scholarly journals Rnf2 (Ring1b) deficiency causes gastrulation arrest and cell cycle inhibition

2003 ◽  
Vol 100 (5) ◽  
pp. 2468-2473 ◽  
Author(s):  
J. W. Voncken ◽  
B. A. J. Roelen ◽  
M. Roefs ◽  
S. de Vries ◽  
E. Verhoeven ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Inhibition

scholarly journals Effects of 4E-BP1 expression on hypoxic cell cycle inhibition and tumor cell proliferation and survival

2008 ◽  
Vol 7 (9) ◽  
pp. 1441-1449 ◽  
Author(s):  
Bryan C. Barnhart ◽  
Jennifer C. Lam ◽  
Regina M. Young ◽  
Peter J. Houghton ◽  
Brian Keith ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Tumor Cell ◽  
Hypoxic Cell ◽  
Tumor Cell Proliferation ◽  
Cell Cycle Inhibition

scholarly journals Ascorbate exerts anti-proliferative effects through cell cycle inhibition and sensitizes tumor cells towards cytostatic drugs

2010 ◽  
Vol 67 (5) ◽  
pp. 1157-1166 ◽  
Author(s):  
Anja Frömberg ◽  
Daniela Gutsch ◽  
Daniel Schulze ◽  
Claudia Vollbracht ◽  
Gabriele Weiss ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Cells ◽  
Cytostatic Drugs ◽  
Cell Cycle Inhibition

Abstract 2357: Src Kinase Inhibition Blocks Thrombin-induced Brain Injuries without Cognitive Side Effects

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Da-Zhi Liu ◽  
Bradley P Ander ◽  
Ali Izadi ◽  
Ken Van ◽  
Xinhua Zhan ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cognitive Deficits ◽  
Neuronal Cell ◽  
Thrombin Injection ◽  
Cell Cycle Reentry ◽  
Cell Cycle Inhibition ◽  
Mature Neurons ◽  
Cognitive Side Effects

Intracerebral hemorrhage (ICH) activates thrombin, a potent mitogen. Thrombin triggers mitosis by modulating several intracellular mitogenic molecules including Src family kinases. These molecules regulate mitogen-activated protein kinases (MAPKs) and cell cycle proteins such as cyclin-dependent kinases (Cdks); and play critical roles in mitogenic signaling pathways and cell cycle progression. Since aberrant cell cycle reentry results in death of mature neurons, cell cycle inhibition appears to be a candidate strategy for the treatment of neurological diseases including ICH. However, this can also block cell cycle (proliferation) of neural progenitor cells (NPCs) and thus impair brain neurogenesis leading to cognitive deficits. We hypothesized that inhibition of cell cycle by blocking mitogenic signaling molecules (i.e., Src family kinase members) blocks cell cycle reentry of mature neurons without injuring NPCs, which will avoid cognitive side effects during cell cycle inhibition treatment for ICH. Our data shows: (1) Thrombin 30U/ml results in apoptosis of mature neurons via neuronal cell cycle reentry in vitro ; (2) PP2 (Src family kinase inhibitor) 0.3 µM attenuates the thrombin-induced neuronal apoptosis via blocking neuronal cell cycle reentry, but does not affect the viability of NPCs at the same doses in vitro ; (3) Intracerebral ventricular thrombin injection (20U, i.c.v.) results in neuron loss in hippocampus and cognitive deficits 5 weeks after thrombin injection in vivo ; (4) PP2 (1mg/kg, i.p.), given immediately after thrombin injection (i.c.v.), blocks the thrombin-induced neuron loss in hippocampus and cognitive deficits, whereas PP2 on its own at the same doses does not affect normal cognition in vivo . These suggest that Src kinase inhibition prevents hippocampal neuron death via blocking neuronal cell cycle reentry after ICH, but does not affect survival of NPCs.

scholarly journals Arginine deprivation in KB cells: I. Effect on cell cycle progress

1977 ◽  
Vol 75 (3) ◽  
pp. 881-888 ◽  
Author(s):  
AS Weissfeld ◽  
H Rouse
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Tritiated Thymidine ◽  
Experimental Period ◽  
Cell Multiplication ◽  
Starvation Period ◽  
Kb Cells ◽  
Insoluble Material ◽  
Cell Cycle Inhibition ◽  
Cellular Dna

When exponentially growing KB cells were deprived of arginine, cell multiplication ceased after 12 h but viability was maintained throughout the experimental period (42-48 h). Although tritiated thymidine ([(3)H]TdR) incorporation into acid-insoluble material declined to 5 percent of the initial rate, the fraction of cells engaged in DNA synthesis, determined by autoradiography, remained constant throughout the starvation period and approximately equal to the synthesizing fraction in exponentially growing controls (40 percent). Continous [(3)H]TdR-labeling indicated that 80 percent of the arginine-starved cells incorporated (3)H at some time during a 48-h deprivation period. Thus, some cells ceased DNA synthesis, whereas some initially nonsynthesizing cells initiated DNA synthesis during starvation. Flow microfluorometric profiles of distribution of cellular DNA contents at the end of the starvation period indicated that essentially no cells had a 4c or G2 complement. If arginine was restored after 30 h of starvation, cultures resumed active, largely asynchronous division after a 16-h lag. Autoradiographs of metaphase figures from cultures continuously labeled with [(3)H]TdR after restoration indicated that all cells in the culture underwent DNA synthesis before dividing. It was concluded that the majority of cells in arginine-starved cultures are arrested in neither a normal G1 nor G2. It is proposed that for an exponential culture, i.e. from most positions in the cell cycle, inhibition of cell growth after arginine with withdrawal centers on the ability of cells to complete replication of their DNA.

scholarly journals BRG1 deletion de‐represses p53 pathways inducing cell cycle inhibition and apoptosis during peri‐gastrulation (541.10)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Ajeet Singh ◽  
Michael C Boyle ◽  
Mark Rubino ◽  
Arpit Tandon ◽  
Ruchir Shah ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Inhibition

scholarly journals Anti-proliferative Effects of Tricyclodecan-9-yl-xanthogenate (D609) Involve Ceramide and Cell Cycle Inhibition

2012 ◽  
Vol 45 (3) ◽  
pp. 455-464 ◽  
Author(s):  
Anchal Gusain ◽  
James F. Hatcher ◽  
Rao Muralikrishna Adibhatla ◽  
Umadevi V. Wesley ◽  
Robert J. Dempsey
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Inhibition
Sign in / Sign up

Export Citation Format

Share Document