
Luigi Cerulo ◽  
Andrea Remo ◽  
Guido Giordano ◽  
Álvaro Gutierrez-Uzquiza ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Rho Gtpases ◽  
Human Cancer ◽  
Genetic Disorders ◽  
Cell Cycle Checkpoint ◽  
Animal Cells ◽  
Normal Tissues ◽  
Checkpoint Pathway ◽  
New Findings ◽  
Cycle Checkpoint

Metastasis is a process by which cancer cells escape from the location of the primary tumor invading normal tissues at distant organs. Chromosomal instability (CIN) is a hallmark of human cancer, associated with metastasis and therapeutic resistance. The centrosome plays a major role in organizing the microtubule cytoskeleton in animal cells regulating cellular architecture and cell division. Loss of centrosome integrity activates the p38-p53-p21 pathway, which results in cell-cycle arrest or senescence and acts as a cell-cycle checkpoint pathway. Structural and numerical centrosome abnormalities can lead to aneuploidy and CIN. New findings derived from studies on cancer and rare genetic disorders suggest that centrosome dysfunction alters the cellular microenvironment through Rho GTPases, p38, and JNK (c-Jun N-terminal Kinase)-dependent signaling in a way that is favorable for pro-invasive secretory phenotypes and aneuploidy tolerance. We here review recent data on how centrosomes act as complex molecular platforms for Rho GTPases and p38 MAPK (Mitogen activated kinase) signaling at the crossroads of CIN, cytoskeleton remodeling, and immune evasion via both cell-autonomous and non-autonomous mechanisms.

scholarly journals The Maize Homologue of the Cell Cycle Checkpoint Protein MAD2 Reveals Kinetochore Substructure and Contrasting Mitotic and Meiotic Localization Patterns

1999 ◽  
Vol 145 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hong-Guo Yu ◽  
Michael G. Muszynski ◽  
R. Kelly Dawe
Keyword(s):  
Cell Cycle ◽  
Spindle Assembly ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Protein ◽  
Microtubule Attachment ◽  
Checkpoint Pathway ◽  
Outer Domain ◽  
Cycle Checkpoint ◽  
Mitosis And Meiosis ◽  
Meiosis I

We have identified a maize homologue of yeast MAD2, an essential component in the spindle checkpoint pathway that ensures metaphase is complete before anaphase begins. Combined immunolocalization of MAD2 and a recently cloned maize CENPC homologue indicates that MAD2 localizes to an outer domain of the prometaphase kinetochore. MAD2 staining was primarily observed on mitotic kinetochores that lacked attached microtubules; i.e., at prometaphase or when the microtubules were depolymerized with oryzalin. In contrast, the loss of MAD2 staining in meiosis was not correlated with initial microtubule attachment but was correlated with a measure of tension: the distance between homologous or sister kinetochores (in meiosis I and II, respectively). Further, the tension-sensitive 3F3/2 phosphoepitope colocalized, and was lost concomitantly, with MAD2 staining at the meiotic kinetochore. The mechanism of spindle assembly (discussed here with respect to maize mitosis and meiosis) is likely to affect the relative contributions of attachment and tension. We support the idea that MAD2 is attachment-sensitive and that tension stabilizes microtubule attachments.

scholarly journals Interactions between p53 and MDM2 in a mammalian cell cycle checkpoint pathway.

1994 ◽  
Vol 91 (7) ◽  
pp. 2684-2688 ◽  
Author(s):  
C. Y. Chen ◽  
J. D. Oliner ◽  
Q. Zhan ◽  
A. J. Fornace ◽  
B. Vogelstein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia

Cell ◽  
1992 ◽  
Vol 71 (4) ◽  
pp. 587-597 ◽  
Author(s):  
Michael B. Kastan ◽  
Qimin Zhan ◽  
Wafik S. El-Deiry ◽  
France Carrier ◽  
Tyler Jacks ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
Ataxia Telangiectasia ◽  
Cell Cycle Checkpoint ◽  
Checkpoint Pathway ◽  
Mammalian Cell Cycle ◽  
Cycle Checkpoint

scholarly journals Chromothripsis: A Cause of Genome Instability in Cancer

2021 ◽  
Vol 3 (4) ◽  
pp. 5-11
Author(s):  
Ishita Agrawal ◽  
Keyword(s):  
Cell Cycle ◽  
Cell Division ◽  
Cell Growth ◽  
Genome Instability ◽  
Cell Cycle Checkpoint ◽  
Genetic Changes ◽  
Checkpoint Pathway ◽  
Cycle Checkpoint

Cancer is a term given to uncontrolled cell growth, which is the result of accumulation of genetic changes during cell division. It can occur due to both genetic and environmental reasons. One such genetic cause of cancer discovered recently is known as Chromothripsis. It is defined as the fragmentation and rearrangement of chromosomes. Researchers are still trying to find the true mechanism underlying Chromothripsis. Two models have been significantly described; first one is the ‘micronuclei hypothesis’, which occurs as a result of chromosome mis-segregation during Mitosis. Second model is based on the ‘telomere crisis’, which occurs due to faulty telomerase enzyme and cell cycle checkpoint pathway. In this letter, we have tried to give brief information about the mechanisms behind Chromothripsis and their role in causing genome instability leading to cancer.

Cell Cycle Checkpoint Genes and Aneuploidy: A Short Review

2001 ◽  
Vol 2 (2) ◽  
pp. 171-180 ◽  
Author(s):  
William Kearns ◽  
Johnson Liu
Keyword(s):  
Cell Cycle ◽  
Short Review ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint ◽  
Checkpoint Genes
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