scholarly journals Demethylation of an nuclear factor-kb (NF-kb) enhancer element orchestrates iNOS induction in osteoarthritis via cell cycle regulation

2015 ◽  
Vol 23 ◽  
pp. A191
Author(s):  
M.C. de Andres ◽  
A. Takahashi ◽  
R.O. Oreffo
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Nuclear Factor ◽  
Enhancer Element ◽  
Cycle Regulation ◽  
Nuclear Factor Kb ◽  
Inos Induction

scholarly journals Identification of cis andtrans Elements Involved in the Cell Cycle Regulation of Multiple Genes in Crithidia fasciculata

1999 ◽  
Vol 19 (9) ◽  
pp. 6174-6182 ◽  
Author(s):  
Riaz Mahmood ◽  
Jane C. Hines ◽  
Dan S. Ray
Keyword(s):  
Cell Cycle ◽  
Reporter Gene ◽  
Cell Cycle Regulation ◽  
Consensus Sequence ◽  
Regulatory Protein ◽  
Gene Transcript ◽  
Nuclear Factor ◽  
Sequence Element ◽  
Crithidia Fasciculata ◽  
Cycle Regulation

ABSTRACT Transcripts of several DNA replication genes, including theRPA1 and TOP2 genes, encoding the large subunit of nuclear replication protein A and the kinetoplast topoisomerase II, accumulate periodically during the cell cycle in the trypanosomatidCrithidia fasciculata. An octamer consensus sequence, CAUAGAAG, present in the 5′ untranslated regions (UTR) of these mRNAs is required for periodic accumulation of the TOP2 andRPA1 transcripts and also for binding of a nuclear factor(s) to the 5′ UTR RNAs of these genes. We show here that insertion of multiple (six) copies of this octamer sequence (6× octamer) into the 5′ UTR of a reporter gene confers periodic accumulation on its transcript. Competition experiments and UV cross-linking studies show that the 6× octamer RNA andTOP2 5′ UTR RNA bind to the same nuclear factor(s). Single-nucleotide substitutions in the 6× octamer that abolish the RNA gel shift also prevent cyclic accumulation of the reporter gene transcript. A protein termed cycling element binding protein, purified by affinity chromatography using 6× octamer RNA as a ligand, binds to RNAs containing wild-type octamers and not to those with mutant octamers. These results define a small sequence element in C. fasciculata mRNAs required for their cell cycle regulation and report the identification and purification of a putative regulatory protein that binds specifically to these elements.

scholarly journals Cell Cycle Regulation of Nuclear Factor p92 DNA-binding Activity by Novel Phase-specific Inhibitors

1996 ◽  
Vol 271 (16) ◽  
pp. 9215-9222 ◽  
Author(s):  
Edgar Grinstein ◽  
Inge Weinert ◽  
Brigitte Droese ◽  
Michele Pagano ◽  
Hans-Dieter Royer
Keyword(s):  
Cell Cycle ◽  
Dna Binding ◽  
Cell Cycle Regulation ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Dna Binding Activity ◽  
Cycle Regulation ◽  
Specific Inhibitors

scholarly journals Genetic variants and cognitive functions in patients with brain tumors

2019 ◽  
Vol 21 (10) ◽  
pp. 1297-1309 ◽  
Author(s):  
Denise D Correa ◽  
Jaya Satagopan ◽  
Axel Martin ◽  
Erica Braun ◽  
Maria Kryza-Lacombe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Dna Repair ◽  
Brain Tumor ◽  
Brain Tumors ◽  
Cell Cycle Regulation ◽  
Cognitive Outcome ◽  
Cholesterol Transport ◽  
Tumor Patients ◽  
Cycle Regulation

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.

scholarly journals Phosphorylation of RCC1 on Serine 11 Facilitates G1/S Transition in HPV E7-Expressing Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 995
Author(s):  
Xiaoyan Hou ◽  
Lijun Qiao ◽  
Ruijuan Liu ◽  
Xuechao Han ◽  
Weifang Zhang
Keyword(s):  
Cell Cycle ◽  
Cervical Cancer ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Mtor Pathway ◽  
Cycle Progression ◽  
Post Translational Modifications ◽  
Hpv E7 ◽  
Cycle Regulation

Persistent infection of high-risk human papillomavirus (HR-HPV) plays a causal role in cervical cancer. Regulator of chromosome condensation 1 (RCC1) is a critical cell cycle regulator, which undergoes a few post-translational modifications including phosphorylation. Here, we showed that serine 11 (S11) of RCC1 was phosphorylated in HPV E7-expressing cells. However, S11 phosphorylation was not up-regulated by CDK1 in E7-expressing cells; instead, the PI3K/AKT/mTOR pathway promoted S11 phosphorylation. Knockdown of AKT or inhibition of the PI3K/AKT/mTOR pathway down-regulated phosphorylation of RCC1 S11. Furthermore, S11 phosphorylation occurred throughout the cell cycle, and reached its peak during the mitosis phase. Our previous data proved that RCC1 was necessary for the G1/S cell cycle progression, and in the present study we showed that the RCC1 mutant, in which S11 was mutated to alanine (S11A) to mimic non-phosphorylation status, lost the ability to facilitate G1/S transition in E7-expressing cells. Moreover, RCC1 S11 was phosphorylated by the PI3K/AKT/mTOR pathway in HPV-positive cervical cancer SiHa and HeLa cells. We conclude that S11 of RCC1 is phosphorylated by the PI3K/AKT/mTOR pathway and phosphorylation of RCC1 S11 facilitates the abrogation of G1 checkpoint in HPV E7-expressing cells. In short, our study explores a new role of RCC1 S11 phosphorylation in cell cycle regulation.

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