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Nfatc3  -  nuclear factor of activated T-cells,...

Rattus norvegicus

 
 
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Disease relevance of Nfatc3_predicted

 

High impact information on Nfatc3_predicted

  • Ang II-induced nuclear translocation of the green fluorescent protein (GFP)-tagged amino-terminal region of NFAT4 (GFP-NFAT4) was suppressed by p115-RGS or BAPTA but not by diphenyleneiodonium [2].
  • These results support the novel concept that NFATc3 controls the excitability of arterial smooth muscle by regulating Kv2.1 expression [3].
  • Consistent with our hypothesis, we found that calcineurin and NFATc3 are obligatory components of the signaling cascade mediating reduced IKv by Ang II [3].

References

  1. The pro-hypertrophic basic helix-loop-helix protein p8 is degraded by the ubiquitin/proteasome system in a protein kinase B/Akt- and glycogen synthase kinase-3-dependent manner, whereas endothelin induction of p8 mRNA and renal mesangial cell hypertrophy require NFAT4. Goruppi, S., Kyriakis, J.M. J. Biol. Chem. (2004) [Pubmed]
  2. Galpha12/13-mediated production of reactive oxygen species is critical for angiotensin receptor-induced NFAT activation in cardiac fibroblasts. Fujii, T., Onohara, N., Maruyama, Y., Tanabe, S., Kobayashi, H., Fukutomi, M., Nagamatsu, Y., Nishihara, N., Inoue, R., Sumimoto, H., Shibasaki, F., Nagao, T., Nishida, M., Kurose, H. J. Biol. Chem. (2005) [Pubmed]
  3. NFATc3 regulates Kv2.1 expression in arterial smooth muscle. Amberg, G.C., Rossow, C.F., Navedo, M.F., Santana, L.F. J. Biol. Chem. (2004) [Pubmed]
 
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