Effects ofHelicobacter pylori infection on cell cycle progression and the expression of cell cycle regulatory proteins

2004 ◽  
Vol 200 (3) ◽  
pp. 334-342 ◽  
Author(s):  
Antonio De Luca ◽  
Maria De Falco ◽  
Salvatore Iaquinto ◽  
Gaetano Iaquinto
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Regulatory Proteins ◽  
Cycle Progression ◽  
Cell Cycle Regulatory Proteins

scholarly journals Transgene Expression of bcl-xL Permits Anti-immunoglobulin (Ig)–induced Proliferation in xid B Cells

1998 ◽  
Vol 187 (7) ◽  
pp. 1081-1091 ◽  
Author(s):  
Nanette Solvason ◽  
Wei Wei Wu ◽  
Nisha Kabra ◽  
Fridjtof Lund-Johansen ◽  
Maria Grazia Roncarolo ◽  
...  
Keyword(s):  
Cell Cycle ◽  
B Cells ◽  
Transgene Expression ◽  
Cell Cycle Progression ◽  
Regulatory Protein ◽  
Ectopic Expression ◽  
Regulatory Proteins ◽  
High Rate ◽  
Cycle Progression ◽  
Cell Cycle Regulatory Proteins

Mutations in the tyrosine kinase, Btk, result in a mild immunodeficiency in mice (xid). While B lymphocytes from xid mice do not proliferate to anti-immunoglobulin (Ig), we show here induction of the complete complement of cell cycle regulatory molecules, though the level of induction is about half that detected in normal B cells. Cell cycle analysis reveals that anti-Ig stimulated xid B cells enter S phase, but fail to complete the cell cycle, exhibiting a high rate of apoptosis. This correlated with a decreased ability to induce the anti-apoptosis regulatory protein, Bcl-xL. Ectopic expression of Bcl-xL in xid B cells permitted anti-Ig induced cell cycle progression demonstrating dual requirements for induction of anti-apoptotic proteins plus cell cycle regulatory proteins during antigen receptor mediated proliferation. Furthermore, our results link one of the immunodeficient traits caused by mutant Btk with the failure to properly regulate Bcl-xL.

Effects of Aqueous Extract of Sophora flavescens on the Expression of Cell Cycle Regulatory Proteins in Human Oral Mucosal Fibroblasts

2003 ◽  
Vol 31 (04) ◽  
pp. 563-572 ◽  
Author(s):  
Hyun-A Kim ◽  
Hyung-Keun You ◽  
Hyung-Shik Shin ◽  
Youn-Chul Kim ◽  
Tai-Hyun Kang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Cyclin E ◽  
Regulatory Proteins ◽  
Cyclin D ◽  
Sophora Flavescens ◽  
Cycle Progression ◽  
Cell Cycle Regulatory Proteins ◽  
Cycle Regulation

Sophorae Radix, the dried roots of Sophora flavescens AITON (Leguminosae), has been used in Oriental traditional medicine for treatment of skin and mucosal ulcers, sores, gastrointestinal hemorrhage, diarrhea, inflammation and arrhythmia. In the present study, we examine the effect of the aqueous extract of Sophorae Radix (AESR) on cell proliferation and cell cycle regulation in human oral mucosal fibroblasts (HOMFs). To study the molecular mechanisms of cell cycle regulation by AESR, we also measured the intracellular levels of cell cycle regulatory proteins such as cyclin D, cyclin-dependent kinases (CDK)-4, CDK-6, cyclin E, CDK-2, p53, p21WAF1/CIP1 and p16INK4 . Cell proliferation was increased in the presence of 10~500 μg/ml of AESR. Maximal growth stimulation was observed in those cells exposed to 100 μg/ml of AESR. Exposure of HOMFs to 100 μg/ml of AESR resulted in an increase of cell cycle progression. The levels of cyclin E and CDK-2 were increased in HOMFs after 100 μg/ml of AESR treatment, but the levels of cyclin D, CDK-4, and CDK-6 were unchanged. After exposure to 100 μg/ml of AESR, the protein levels of p16INK4A and p53 were decreased as compared to that of the control group, but the level of p21WAF1/CIP1 was similar in the cells treated with 100 μg/ml of AESR and untreated cells. The results suggest that AESR may increase cell proliferation and cell cycle progression in HOMFs, which is linked to increased cellular levels of cyclin E and CDK-2 and decreased cellular levels of p53 and p16INK4A . Further studies are necessary to clarify the active constituents of AESR responsible for such biomolecular activities.

