ISSN:
0730-2312
Keywords:
monoiodoacetic acid
;
sulfhydryl reagent
;
modulation of signal transduction
;
redox-linked
;
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Biology
,
Chemistry and Pharmacology
,
Medicine
Notes:
Actions of monoiodoacetic acid (MIA) as a sulfhydryl reagent on the different stages of the T cell receptor (TCR)-mediated signal transduction were examined. MIA (1 mM) prevented anti-TCR (CD3) monoclonal antibody (mAb)-induced energy-dependent receptor capping but at the same time promoted the anti-CD3 mAb/mitogen-induced tyrosine phosphorylation of the T cell activation-linked cellular proteins of 120, 80, 70, 56, and 40 KDa. Relatively low concentration (0.01 mM) of MIA further promoted anti-CD3 mAb-induced transcription of c-fos, production of IL-2, and cell surface expression of IL-2 receptors. The MIA-promoted TCR-mediated IL-2 production actually required signal transduction that could be inhibited by cyclosporin A, genistein, or H-7. In contrast, the same concentration of MIA as promoted the signal transduction for cell activation severely inhibited the anti-CD3 mAb-triggered signal delivery for cell proliferation, selectively at its early stage. We conclude from these results that MIA differentially affects various steps of signaling into T lymphocytes, suggesting that there exist multiple sites of MIA-sensitive or redox-linked control in the signal cascade. © 1995 Wiley-Liss, Inc.
Additional Material:
9 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/jcb.240590105
