NFATC2

Nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 2

PDB rendering based on 1a02.
Identifiers
Symbols NFATC2; NFAT1; NFATP
External IDs OMIM600490 MGI102463 HomoloGene7861 GeneCards: NFATC2 Gene
Orthologs
Species Human Mouse
Entrez 4773 18019
Ensembl ENSG00000101096 ENSMUSG00000027544
UniProt Q13469 Q6P3F6
RefSeq (mRNA) NM_001136021.1 NM_001037177
RefSeq (protein) NP_001129493.1 NP_001032254
Location (UCSC) Chr 20:
50 – 50.18 Mb
Chr 2:
168.3 – 168.43 Mb
PubMed search [1] [2]

Nuclear factor of activated T-cells, cytoplasmic 2 is a protein that in humans is encoded by the NFATC2 gene.[1]

This gene is a member of the nuclear factor of activated T cells (NFAT) family. The product of this gene is a DNA-binding protein with a REL-homology region (RHR) and an NFAT-homology region (NHR). This protein is present in the cytosol and only translocates to the nucleus upon T cell receptor (TCR) stimulation, where it becomes a member of the nuclear factors of activated T cells transcription complex. This complex plays a central role in inducing gene transcription during the immune response. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.[2]
NFAT transcription factors are implicated in breast cancer, more specifically in the process of cell motility at the basis of metastasis formation. Indeed NFAT1 (NFATC2) is pro-invasive and pro-migratory in breast carcinoma [3] [4]

Contents

Interactions

NFATC2 has been shown to interact with MEF2D,[5] EP300,[6] IRF4[7] and Protein kinase Mζ.[8]

See also

References

  1. ^ Northrop JP, Ho SN, Chen L, Thomas DJ, Timmerman LA, Nolan GP, Admon A, Crabtree GR (Jul 1994). "NF-AT components define a family of transcription factors targeted in T-cell activation". Nature 369 (6480): 497–502. doi:10.1038/369497a0. PMID 8202141. 
  2. ^ "Entrez Gene: NFATC2 nuclear factor of activated T-cells, cytoplasmic, calcineurin-dependent 2". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=4773. 
  3. ^ Jauliac, S; López-Rodriguez, C, Shaw, LM, Brown, LF, Rao, A, Toker, A (2002 Jul). "The role of NFAT transcription factors in integrin-mediated carcinoma invasion.". Nature cell biology 4 (7): 540–4. doi:10.1038/ncb816. PMID 12080349. 
  4. ^ Yoeli-Lerner, M; Yiu, GK, Rabinovitz, I, Erhardt, P, Jauliac, S, Toker, A (2005 Nov 23). "Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT.". Molecular cell 20 (4): 539–50. doi:10.1016/j.molcel.2005.10.033. PMID 16307918. 
  5. ^ Youn, H D; Chatila T A, Liu J O (Aug. 2000). "Integration of calcineurin and MEF2 signals by the coactivator p300 during T-cell apoptosis". EMBO J. (ENGLAND) 19 (16): 4323–4331. doi:10.1093/emboj/19.16.4323. ISSN 0261-4189. PMC 302027. PMID 10944115. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=302027. 
  6. ^ García-Rodríguez, C; Rao A (Jun. 1998). "Nuclear factor of activated T cells (NFAT)-dependent transactivation regulated by the coactivators p300/CREB-binding protein (CBP)". J. Exp. Med. (UNITED STATES) 187 (12): 2031–2036. doi:10.1084/jem.187.12.2031. ISSN 0022-1007. PMC 2212364. PMID 9625762. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2212364. 
  7. ^ Rengarajan, Jyothi; Mowen Kerri A, McBride Kathryn D, Smith Erica D, Singh Harinder, Glimcher Laurie H (Apr. 2002). "Interferon regulatory factor 4 (IRF4) interacts with NFATc2 to modulate interleukin 4 gene expression". J. Exp. Med. (United States) 195 (8): 1003–1012. doi:10.1084/jem.20011128. ISSN 0022-1007. PMC 2193700. PMID 11956291. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2193700. 
  8. ^ San-Antonio, Belén; Iñiguez Miguel A, Fresno Manuel (Jul. 2002). "Protein kinase Czeta phosphorylates nuclear factor of activated T cells and regulates its transactivating activity". J. Biol. Chem. (United States) 277 (30): 27073–27080. doi:10.1074/jbc.M106983200. ISSN 0021-9258. PMID 12021260. 

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.