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Inhibition of cyclosporin-resistant B-cell antigen responses by pyrazoles: a tool for the identification of novel molecular mechanisms of B-cell activation.
Transplant Proc
May 2001
Department of Transplantation Research, Basel, Switzerland.
Spontaneous mutations in the human immunodeficiency virus type 1 gag gene that affect viral replication in the presence of cyclosporins.
J Virol
June 1996
Sandoz Forschungsinstitut, Vienna, Austria.
Human immunodeficiency virus type 1 mutants that are resistant to inhibition by cyclosporins arise spontaneously in vitro during propagation in a HeLa-CD4+ cell line in the presence of a nonimmunosuppressive analog of cyclosporin A. Interestingly, the phenotype of all of the mutants examined is drug resistant and drug dependent, with both cyclosporin A and its analog. Four independently isolated mutants have been analyzed genetically by construction of recombinant proviruses in the NL4-3 parental strain background and subsequent testing of the chimeric viruses in HeLa cells.
View Article and Find Full Text PDFNuclear association of a T-cell transcription factor blocked by FK-506 and cyclosporin A.
Nature
August 1991
Beckman Center for Molecular and Genetic Medicine, Howard Hughes Medical Institute, Stanford University Medical School, California 94305.
Cyclosporin A and FK506 inhibit T- and B-cell activation and other processes essential to an effective immune response. In T lymphocytes these drugs disrupt an unknown step in the transmission of signals from the T-cell antigen receptor to cytokine genes that coordinate the immune response. The putative intracellular receptors for FK506 and cyclosporin are cis-trans prolyl isomerases.
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