scholarly journals Precocious centriole disengagement and centrosome fragmentation induced by mitotic delay

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Menuka Karki ◽  
Neda Keyhaninejad ◽  
Charles B. Shuster
Keyword(s):  
Mitotic Delay

The wee1 protein kinase is required for radiation-induced mitotic delay

Nature ◽  
1992 ◽  
Vol 356 (6367) ◽  
pp. 353-355 ◽  
Author(s):  
Roy Rowley ◽  
James Hudson ◽  
Paul G. Young
Keyword(s):  
Protein Kinase ◽  
Mitotic Delay ◽  
Radiation Induced

scholarly journals Radiation-Induced Mitotic Delay in L Cells

1967 ◽  
Vol 30 (1) ◽  
pp. 155 ◽  
Author(s):  
G. F. Whitmore ◽  
J. E. Till ◽  
S. Gulyas
Keyword(s):  
L Cells ◽  
Mitotic Delay ◽  
Radiation Induced

scholarly journals A brain-penetrant microtubule-targeting agent that disrupts hallmarks of glioma tumorigenesis

2020 ◽  
Author(s):  
Eric A Horne ◽  
Philippe Diaz ◽  
Patrick J Cimino ◽  
Erik Jung ◽  
Cong Xu ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Mouse Model ◽  
Immunofluorescence Analysis ◽  
In Vivo Antitumor Activity ◽  
Microtubule Targeting Agents ◽  
Mitotic Delay ◽  
Tumor Mouse Model ◽  
In Vivo Testing ◽  
New Chemical Entity

Abstract Background Glioma is sensitive to microtubule-targeting agents (MTAs), but most MTAs do not cross the blood brain barrier (BBB). To address this limitation, we developed the new chemical entity, ST-401, a brain-penetrant MTA. Methods Synthesis of ST-401. Measures of MT assembly and dynamics. Cell proliferation and viability of patient-derived (PD) glioma in culture. Measure of tumor microtube (TM) parameters using immunofluorescence analysis and machine learning-based workflow. Pharmacokinetics (PK) and experimental toxicity in mice. In vivo antitumor activity in the RCAS/tv-a PDGFB-driven glioma (PDGFB-glioma) mouse model. Results We discovered that ST-401 disrupts microtubule (MT) function through gentle and reverisible reduction in MT assembly that triggers mitotic delay and cell death in interphase. ST-401 inhibits the formation of TMs, MT-rich structures that connect glioma to a network that promotes resistance to DNA damage. PK analysis of ST-401 in mice shows brain penetration reaching antitumor concentrations, and in vivo testing of ST-401 in a xenograft flank tumor mouse model demonstrates significant antitumor activity and no over toxicity in mice. In the PDGFB-glioma mouse model, ST-401 enhances the therapeutic efficacies of temozolomide (TMZ) and radiation therapy (RT). Conclusion Our study identifies hallmarks of glioma tumorigenesis that are sensitive to MTAs and reports ST-401 as a promising chemical scaffold to develop brain-penetrant MTAs.

scholarly journals The inhibition of Aurora A abrogates the mitotic delay induced by microtubule perturbing agents

Cell Cycle ◽  
2009 ◽  
Vol 8 (6) ◽  
pp. 876-888 ◽  
Author(s):  
Deborah R. Wysong ◽  
Arijit Chakravarty ◽  
Kara Hoar ◽  
Jeffrey A. Ecsedy
Keyword(s):  
Aurora A ◽  
Mitotic Delay

Mitotic Delay in More Mature Erythroblasts of the Dog, Induced in Vivo by Sublethal Doses of X-Rays

1964 ◽  
Vol 21 (3) ◽  
pp. 413 ◽  
Author(s):  
N. Odartchenko ◽  
H. Cottier ◽  
L. E. Feinendegen ◽  
V. P. Bond
Keyword(s):  
X Rays ◽  
Mitotic Delay ◽  
Sublethal Doses

scholarly journals Growth-Dependent Activation of Protein Kinases Suggests a Mechanism for Measuring Cell Growth

Genetics ◽  
2020 ◽  
Vol 215 (3) ◽  
pp. 729-746 ◽  
Author(s):  
Akshi Jasani ◽  
Tiffany Huynh ◽  
Douglas R. Kellogg
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Genetic Studies ◽  
Gene Deletions ◽  
Measuring Cell ◽  
Anionic Phospholipids ◽  
Link Type ◽  
Mitotic Delay ◽  
Dependent Signal ◽  
Bud Growth

In all cells, progression through the cell cycle occurs only when sufficient growth has occurred. Thus, cells must translate growth into a proportional signal that can be used to measure and transmit information about growth. Previous genetic studies in budding yeast suggested that related kinases called Gin4 and Hsl1 could function in mechanisms that measure bud growth; however, interpretation of the data was complicated by the use of gene deletions that cause complex terminal phenotypes. Here, we used the first conditional alleles of Gin4 and Hsl1 to more precisely define their functions. We show that excessive bud growth during a prolonged mitotic delay is an immediate consequence of inactivating Gin4 and Hsl1. Thus, acute loss of Gin4 and Hsl1 causes cells to behave as though they cannot detect that bud growth has occurred. We further show that Gin4 and Hsl1 undergo gradual hyperphosphorylation during bud growth that is dependent upon growth and correlated with the extent of growth. Moreover, gradual hyperphosphorylation of Gin4 during bud growth requires binding to anionic phospholipids that are delivered to the growing bud. While alternative models are possible, the data suggest that signaling lipids delivered to the growing bud generate a growth-dependent signal that could be used to measure bud growth.

scholarly journals The Budding Yeast Nuclear Envelope Adjacent to the Nucleolus Serves as a Membrane Sink during Mitotic Delay

2012 ◽  
Vol 22 (12) ◽  
pp. 1128-1133 ◽  
Author(s):  
Keren L. Witkin ◽  
Yolanda Chong ◽  
Sichen Shao ◽  
Micah T. Webster ◽  
Sujoy Lahiri ◽  
...  
Keyword(s):  
Nuclear Envelope ◽  
Budding Yeast ◽  
Mitotic Delay
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