Characterization of binding activity between nuclear factor of activated T cells and calcineurin by amplified luminescent proximity homogeneous assay

2006 ◽  
Vol 312 (1-2) ◽  
pp. 105-110 ◽  
Author(s):  
Noriko Kitamura ◽  
Osamu Kaminuma ◽  
Fujiko Kitamura ◽  
Shoichiro Miyatake
Keyword(s):  
T Cells ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Homogeneous Assay

A novel monitoring of immunosuppression in recipients with DNA-binding activity of nuclear factor in activated T cells

1997 ◽  
Vol 29 (1-2) ◽  
pp. 1172-1173
Author(s):  
K. Akioka ◽  
H. Nakajima ◽  
I. Fujiwara ◽  
N. Yoshimura ◽  
T. Matsuda ◽  
...  
Keyword(s):  
T Cells ◽  
Dna Binding ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Dna Binding Activity

scholarly journals A potential role for nuclear factor of activated T-cells in receptor tyrosine kinase and G-protein-coupled receptor agonist-induced cell proliferation

2002 ◽  
Vol 368 (1) ◽  
pp. 183-190 ◽  
Author(s):  
Chandrahasa R. YELLATURU ◽  
Salil K. GHOSH ◽  
R.K. RAO ◽  
Lisa K. JENNINGS ◽  
Aviv HASSID ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Dna Synthesis ◽  
G Protein ◽  
Receptor Tyrosine Kinase ◽  
Binding Activity ◽  
Nuclear Factor ◽  
Activated T Cells ◽  
Dna Binding Activity ◽  
G Protein Coupled

We have studied the role of nuclear factor of activated T-cells (NFAT) transcription factors in the induction of vascular smooth muscle cell (VSMC) growth by platelet-derived growth factor-BB (PDGF-BB) and thrombin, the receptor tyrosine kinase (RTK) and G-protein-coupled receptor (GPCR) agonists, respectively. NFATc1 but not NFATc2 or NFATc3 was translocated from the cytoplasm to the nucleus upon treatment of VSMCs with PDGF-BB or thrombin. Translocation of NFATc1 was followed by an increase in NFAT—DNA binding activity and NFAT-dependent reporter gene expression. Cyclosporin A (CsA), a potent and specific inhibitor of calcineurin, a calcium/calmodulin-dependent serine phosphatase involved in the dephosphorylation and activation of NFATs, blocked NFAT—DNA binding activity and NFAT-dependent reporter gene expression induced by PDGF-BB and thrombin. CsA also completely inhibited PDGF-BB- and thrombin-induced VSMC growth, as measured by DNA synthesis and cell number. In addition, forced expression of the NFAT-competing peptide VIVIT for calcineurin binding significantly attenuated the DNA synthesis induced by PDGF-BB and thrombin in VSMCs. Together, these findings for the first time demonstrate a role for NFATs in RTK and GPCR agonist-induced growth in VSMCs.

scholarly journals Erythromycin Inhibits Transcriptional Activation of NF-κB, but not NFAT, through Calcineurin-Independent Signaling in T Cells

1999 ◽  
Vol 43 (11) ◽  
pp. 2678-2684 ◽  
Author(s):  
Yosuke Aoki ◽  
Peter N. Kao
Keyword(s):  
T Cells ◽  
Dna Binding ◽  
Transcriptional Activation ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Binding Activity ◽  
Cytokine Gene Expression ◽  
Nuclear Factor ◽  
Mobility Shift ◽  
Activated T Cells

ABSTRACT The molecular mechanism of the anti-inflammatory effect of erythromycin (EM) was investigated at the level of transcriptional regulation of cytokine gene expression in T cells. EM (>10−6 M) significantly inhibited interleukin-8 (IL-8) expression but not IL-2 expression from T cells induced with 20 ng of phorbol 12-myristate 13-acetate (PMA) per ml plus 2 μM calcium ionophore (P-I). In electrophoretic mobility shift assays EM at 10−7 to 10−5 M concentrations inhibited nuclear factor kappa B (NF-κB) DNA-binding activities induced by P-I. Reporter gene assays also showed that EM (10−5 M) inhibited IL-8 NF-κB transcription by 37%. The inhibitory effects of EM on transcriptional activation of IL-2 and DNA-binding activity of nuclear factor of activated T cells (NFAT) were not seen in T cells. On the other hand, FK506, which is also a macrolide derivative, inhibited transcriptional activation of both NF-κB and NFAT more strongly than EM did. The mechanism of EM inhibition of transactivation of NF-κB was further investigated in transiently transfected T cells that express calcineurin A and B subunits. Expression of calcineurin did not render transactivation of NF-κB in T cells more resistant to EM, while the inhibitory effect of FK506 on transactivation of NF-κB was attenuated. These findings indicate that EM is capable of inhibiting expression of the IL-8 gene in T cells through transcriptional inhibition and that this inhibition is mediated through a non-calcineurin-dependent signaling event in T lymphocytes.

Sign in / Sign up

Export Citation Format

Share Document