scholarly journals Cellular localization and cell cycle regulation by a temperature-sensitive p53 protein.

1991 ◽  
Vol 5 (2) ◽  
pp. 151-159 ◽  
Author(s):  
J Martinez ◽  
I Georgoff ◽  
J Martinez ◽  
A J Levine

1996 ◽  
Vol 109 (12) ◽  
pp. 2865-2874 ◽  
Author(s):  
H. Bastians ◽  
H. Ponstingl

We identified a novel human protein serine/threonine phosphatase cDNA, designated protein phosphatase 6 (PP6) by using a homology-based polymerase chain reaction. The predicted amino acid sequence indicates a 35 kDa protein showing high homology to other protein phosphatases including human PP2A (57%), human PP4 (59%), rat PPV (98%), Drosophila PPV (74%), Schizosaccharomyces pombe ppe1 (68%) and Saccharomyces cerevisiae Sit4p (61%). In human cells, three forms of PP6 mRNA were found with highest levels of expression in testis, heart and skeletal muscle. The PP6 protein was detected in lysates of human heart muscle and in bull testis. Complementation studies using a temperature sensitive mutant strain of S. cerevisiae SIT4, which is required for the G1 to S transition of the cell cycle, showed that PP6 can rescue the mutant growth arrest. In addition, a loss of function mutant of S. pombe ppe1, described as a gene interacting with the pim1/spi1 mitotic checkpoint and involved in cell shape control, can be complemented by expression of human PP6. These data indicate that human PP6 is a functional homologue of budding yeast Sit4p and fission yeast ppe1, implying a function of PP6 in cell cycle regulation.



1998 ◽  
Vol 9 (12) ◽  
pp. 3273-3297 ◽  
Author(s):  
Paul T. Spellman ◽  
Gavin Sherlock ◽  
Michael Q. Zhang ◽  
Vishwanath R. Iyer ◽  
Kirk Anders ◽  
...  

We sought to create a comprehensive catalog of yeast genes whose transcript levels vary periodically within the cell cycle. To this end, we used DNA microarrays and samples from yeast cultures synchronized by three independent methods: α factor arrest, elutriation, and arrest of a cdc15 temperature-sensitive mutant. Using periodicity and correlation algorithms, we identified 800 genes that meet an objective minimum criterion for cell cycle regulation. In separate experiments, designed to examine the effects of inducing either the G1 cyclin Cln3p or the B-type cyclin Clb2p, we found that the mRNA levels of more than half of these 800 genes respond to one or both of these cyclins. Furthermore, we analyzed our set of cell cycle–regulated genes for known and new promoter elements and show that several known elements (or variations thereof) contain information predictive of cell cycle regulation. A full description and complete data sets are available at http://cellcycle-www.stanford.edu



2006 ◽  
Vol 84 (4) ◽  
pp. 640-650 ◽  
Author(s):  
Hong Wang ◽  
Yongming Zhou ◽  
Larry C. Fowke

The cell division cycle in plants as in other eukaryotes is controlled by the cyclin-dependent kinase (CDK). This CDK paradigm determines that developmental cues and environmental signals need to impinge on the CDK complex to affect the cell cycle. An important part of understanding cell cycle regulation is to understand how CDK is regulated by various factors. In addition, there are features that set the cell cycle regulation in plants apart from that in other eukaryotes such as animals. Our knowledge of the molecular mechanisms that underlie the differences is poor. A family of plant CDK inhibitor proteins has been identified. The plant CDK inhibitors share similarity with a family of animal CDK inhibitors in a small region, while most of the sequence and the structural layout of the plant CDK inhibitors are different from the animal counterparts. Studies of plant CDK inhibitors have been performed mostly with the CDK inhibitors from Arabidopsis called ICKs (also referred to as KRPs). ICKs interact with D-type cyclins and A-type CDK. Overexpression of ICKs has been shown to affect cell division, plant growth, and morphogenesis. Studies of ICKs have also provided insightful information on the control of endoreduplication in plants. These aspects as well as cellular localization and protein regulation of ICKs are reviewed.



10.2741/a501 ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. d121-137 ◽  
Author(s):  
John W Ludlow






2019 ◽  
Vol 21 (10) ◽  
pp. 1297-1309 ◽  
Author(s):  
Denise D Correa ◽  
Jaya Satagopan ◽  
Axel Martin ◽  
Erica Braun ◽  
Maria Kryza-Lacombe ◽  
...  

AbstractBackgroundPatients with brain tumors treated with radiotherapy (RT) and chemotherapy (CT) often experience cognitive dysfunction. We reported that single nucleotide polymorphisms (SNPs) in the APOE, COMT, and BDNF genes may influence cognition in brain tumor patients. In this study, we assessed whether genes associated with late-onset Alzheimer’s disease (LOAD), inflammation, cholesterol transport, dopamine and myelin regulation, and DNA repair may influence cognitive outcome in this population.MethodsOne hundred and fifty brain tumor patients treated with RT ± CT or CT alone completed a neurocognitive assessment and provided a blood sample for genotyping. We genotyped genes/SNPs in these pathways: (i) LOAD risk/inflammation/cholesterol transport, (ii) dopamine regulation, (iii) myelin regulation, (iv) DNA repair, (v) blood–brain barrier disruption, (vi) cell cycle regulation, and (vii) response to oxidative stress. White matter (WM) abnormalities were rated on brain MRIs.ResultsMultivariable linear regression analysis with Bayesian shrinkage estimation of SNP effects, adjusting for relevant demographic, disease, and treatment variables, indicated strong associations (posterior association summary [PAS] ≥ 0.95) among tests of attention, executive functions, and memory and 33 SNPs in genes involved in: LOAD/inflammation/cholesterol transport (eg, PDE7A, IL-6), dopamine regulation (eg, DRD1, COMT), myelin repair (eg, TCF4), DNA repair (eg, RAD51), cell cycle regulation (eg, SESN1), and response to oxidative stress (eg, GSTP1). The SNPs were not significantly associated with WM abnormalities.ConclusionThis novel study suggests that polymorphisms in genes involved in aging and inflammation, dopamine, myelin and cell cycle regulation, and DNA repair and response to oxidative stress may be associated with cognitive outcome in patients with brain tumors.



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