Document Detail


HTLV-I Tax induces and associates with Crk-associated substrate lymphocyte type (Cas-L).
MedLine Citation:
PMID:  15592516     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Satoshi Iwata; Akiko Souta-Kuribara; Akio Yamakawa; Takahiro Sasaki; Takatsune Shimizu; Osamu Hosono; Hiroshi Kawasaki; Hirotoshi Tanaka; Nam H Dang; Toshiki Watanabe; Naomichi Arima; Chikao Morimoto
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Oncogene     Volume:  24     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-02-11     Completed Date:  2005-03-14     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  England    
Other Details:
Languages:  eng     Pagination:  1262-71     Citation Subset:  IM    
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.
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MeSH Terms
Descriptor/Qualifier:
Adaptor Proteins, Signal Transducing
Cadmium Chloride / pharmacology
Cell Line, Transformed
Cell Movement / genetics,  physiology
Cytosol / chemistry
Gene Products, tax / analysis,  metabolism*
Human T-lymphotropic virus 1 / metabolism
Humans
Immunoprecipitation
Leukemia, T-Cell / virology*
Leukocytes, Mononuclear / chemistry,  drug effects,  physiology
NF-kappa B / physiology
Phosphoproteins / analysis,  metabolism,  physiology*
Phosphorylation
Transcriptional Activation / physiology
Two-Hybrid System Techniques
Up-Regulation
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Gene Products, tax; 0/NEDD9 protein, human; 0/NF-kappa B; 0/Phosphoproteins; 10108-64-2/Cadmium Chloride

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