ATF3

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Activating transcription factor 3
Identifiers
Symbol ATF3
External IDs OMIM603148 MGI109384 HomoloGene1265 GeneCards: ATF3 Gene
RNA expression pattern
PBB GE ATF3 202672 s at tn.png
More reference expression data
Orthologs
Species Human Mouse
Entrez 467 11910
Ensembl ENSG00000162772 ENSMUSG00000026628
UniProt P18847 Q60765
RefSeq (mRNA) NM_001030287 NM_007498
RefSeq (protein) NP_001025458 NP_031524
Location (UCSC) Chr 1:
212.74 – 212.79 Mb
Chr 1:
191.17 – 191.18 Mb
PubMed search [1] [2]

Cyclic AMP-dependent transcription factor ATF-3 is a protein that, in humans, is encoded by the ATF3 gene.[1]

Function[edit]

Activating transcription factor 3 is a member of the mammalian activation transcription factor/cAMP responsive element-binding (CREB) protein family of transcription factors. Multiple transcript variants encoding two different isoforms have been found for this gene. The longer isoform represses rather than activates transcription from promoters with ATF binding elements. The shorter isoform (deltaZip2) lacks the leucine zipper protein-dimerization motif and does not bind to DNA, and it stimulates transcription, it is presumed, by sequestering inhibitory co-factors away from the promoter. It is possible that alternative splicing of the ATF3 gene may be physiologically important in the regulation of target genes.[2]

Clinical significance[edit]

ATF-3 is widely used as a marker for injured dorsal root ganglion neurons in Pain Research.[3]

See also[edit]

Interactions[edit]

ATF3 has been shown to interact with:

References[edit]

  1. ^ Chen BP, Liang G, Whelan J, Hai T (June 1994). "ATF3 and ATF3 delta Zip. Transcriptional repression versus activation by alternatively spliced isoforms". J Biol Chem 269 (22): 15819–26. PMID 7515060. 
  2. ^ "Entrez Gene: ATF3 activating transcription factor 3". 
  3. ^ Lindå H, Sköld MK, Ochsmann T (2011). "Activating transcription factor 3, a useful marker for regenerative response after nerve root injury". Front Neurol 2: 30. doi:10.3389/fneur.2011.00030. PMC 3099310. PMID 21629765. 
  4. ^ Pearson AG, Gray CW, Pearson JF, Greenwood JM, During MJ, Dragunow M (December 2003). "ATF3 enhances c-Jun-mediated neurite sprouting". Brain Res. Mol. Brain Res. 120 (1): 38–45. doi:10.1016/j.molbrainres.2003.09.014. PMID 14667575. 
  5. ^ a b Chen BP, Wolfgang CD, Hai T (March 1996). "Analysis of ATF3, a transcription factor induced by physiological stresses and modulated by gadd153/Chop10". Mol. Cell. Biol. 16 (3): 1157–68. PMC 231098. PMID 8622660. 
  6. ^ Hai T, Curran T (May 1991). "Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity". Proc. Natl. Acad. Sci. U.S.A. 88 (9): 3720–4. doi:10.1073/pnas.88.9.3720. PMC 51524. PMID 1827203. 
  7. ^ Chu HM, Tan Y, Kobierski LA, Balsam LB, Comb MJ (January 1994). "Activating transcription factor-3 stimulates 3',5'-cyclic adenosine monophosphate-dependent gene expression". Mol. Endocrinol. 8 (1): 59–68. doi:10.1210/mend.8.1.8152431. PMID 8152431. 
  8. ^ Stelzl U, Worm U, Lalowski M, Haenig C, Brembeck FH, Goehler H, Stroedicke M, Zenkner M, Schoenherr A, Koeppen S, Timm J, Mintzlaff S, Abraham C, Bock N, Kietzmann S, Goedde A, Toksöz E, Droege A, Krobitsch S, Korn B, Birchmeier W, Lehrach H, Wanker EE (September 2005). "A human protein-protein interaction network: a resource for annotating the proteome". Cell 122 (6): 957–68. doi:10.1016/j.cell.2005.08.029. PMID 16169070. 
  9. ^ Yan C, Wang H, Boyd DD (March 2002). "ATF3 represses 72-kDa type IV collagenase (MMP-2) expression by antagonizing p53-dependent trans-activation of the collagenase promoter". J. Biol. Chem. 277 (13): 10804–12. doi:10.1074/jbc.M112069200. PMID 11792711. 
  10. ^ Kang Y, Chen CR, Massagué J (April 2003). "A self-enabling TGFbeta response coupled to stress signaling: Smad engages stress response factor ATF3 for Id1 repression in epithelial cells". Mol. Cell 11 (4): 915–26. doi:10.1016/s1097-2765(03)00109-6. PMID 12718878. 

Further reading[edit]

External links[edit]

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