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Article: Modulation of nuclear factor-κB by human T cell leukemia virus type 1 tax protein: Implications for oncogenesis and inflammation

TitleModulation of nuclear factor-κB by human T cell leukemia virus type 1 tax protein: Implications for oncogenesis and inflammation
Authors
KeywordsAdult T cell leukemia (ATL)
HTLV-1 Tax
Human T cell leukemia virus (HTLV-1)
IKK
Inflammation
NF-κB
NIK
Issue Date2006
Citation
Immunologic Research, 2006, v. 34 n. 1, p. 1-12 How to Cite?
AbstractActivation of the nuclear factor kappa B (NF-κB) transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. While the main function of NF-κB is to promote the host's immune response, the NF-κB pathway is frequently dysregulated by invading viral pathogens. Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses. Here, we review current thinking on how Tax may affect both diseases through activation of NF-κB signaling. © 2006 Humana Press Inc.
Persistent Identifierhttp://hdl.handle.net/10722/157446
ISSN
2023 Impact Factor: 3.3
2023 SCImago Journal Rankings: 0.870
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPeloponese Jr, JMen_US
dc.contributor.authorYeung, MLen_US
dc.contributor.authorJeang, KTen_US
dc.date.accessioned2012-08-08T08:50:02Z-
dc.date.available2012-08-08T08:50:02Z-
dc.date.issued2006en_US
dc.identifier.citationImmunologic Research, 2006, v. 34 n. 1, p. 1-12en_US
dc.identifier.issn0257-277Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/157446-
dc.description.abstractActivation of the nuclear factor kappa B (NF-κB) transcription factor family by different stimuli, such as inflammatory cytokines, stress inducers, or pathogens, results in innate and adaptive immunity. While the main function of NF-κB is to promote the host's immune response, the NF-κB pathway is frequently dysregulated by invading viral pathogens. Human T cell leukemia virus type 1 (HTLV-1) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL) and an inflammatory disease named tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). HTLV-1 encodes an oncoprotein, Tax, which plays a significant role in the initiation of cellular transformation and the elicitation of the host's inflammatory responses. Here, we review current thinking on how Tax may affect both diseases through activation of NF-κB signaling. © 2006 Humana Press Inc.en_US
dc.languageengen_US
dc.relation.ispartofImmunologic Researchen_US
dc.subjectAdult T cell leukemia (ATL)-
dc.subjectHTLV-1 Tax-
dc.subjectHuman T cell leukemia virus (HTLV-1)-
dc.subjectIKK-
dc.subjectInflammation-
dc.subjectNF-κB-
dc.subjectNIK-
dc.subject.meshAnimalsen_US
dc.subject.meshCell Transformation, Neoplastic - Immunologyen_US
dc.subject.meshGene Products, Tax - Immunologyen_US
dc.subject.meshHtlv-I Infections - Immunologyen_US
dc.subject.meshHuman T-Lymphotropic Virus 1 - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshInflammation - Immunologyen_US
dc.subject.meshNf-Kappa B - Immunologyen_US
dc.titleModulation of nuclear factor-κB by human T cell leukemia virus type 1 tax protein: Implications for oncogenesis and inflammationen_US
dc.typeArticleen_US
dc.identifier.emailYeung, ML:pmlyeung@hku.hken_US
dc.identifier.authorityYeung, ML=rp01402en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1385/IR:34:1:1en_US
dc.identifier.pmid16720895-
dc.identifier.scopuseid_2-s2.0-33646870117en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646870117&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume34en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage12en_US
dc.identifier.isiWOS:000237855100001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridPeloponese Jr, JM=6602547774en_US
dc.identifier.scopusauthoridYeung, ML=8350940900en_US
dc.identifier.scopusauthoridJeang, KT=7004824803en_US
dc.identifier.issnl0257-277X-

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