Results 41 to 50 of about 775,653 (341)

The anaphase-promoting complex or cyclosome supports cell survival in response to endoplasmic reticulum stress. [PDF]

open access: yesPLoS ONE, 2012
The anaphase-promoting complex or cyclosome (APC/C) is a multi-subunit ubiquitin ligase that regulates exit from mitosis and G1 phase of the cell cycle.
Meifan Chen   +2 more
doaj   +1 more source

Pulsatile MAPK Signaling Modulates p53 Activity to Control Cell Fate Decisions at the G2 Checkpoint for DNA Damage

open access: yesCell Reports, 2020
Summary: Cell-autonomous changes in p53 expression govern the duration and outcome of cell-cycle arrest at the G2 checkpoint for DNA damage. Here, we report that mitogen-activated protein kinase (MAPK) signaling integrates extracellular cues with p53 ...
Siddharth De   +3 more
doaj   +1 more source

Cell cycle checkpoint in cancer: a therapeutically targetable double-edged sword

open access: yesJournal of experimental & clinical cancer research : CR, 2016
Major currently used anticancer therapeutics either directly damage DNA or target and upset basic cell division mechanisms like DNA replication and chromosome segregation.
R. Visconti, R. Della Monica, D. Grieco
semanticscholar   +1 more source

Phosphorylation of the MBF repressor Yox1p by the DNA replication checkpoint keeps the G1/S cell-cycle transcriptional program active.

open access: yesPLoS ONE, 2011
BackgroundIn fission yeast Schizosaccharomyces pombe G1/S cell-cycle regulated transcription depends upon MBF. A negative feedback loop involving Nrm1p and Yox1p bound to MBF leads to transcriptional repression as cells exit G1 phase. However, activation
Catia Caetano   +2 more
doaj   +1 more source

Cell Cycle Regulation by Checkpoints [PDF]

open access: yes, 2014
Cell cycle checkpoints are surveillance mechanisms that monitor the order, integrity, and fidelity of the major events of the cell cycle. These include growth to the appropriate cell size, the replication and integrity of the chromosomes, and their accurate segregation at mitosis. Many of these mechanisms are ancient in origin and highly conserved, and
Kevin J, Barnum, Matthew J, O'Connell
openaire   +2 more sources

Intrinsic checkpoint deficiency during cell cycle re-entry from quiescence

open access: yesbioRxiv, 2019
The authors find that human cells re-entering the cell cycle from quiescence have both an impaired p53-dependent DNA replication origin licensing checkpoint and slow origin licensing.
J. Matson   +5 more
semanticscholar   +1 more source

bir1 deletion causes malfunction of the spindle assembly checkpoint and apoptosis in yeast

open access: yesFrontiers in Oncology, 2012
Cell division in yeast is a highly regulated and well studied event. Various checkpoints are placed throughout the cell cycle to ensure faithful segregation of sister chromatids.
Qun eRen   +5 more
doaj   +1 more source

Mammalian cells lack checkpoints for tetraploidy, aberrant centrosome number, and cytokinesis failure

open access: yesBMC Cell Biology, 2005
Background Mammalian cells have been reported to have a p53-dependent tetraploidy checkpoint that blocks cell cycle progression in G1 in response to failure of cell division.
Stearns Tim, Wong Connie
doaj   +1 more source

Cell cycle checkpoint control [PDF]

open access: yesExperimental & Molecular Medicine, 1997
Genetic instability is considered to be a major driving force of malignancy of cancer cells, and at least some of cancer-associated genetic instability is known to be caused by defects in the cell cycle checkpoint control. Patients of the cancer-prone genetic disorder ataxia telangiectagia frequently develop malignant lymphoma and their cells are ...
Hiroshi Murakami, Hiroto Okayama
openaire   +1 more source

Organoids in pediatric cancer research

open access: yesFEBS Letters, EarlyView.
Organoid technology has revolutionized cancer research, yet its application in pediatric oncology remains limited. Recent advances have enabled the development of pediatric tumor organoids, offering new insights into disease biology, treatment response, and interactions with the tumor microenvironment.
Carla RĂ­os Arceo, Jarno Drost
wiley   +1 more source

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