scholarly journals The Rho GTPase Effector ROCK Regulates Cyclin A, Cyclin D1, and p27Kip1 Levels by Distinct Mechanisms

2006 ◽  
Vol 26 (12) ◽  
pp. 4612-4627 ◽  
Author(s):  
Daniel R. Croft ◽  
Michael F. Olson
Keyword(s):  
Cell Cycle ◽  
Cyclin D1 ◽  
Cell Cycle Progression ◽  
Rho Gtpase ◽  
Cyclin A ◽  
Regulatory Proteins ◽  
Mitogen Activated Protein Kinase ◽  
Lim Kinase ◽  
Cycle Progression ◽  
Cell Cycle Regulatory Proteins

ABSTRACT The members of the Rho GTPase family are well known for their regulation of actin cytoskeletal structures. In addition, they influence progression through the cell cycle. The RhoA and RhoC proteins regulate numerous effector proteins, with a central and vital signaling role mediated by the ROCK I and ROCK II serine/threonine kinases. The requirement for ROCK function in the proliferation of numerous cell types has been revealed by studies utilizing ROCK-selective inhibitors such as Y-27632. However, the mechanisms by which ROCK signaling promotes cell cycle progression have not been thoroughly characterized. Using a conditionally activated ROCK-estrogen receptor fusion protein, we found that ROCK activation is sufficient to stimulate G1/S cell cycle progression in NIH 3T3 mouse fibroblasts. Further analysis revealed that ROCK acts via independent pathways to alter the levels of cell cycle regulatory proteins: cyclin D1 and p21Cip1 elevation via Ras and the mitogen-activated protein kinase pathway, increased cyclin A via LIM kinase 2, and reduction of p27Kip1 protein levels. Therefore, the influence of ROCK on cell cycle regulatory proteins occurs by multiple independent mechanisms.

scholarly journals p38 mitogen-activated protein kinase contributes to cell cycle regulation by cAMP in FRTL-5 thyroid cells

2005 ◽  
Vol 153 (1) ◽  
pp. 123-133 ◽  
Author(s):  
C Corrèze ◽  
J-P Blondeau ◽  
M Pomérance
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Cyclin E ◽  
Regulatory Proteins ◽  
Thyroid Cells ◽  
Cycle Progression ◽  
Mapk Activity ◽  
Mitogen Activated Protein ◽  
Cell Cycle Regulatory Proteins ◽  
P38 Mapks

Objective: Thyrotropin activates the cAMP pathway in thyroid cells, and stimulates cell cycle progression in cooperation with insulin or insulin-like growth factor-I. Because p38 mitogen-activated protein kinases (p38 MAPKs) were stimulated by cAMP in the FRTL-5 rat thyroid cell line, we investigated (i) the effect of the specific inhibition of p38 MAPKs on FRTL-5 cell proliferation and (ii) the mechanism of action of p38 MAPKs on cell cycle control, by studying the expression and/or the activity of several cell cycle regulatory proteins in FRTL-5 cells. Methods: DNA synthesis was monitored by incorporation of [3H]thymidine into DNA and the cell cycle distribution was assessed by fluorescence-activated cell sorter analysis. Expression of cell cycle regulatory proteins was determined by Western blot analysis. Cyclin-dependent kinase 2 (Cdk2) activity associated to cyclin E was immunoprecipitated and was measured by an in vitro kinase assay. Results: SB203580, an inhibitor of α and β isoforms of p38 MAPKs, but not its inactive analog SB202474, inhibited DNA synthesis and the G1-S transition induced by forskolin plus insulin. SB203580 inhibited specifically p38 MAPK activity but not other kinase activities such as Akt and p70-S6 kinase. Treatment of FRTL-5 cells with SB203580 decreased total and cyclin E-associated Cdk2 kinase activity stimulated with forskolin and insulin. However, inhibition of p38 MAPKs by SB203580 was without effect on total cyclin E and Cdk2 levels. The decrease in Cdk2 kinase activity caused by SB203580 treatment was not due to an increased expression of p21Cip1 or p27Kip1 inhibitory proteins. In addition, SB203580 affected neither Cdc25A phosphatase expression nor Cdk2 Tyr-15 phosphorylation. Inhibition of p38 MAPKs decreased Cdk2-cyclin E activation by regulating the subcellular localization of Cdk2 and its phosphorylation on Thr-160. Conclusions: These results indicate that p38 MAPK activity is involved in the regulation of cell cycle progression in FRTL-5 thyroid cells, at least in part by increasing nuclear Cdk2 activity.

