Paclitaxel inhibits osteoclast formation and bone resorption via influencing mitotic cell cycle arrest and RANKL-induced activation of NF-κB and ERK

2012 ◽  
Vol 113 (3) ◽  
pp. 946-955 ◽  
Author(s):  
Estabelle S. M. Ang ◽  
Nathan J. Pavlos ◽  
Shek Man Chim ◽  
Hao Tian Feng ◽  
Robin M. Scaife ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Resorption ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Osteoclast Formation ◽  
Mitotic Cell Cycle ◽  
Cycle Arrest

scholarly journals NF-κB Promotes Survival during Mitotic Cell Cycle Arrest

2003 ◽  
Vol 279 (2) ◽  
pp. 1482-1490 ◽  
Author(s):  
Pratibha Mistry ◽  
Karl Deacon ◽  
Sharad Mistry ◽  
Jonathan Blank ◽  
Rajnikant Patel
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Mitotic Cell Cycle ◽  
Cycle Arrest

scholarly journals CDC44: a putative nucleotide-binding protein required for cell cycle progression that has homology to subunits of replication factor C.

1994 ◽  
Vol 14 (1) ◽  
pp. 255-267 ◽  
Author(s):  
E A Howell ◽  
M A McAlear ◽  
D Rose ◽  
C Holm
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Large Subunit ◽  
Mitotic Cell ◽  
Predicted Amino Acid Sequence ◽  
Replication Factor C ◽  
Replication Factor ◽  
Cycle Arrest ◽  
Factor C

To investigate the means by which a cell regulates the progression of the mitotic cell cycle, we characterized cdc44, a mutation that causes Saccharomyces cerevisiae cells to arrest before mitosis. CDC44 encodes a 96-kDa basic protein with significant homology to a human protein that binds DNA (PO-GA) and to three subunits of human replication factor C (also called activator 1). The hypothesis that Cdc44p is involved in DNA metabolism is supported by the observations that (i) levels of mitotic recombination suggest elevated rates of DNA damage in cdc44 mutants and (ii) the cell cycle arrest observed in cdc44 mutants is alleviated by the DNA damage checkpoint mutations rad9, mec1, and mec2. The predicted amino acid sequence of Cdc44p contains GTPase consensus sites, and mutations in these regions cause a conditional cell cycle arrest. Taken together, these observations suggest that the essential CDC44 gene may encode the large subunit of yeast replication factor C.

CDC44: a putative nucleotide-binding protein required for cell cycle progression that has homology to subunits of replication factor C

1994 ◽  
Vol 14 (1) ◽  
pp. 255-267
Author(s):  
E A Howell ◽  
M A McAlear ◽  
D Rose ◽  
C Holm
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Large Subunit ◽  
Mitotic Cell ◽  
Predicted Amino Acid Sequence ◽  
Replication Factor C ◽  
Replication Factor ◽  
Cycle Arrest ◽  
Factor C

To investigate the means by which a cell regulates the progression of the mitotic cell cycle, we characterized cdc44, a mutation that causes Saccharomyces cerevisiae cells to arrest before mitosis. CDC44 encodes a 96-kDa basic protein with significant homology to a human protein that binds DNA (PO-GA) and to three subunits of human replication factor C (also called activator 1). The hypothesis that Cdc44p is involved in DNA metabolism is supported by the observations that (i) levels of mitotic recombination suggest elevated rates of DNA damage in cdc44 mutants and (ii) the cell cycle arrest observed in cdc44 mutants is alleviated by the DNA damage checkpoint mutations rad9, mec1, and mec2. The predicted amino acid sequence of Cdc44p contains GTPase consensus sites, and mutations in these regions cause a conditional cell cycle arrest. Taken together, these observations suggest that the essential CDC44 gene may encode the large subunit of yeast replication factor C.

scholarly journals A RAD9-dependent cell cycle arrest in response to unresolved recombination intermediates in Saccharomyces cerevisiae

2019 ◽  
Author(s):  
Hardeep Kaur ◽  
GN Krishnaprasad ◽  
Michael Lichten
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Damage ◽  
Cell Division ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Cycle Arrest ◽  
Associated Lesions

AbstractIn Saccharomyces cerevisiae, the conserved Sgs1-Top3-Rmi1 helicase-decatenase regulates homologous recombination by limiting accumulation of recombination intermediates that are precursors of crossovers. In vitro studies have suggested that the dissolution of double-Holliday junction joint molecules by Sgs1-driven convergent junction migration and Top3-Rmi1 mediated strand decatenation could be responsible for this. To ask if dissolution occurs in vivo, we conditionally depleted Sgs1 and/or Rmi1 during return to growth, a procedure where recombination intermediates formed during meiosis are resolved when cells resume the mitotic cell cycle. Sgs1 depletion during return to growth delayed joint molecule resolution, but ultimately most were resolved and cells divided normally. In contrast, Rmi1 depletion resulted in delayed and incomplete joint molecule resolution, and most cells did not divide. rad9Δ mutation restored cell division in Rmi1-depleted cells, indicating that the DNA damage checkpoint caused this cell cycle arrest. Restored cell division in rad9Δ, Rmi1-depleted cells frequently produced anucleate cells, consistent with the suggestion that persistent recombination intermediates prevented chromosome segregation. Our findings indicate that Sgs1-Top3-Rmi1 acts in vivo, as it does in vitro, to promote recombination intermediate resolution by dissolution. They also indicate that, in the absence of Top3-Rmi1 activity, unresolved recombination intermediates persist and activate the DNA damage response, which is usually thought to be activated by much earlier DNA damage-associated lesions.

Helicobacter pylori induces cell cycle arrest of T-lymphocytes

2005 ◽  
Vol 43 (05) ◽  
Author(s):  
M Gerhard ◽  
C Schmees ◽  
R Rad ◽  
P Voland ◽  
T Treptau ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Helicobacter Pylori ◽  
T Lymphocytes ◽  
Cell Cycle Arrest ◽  
Cycle Arrest
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