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Tytuł artykułu

The latent cytomegalovirus decreases telomere length by microcompetition

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
Reduced telomere length has been associated with aging and age-related diseases. Latent infection with the Cytomegalovirus (CMV) induces telomere shortening in the infected cells. Latent CMV infection may cause reduced telomere length via GABP transcription factor deficiency, according to the Microcompetition Theory. Microcompetition and viral-induced transcription factor deficiency is important since most people harbor a latent viral infection.
Wydawca

Czasopismo
Rocznik
Tom
10
Numer
1
Opis fizyczny
Daty
otrzymano
2015-04-26
zaakceptowano
2015-04-30
online
2015-05-27
Twórcy
  • The Center for the Biology of Chronic Disease
    (CBCD), Valley Cottage, NY 10989, USA
  • The Center for the Biology of Chronic Disease
    (CBCD), Valley Cottage, NY 10989, USA
Bibliografia
  • [1] Drury S.S., Theall K., Gleason M.M., Smyke A.T., De Vivo I.,Wong J.Y.Y. et al., Telomere length and early severe socialdeprivation: linking early adversity and cellular aging, Mol.Psychiatry, 2012, 17(7), 719-727[Crossref]
  • [2] van de Berg P.J., Griffiths S.J., Yong S.L., Macaulay R.,Bemelman F.J., Jackson S. et al., Cytomegalovirus InfectionReduces Telomere Length of the Circulating T Cell Pool, J.Immunol. 2010, 184, 3417-3423[WoS]
  • [3] Polansky H., Microcompetition with Foreign DNA and the Originof Chronic Disease., The Center for the Biology of ChronicDisease, New York, 2003
  • [4] Liu B.H., Wang X., Ma Y.X., Wang S., CMV Enhancer/HumanPDGF-Beta Promoter for Neuron-Specific Transgene Expression,Gene Ther., 2004, 11(1), 52-60[Crossref]
  • [5] Slobedman B., Mocarski E.S., Quantitative Analysis of LatentHuman Cytomegalovirus, J. Virol., 1999, 73(6), 4806-4812
  • [6] Adam G.I., Miller S.J., Ulleras E., Franklin G.C., Cell-Type-Specific Modulation of PDGF-B Regulatory Elements via ViralEnhancer Competition: A Caveat for the Use of ReferencePlasmids in Transient Transfection Assays, Gene, 1996, 178(1),25-29
  • [7] Yu S., Cui K., Jothi R., Zhao D.M., Jing X., Zhao K. et al., GABPcontrols a critical transcription regulatory module that isessential for maintenance and differentiation of hematopoieticstem/progenitor cells, Blood, 2011, 117(7), 2166-2178[WoS]
  • [8] Sarek G., Vannier J.B., Panier S., Petrini J.H.J., Boulton S.J.,TRF2 Recruits RTEL1 to Telomeres in S Phase to Promote T-LoopUnwinding, Molecular Cell, 2015, 57(4), 622-635[Crossref]
  • [9] Spyridopoulos I., Hoffmann J., Aicher A., Brummendorf T.H.,Doerr H.W., Zeiher A.M. et al., Accelerated Telomere Shorteningin Leukocyte Subpopulations of Patients With Coronary HeartDisease, Circulation, 2009, 120, 1364-1372[WoS]
  • [10] Nan W.Q., Ling Z., Bing C., The influence of the telomeretelomerasesystem on diabetes mellitus and its vascularcomplications, Expert Opin. Ther. Targets., 2015, 19(6)
  • [11] Ji Y.N., An L., Zhan P., Chen X.H., Cytomegalovirus infection andcoronary heart disease risk: a meta-analysis, Molecular BiologyReports, 2012, 39(6), 6537-6546[WoS][Crossref]
  • [12] Mendy A., Gasana J., Vieira E.R., Diallo H., Prospective studyof cytomegalovirus seropositivity and risk of mortality fromdiabetes, Acta Diabetol., 2014, 51, 723-729[WoS]
  • [13] Green M., Michaels M.G., Epstein-Barr Virus Infectionand Posttransplant Lymphoproliferative Disorder, Am. J.Transplant., 2013, 13(s3), 41-54[Crossref][WoS]
  • [14] Reddehase M.J., Cytomegaloviruses: From MolecularPathogenesis to Intervention. Volume 2, Horizon ScientificPress, United Kingdom, 2013
  • [15] Bernstein D.I., Bellamy A.R., Hook III E.W., Levin M.J., WaldA., Ewell M.G. et al., Epidemiology, Clinical Presentation, andAntibody Response to Primary Infection With Herpes SimplexVirus Type 1 and Type 2 in Young Women, Clin. Infect. Dis.,2013, 56(3), 344-351[Crossref]
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_1515_med-2015-0042
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