2004
DOI: 10.1182/blood-2003-12-4251
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Transcriptional activation of hTERT through the NF-κB pathway in HTLV-I–transformed cells

Abstract: In immortal cells, the existence of a mechanism for the maintenance of telomere length is critical. In most cases this is achieved by the reactivation of telomerase, a cellular reverse transcriptase that prevents telomere shortening. Here we report that the telomerase gene

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Cited by 121 publications
(132 citation statements)
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References 70 publications
(74 reference statements)
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“…This hypothesis is consistent with previous findings that hTERT protein interacts directly with NF-κB p65, an effect reversed by the IKK inhibitor PS-1145 or NF-κB nuclear translocation inhibitor SN-50 in human multiple myeloma MM.1S cells [76]. It is also in line with the findings that NF-κB transactivates c-myc to stimulate hTERT promoter activity, which can be induced by human T-cell lymphotropic virus type-I in primary T cells in vitro and in adult T-cell leukemia/lymphoma samples ex vivo [77]. However, what is not yet clear includes the protein motifs that mediate the molecular interactions between the hTERT and NF-κB p65 proteins, and the biological consequence of LMP1 signalling in the maintenance of telomeres.…”
Section: Regulation Of Telomerase Activity By the Ebv Proteinssupporting
confidence: 74%
“…This hypothesis is consistent with previous findings that hTERT protein interacts directly with NF-κB p65, an effect reversed by the IKK inhibitor PS-1145 or NF-κB nuclear translocation inhibitor SN-50 in human multiple myeloma MM.1S cells [76]. It is also in line with the findings that NF-κB transactivates c-myc to stimulate hTERT promoter activity, which can be induced by human T-cell lymphotropic virus type-I in primary T cells in vitro and in adult T-cell leukemia/lymphoma samples ex vivo [77]. However, what is not yet clear includes the protein motifs that mediate the molecular interactions between the hTERT and NF-κB p65 proteins, and the biological consequence of LMP1 signalling in the maintenance of telomeres.…”
Section: Regulation Of Telomerase Activity By the Ebv Proteinssupporting
confidence: 74%
“…As expected, reactivation of the human telomerase gene catalytic subunit (hTERT) and increased telomerase activity is commonly found in HTLV-I infected cell lines in vitro and in ex vivo ATL cells [114][115][116][117][118]. Recent studies demonstrate Tax, through its NF-kB inducing activity, stimulates hTERT expression in HTLV-I-infected cells, allowing maintenance of long telomeres and avoidance of replicative senescence [118]. However, in the presence of antigenic stimulation of T-lymphocytes bearing Tax, hTERT mRNA induction is diminished [118,119].…”
Section: Molecular Pathogenesismentioning
confidence: 89%
“…These effects increase the occurrence and accumulation of somatic mutations and predispose HTLV-I infected cells to chromosome instability. As expected, reactivation of the human telomerase gene catalytic subunit (hTERT) and increased telomerase activity is commonly found in HTLV-I infected cell lines in vitro and in ex vivo ATL cells [114][115][116][117][118]. Recent studies demonstrate Tax, through its NF-kB inducing activity, stimulates hTERT expression in HTLV-I-infected cells, allowing maintenance of long telomeres and avoidance of replicative senescence [118].…”
Section: Molecular Pathogenesismentioning
confidence: 90%
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“…Antiviral therapy with zidovudine (AZT) and interferon-alpha (IFN-a) in these patients has produced longterm clinical remissions in human trials (Gill et al, 1995;Hermine et al, 1995;Matutes et al, 2001;White et al, 2001). In HTLV-I-infected cells, Tax stimulates endogenous hTERT promoter (Sinha-Datta et al, 2004). However despite strong telomerase activity, HTLV-Iinfected cells retain short telomeres and enduring treatment of HTLV-I-infected cells with AZT result in telomere attrition and reactivation of p53 transcriptional activities .…”
Section: Introductionmentioning
confidence: 99%