scholarly journals In silico APC/C substrate discovery reveals cell cycle degradation of chromatin regulators including UHRF1

2020 ◽  
Author(s):  
Jennifer L. Kernan ◽  
Raquel C. Martinez-Chacin ◽  
Xianxi Wang ◽  
Rochelle L. Tiedemann ◽  
Thomas Bonacci ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Methylation ◽  
In Silico ◽  
Cell Cycle Progression ◽  
Vital Role ◽  
Regulatory Proteins ◽  
Phase Cell ◽  
Cell Physiology ◽  
Cycle Progression ◽  
Chromatin Regulator

AbstractThe Anaphase-Promoting Complex/Cyclosome (APC/C) is an E3 ubiquitin ligase and critical regulator of cell cycle progression. Despite its vital role, it has remained challenging to globally map APC/C substrates. By combining orthogonal features of known substrates, we predicted APC/C substrates in silico. This analysis identified many known substrates and suggested numerous candidates. Unexpectedly, chromatin regulatory proteins are enriched among putative substrates and we show that several chromatin proteins bind APC/C, oscillate during the cell cycle and are degraded following APC/C activation, consistent with being direct APC/C substrates. Additional analysis revealed detailed mechanisms of ubiquitylation for UHRF1, a key chromatin regulator involved in histone ubiquitylation and DNA methylation maintenance. Disrupting UHRF1 degradation at mitotic exit accelerates G1-phase cell cycle progression and perturbs global DNA methylation patterning in the genome. We conclude that APC/C coordinates crosstalk between cell cycle and chromatin regulatory proteins. This has potential consequences in normal cell physiology, where the chromatin environment changes depending on proliferative state, as well as in disease.

scholarly journals Antineoplastic Effects of Honokiol on Melanoma

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ruth Guillermo-Lagae ◽  
Sreevidya Santha ◽  
Milton Thomas ◽  
Emily Zoelle ◽  
Jonathan Stevens ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Malignant Melanoma ◽  
Cell Viability ◽  
Cell Cycle Progression ◽  
Regulatory Proteins ◽  
M Phase ◽  
Cell Cycle Regulatory Proteins ◽  
In Vitro Effects

Honokiol, a plant lignan has been shown to have antineoplastic effects against nonmelanoma skin cancer developments in mice. In this study, antineoplastic effects of honokiol were investigated in malignant melanoma models. In vitro effects of honokiol treatment on SKMEL-2 and UACC-62 melanoma cells were evaluated by measuring the cell viability, proliferation, apoptosis, cell cycle analysis, and expressions of various proteins associated with cell cycle progression and apoptosis. For the in vivo study, male nude mice inoculated with SKMEL-2 or UACC-62 cells received injections of sesame oil or honokiol for two to seven weeks. In vitro honokiol treatment caused significant decrease in cell viability, proliferation, cell cycle arrest, increased apoptosis, and modulation of apoptotic and cell cycle regulatory proteins. Honokiol caused an accumulation of cells in the G2/M phase of the cell cycle in SKMEL-2 and G0/G1 phase in UACC-62 cells. An elevated level of caspases and PARP were observed in both cell lines treated with honokiol. A decrease in the expression of various cell cycle regulatory proteins was also observed in honokiol treated cells. Honokiol caused a significant reduction of tumor growth in SKMEL-2 and UACC-62 melanoma xenografts. These findings suggest that honokiol is a good candidate for further studies as a possible treatment for malignant melanoma.

