|  Help  |  About  |  Contact Us

Publication : Calcineurin-dependent nuclear translocation of a murine transcription factor NFATx: molecular cloning and functional characterization.

First Author  Liu J Year  1997
Journal  Mol Biol Cell Volume  8
Issue  1 Pages  157-70
PubMed ID  9017603 Mgi Jnum  J:38327
Mgi Id  MGI:85703 Doi  10.1091/mbc.8.1.157
Citation  Liu J, et al. (1997) Calcineurin-dependent nuclear translocation of a murine transcription factor NFATx: molecular cloning and functional characterization. Mol Biol Cell 8(1):157-70
abstractText  Members of the nuclear factor of activated T cells (NFAT) are involved in the induction of a number of cytokine genes. We report here cDNA cloning and chromosomal localization of a murine homologue of human NFATx, designated as mNFATx1, and its splicing variants nMFATx2 and m Delta NFATx. Northern blot analysis showed mNFATx1 to be predominantly expressed in the thymus. NMFATx1, but not m Delta NFATx, produced in COS-7 cells, bound to all NFAT-binding sites of the interleukin (IL)-2 and IL-4 promoters tested. Immunofluorescence assay showed that both mNFATx1 and m Delta NFATx introduced into COS-7 cells localized predominantly to the cytoplasm, but did translocate to the nucleus, either by cotransfection with an active form of calcineurin or wild-type calcineurin followed by stimulation with calcium ionophore. Translocation of mNFATx1 correlated well with activation of the murine IL-2 promoter; mNFATx1 translocated under conditions described above, in combination with phorbol 12- myristate 13-acetate, activated the transiently transfected murine IL-2 promoter. Thus, nuclear- translocated mNFATx1 is involved in activation of the IL-2 promoter. These results provide the first evidence for the requirement of calcineurin in the control of mNFATx imported from the cytoplasm to the nucleus and implies that mNFATx may possibly be a substrate of calcineurin in vivo.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

10 Bio Entities

Trail: Publication

0 Expression