rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
7
|
pubmed:dateCreated |
2005-2-11
|
pubmed:abstractText |
Crk-associated substrate lymphocyte type (Cas-L) is a docking protein that is heavily tyrosine phosphorylated by the engagement of beta1 integrins in T cells. In the present study, we attempted to evaluate the role of Cas-L in the pathophysiology of adult T-cell leukemia (ATL). Examination of peripheral blood mononuclear cells from ATL patients as well as ATL-derived T cell lines showed an elevation of Cas-L in these cells. We showed that tyrosine phosphorylation as well as expression of Cas-L was markedly elevated through the induction of human T-lymphotropic virus type I (HTLV-I) Tax in JPX-9 cells, with these cells showing marked motile behavior on the ligands for integrins. We next performed yeast two-hybrid screening of cDNA library from an HTLV-I-transformed T cell line, which resulted in the identification of Tax as a putative binding partner for Cas-L. Co-precipitation experiments revealed that the serine-rich region of Cas-L might serve as the binding site with the highest affinity for Tax. Co-localization study showed that Tax and Cas-L partly merged in the cytoplasm. Finally, we showed that exogenous Cas-L inhibited Tax-mediated transactivation of nuclear factor kappaB (NF-kappaB), while Tax-independent activation of NF-kappaB remained intact, hence indicating that Cas-L might specifically regulate Tax-NF-kappaB pathway.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0950-9232
|
pubmed:author |
pubmed-author:ArimaNaomichiN,
pubmed-author:DangNam HNH,
pubmed-author:HosonoOsamuO,
pubmed-author:IwataSatoshiS,
pubmed-author:KawasakiHiroshiH,
pubmed-author:MorimotoChikaoC,
pubmed-author:SasakiTakahiroT,
pubmed-author:ShimizuTakatsuneT,
pubmed-author:Souta-KuribaraAkikoA,
pubmed-author:TanakaHirotoshiH,
pubmed-author:WatanabeToshikiT,
pubmed-author:YamakawaAkioA
|
pubmed:issnType |
Print
|
pubmed:day |
10
|
pubmed:volume |
24
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1262-71
|
pubmed:dateRevised |
2008-11-21
|
pubmed:meshHeading |
pubmed-meshheading:15592516-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:15592516-Cadmium Chloride,
pubmed-meshheading:15592516-Cell Line, Transformed,
pubmed-meshheading:15592516-Cell Movement,
pubmed-meshheading:15592516-Cytosol,
pubmed-meshheading:15592516-Gene Products, tax,
pubmed-meshheading:15592516-Human T-lymphotropic virus 1,
pubmed-meshheading:15592516-Humans,
pubmed-meshheading:15592516-Immunoprecipitation,
pubmed-meshheading:15592516-Leukemia, T-Cell,
pubmed-meshheading:15592516-Leukocytes, Mononuclear,
pubmed-meshheading:15592516-NF-kappa B,
pubmed-meshheading:15592516-Phosphoproteins,
pubmed-meshheading:15592516-Phosphorylation,
pubmed-meshheading:15592516-Transcriptional Activation,
pubmed-meshheading:15592516-Two-Hybrid System Techniques,
pubmed-meshheading:15592516-Up-Regulation
|
pubmed:year |
2005
|
pubmed:articleTitle |
HTLV-I Tax induces and associates with Crk-associated substrate lymphocyte type (Cas-L).
|
pubmed:affiliation |
Division of Clinical Immunology, Advanced Clinical Research Center, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|