scholarly journals Phylogenetic analysis of cell-cycle regulatory proteins within the Symbiodiniaceae

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Lucy M. Gorman ◽  
Shaun P. Wilkinson ◽  
Sheila A. Kitchen ◽  
Clinton A. Oakley ◽  
Arthur R. Grossman ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Phylogenetic Position ◽  
Cellular Mechanisms ◽  
Free Living ◽  
Cycle Progression ◽  
Altered Expression ◽  
Cyclin Dependent Kinases ◽  
Cell Cycle Regulatory Proteins ◽  
Cyclin Gene

AbstractIn oligotrophic waters, cnidarian hosts rely on symbiosis with their photosynthetic dinoflagellate partners (family Symbiodiniaceae) to obtain the nutrients they need to grow, reproduce and survive. For this symbiosis to persist, the host must regulate the growth and proliferation of its symbionts. One of the proposed regulatory mechanisms is arrest of the symbiont cell cycle in the G1 phase, though the cellular mechanisms involved remain unknown. Cell-cycle progression in eukaryotes is controlled by the conserved family of cyclin-dependent kinases (CDKs) and their partner cyclins. We identified CDKs and cyclins in different Symbiodiniaceae species and examined their relationship to homologs in other eukaryotes. Cyclin proteins related to eumetazoan cell-cycle-related cyclins A, B, D, G/I and Y, and transcriptional cyclin L, were identified in the Symbiodiniaceae, alongside several alveolate-specific cyclin A/B proteins, and proteins related to protist P/U-type cyclins and apicomplexan cyclins. The largest expansion of Symbiodiniaceae cyclins was in the P/U-type cyclin groups. Proteins related to eumetazoan cell-cycle-related CDKs (CDK1) were identified as well as transcription-related CDKs. The largest expansion of CDK groups was, however, in alveolate-specific groups which comprised 11 distinct CDK groups (CDKA-J) with CDKB being the most widely distributed CDK protein. As a result of its phylogenetic position, conservation across Symbiodiniaceae species, and the presence of the canonical CDK motif, CDKB emerged as a likely candidate for a Saccharomyces cerevisiae Cdc28/Pho85-like homolog in Symbiodiniaceae. Similar to cyclins, two CDK-groups found in Symbiodiniaceae species were solely associated with apicomplexan taxa. A comparison of Breviolum minutum CDK and cyclin gene expression between free-living and symbiotic states showed that several alveolate-specific CDKs and two P/U-type cyclins exhibited altered expression in hospite, suggesting that symbiosis influences the cell cycle of symbionts on a molecular level. These results highlight the divergence of Symbiodiniaceae cell-cycle proteins across species. These results have important implications for host control of the symbiont cell cycle in novel cnidarian–dinoflagellate symbioses.

scholarly journals Nuclear envelope influences on cell-cycle progression

2011 ◽  
Vol 39 (6) ◽  
pp. 1742-1746 ◽  
Author(s):  
Vlastimil Srsen ◽  
Nadia Korfali ◽  
Eric C. Schirmer
Keyword(s):  
Cell Cycle ◽  
Nuclear Envelope ◽  
Cell Cycle Progression ◽  
Membrane System ◽  
Regulatory Proteins ◽  
Cycle Progression ◽  
Cytoplasmic Surface ◽  
Dynamic Interface ◽  
Gene Regulatory ◽  
Cycle Regulation

The nuclear envelope is a complex double membrane system that serves as a dynamic interface between the nuclear and cytoplasmic compartments. Among its many roles is to provide an anchor for gene regulatory proteins on its nucleoplasmic surface and for the cytoskeleton on its cytoplasmic surface. Both sets of anchors are proteins called NETs (nuclear envelope transmembrane proteins), embedded respectively in the inner or outer nuclear membranes. Several lines of evidence indicate that the nuclear envelope contributes to cell-cycle regulation. These contributions come from both inner and outer nuclear membrane NETs and appear to operate through several distinct mechanisms ranging from sequestration of gene-regulatory proteins to activating kinase cascades.

Sign in / Sign up

Export Citation Format

Share Document