Publikationsdatum:
1995-07-07
Beschreibung:
Human T cell lymphotropic virus I (HTLV-I) is the etiological agent for adult T cell leukemia and tropical spastic paraparesis (also termed HTLV-I-associated myelopathy). HTLV-I-infected peripheral blood T cells exhibit an initial phase of interleukin-2 (IL-2)-dependent growth; over time, by an unknown mechanism, the cells become IL-2-independent. Whereas the Jak kinases Jak1 and Jak3 and the signal transducer and activator of transcription proteins Stat3 and Stat5 are activated in normal T cells in response to IL-2, this signaling pathway was constitutively activated in HTLV-I-transformed cells. In HTLV-I-infected cord blood lymphocytes, the transition from IL-2-dependent to IL-2-independent growth correlated with the acquisition of a constitutively activated Jak-STAT pathway, which suggests that this pathway participates in HTLV-I-mediated T cell transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Migone, T S -- Lin, J X -- Cereseto, A -- Mulloy, J C -- O'Shea, J J -- Franchini, G -- Leonard, W J -- New York, N.Y. -- Science. 1995 Jul 7;269(5220):79-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7604283" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Base Sequence
;
Cell Line, Transformed
;
*Cell Transformation, Viral
;
Cells, Cultured
;
DNA-Binding Proteins/*metabolism
;
Enzyme Activation
;
Fetal Blood/cytology
;
Human T-lymphotropic virus 1/*physiology
;
Humans
;
Interleukin-2/pharmacology
;
Janus Kinase 1
;
Janus Kinase 3
;
*Milk Proteins
;
Molecular Sequence Data
;
Phosphorylation
;
Protein-Tyrosine Kinases/*metabolism
;
Receptors, Interleukin-2/metabolism
;
STAT3 Transcription Factor
;
STAT5 Transcription Factor
;
Signal Transduction
;
T-Lymphocytes/metabolism/*virology
;
Trans-Activators/*metabolism
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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