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GATA binding protein 2, also known as GATA2, is a human gene. The protein encoded by this gene is a transcription factor.[1]

The GATA family of transcription factors, which contain zinc fingers in their DNA binding domain, have emerged as candidate regulators of gene expression in hematopoietic cells.[2] GATA1 is essential for normal primitive and definitive erythropoiesis and is expressed at high levels in erythroid cells, mast cells, and megakaryocytes. GATA2 is expressed in hematopoietic progenitors, including early erythroid cells, mast cells, and megakaryocytes, and also in nonhematopoietic embryonic stem cells. In chicken erythroid progenitors, forced expression of GATA2 promotes proliferation at the expense of differentiation.[3] GATA3 expression is restricted to T-lymphoid cells and some nonhematopoietic cell types, including embryonic stem cells.[4]

Contents

Interactions

GATA2 has been shown to interact with Pituitary-specific positive transcription factor 1,[5] HDAC3,[6] Zinc finger and BTB domain-containing protein 16,[7] LMO2,[8] Promyelocytic leukemia protein[9] and SPI1.[10]

See also

References

  1. ^ Lee ME, Temizer DH, Clifford JA, Quertermous T (25 August 1991). "Cloning of the GATA-binding protein that regulates endothelin-1 gene expression in endothelial cells". J. Biol. Chem. 266 (24): 16188–92. PMID 1714909. http://www.jbc.org/cgi/content/abstract/266/24/16188.  
  2. ^ Tsai FY, Keller G, Kuo FC, Weiss M, Chen J, Rosenblatt M, Alt FW, Orkin SH (September 1994). "An early haematopoietic defect in mice lacking the transcription factor GATA-2". Nature 371 (6494): 221–6. doi:10.1038/371221a0. PMID 8078582.  
  3. ^ Briegel K, Lim KC, Plank C, Beug H, Engel JD, Zenke M (June 1993). "Ectopic expression of a conditional GATA-2/estrogen receptor chimera arrests erythroid differentiation in a hormone-dependent manner". Genes Dev. 7 (6): 1097–109. doi:10.1101/gad.7.6.1097. PMID 8504932.  
  4. ^ "Entrez Gene: GATA2 GATA binding protein 2". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=2624.  
  5. ^ Dasen, J S; O'Connell S M, Flynn S E, Treier M, Gleiberman A S, Szeto D P, Hooshmand F, Aggarwal A K, Rosenfeld M G (May. 1999). "Reciprocal interactions of Pit1 and GATA2 mediate signaling gradient-induced determination of pituitary cell types". Cell (UNITED STATES) 97 (5): 587–98. doi:10.1016/S0092-8674(00)80770-9. ISSN 0092-8674. PMID 10367888.  
  6. ^ Ozawa, Y; Towatari M, Tsuzuki S, Hayakawa F, Maeda T, Miyata Y, Tanimoto M, Saito H (Oct. 2001). "Histone deacetylase 3 associates with and represses the transcription factor GATA-2". Blood (United States) 98 (7): 2116–23. doi:10.1182/blood.V98.7.2116. ISSN 0006-4971. PMID 11567998.  
  7. ^ Tsuzuki, Shinobu; Enver Tariq (May. 2002). "Interactions of GATA-2 with the promyelocytic leukemia zinc finger (PLZF) protein, its homologue FAZF, and the t(11;17)-generated PLZF-retinoic acid receptor alpha oncoprotein". Blood (United States) 99 (9): 3404–10. doi:10.1182/blood.V99.9.3404. ISSN 0006-4971. PMID 11964310.  
  8. ^ Osada, H; Grutz G, Axelson H, Forster A, Rabbitts T H (Oct. 1995). "Association of erythroid transcription factors: complexes involving the LIM protein RBTN2 and the zinc-finger protein GATA1". Proc. Natl. Acad. Sci. U.S.A. (UNITED STATES) 92 (21): 9585–9. doi:10.1073/pnas.92.21.9585. ISSN 0027-8424. PMID 7568177.  
  9. ^ Tsuzuki, S; Towatari M, Saito H, Enver T (Sep. 2000). "Potentiation of GATA-2 activity through interactions with the promyelocytic leukemia protein (PML) and the t(15;17)-generated PML-retinoic acid receptor alpha oncoprotein". Mol. Cell. Biol. (UNITED STATES) 20 (17): 6276–86. doi:10.1128/MCB.20.17.6276-6286.2000. ISSN 0270-7306. PMID 10938104.  
  10. ^ Zhang, P; Behre G, Pan J, Iwama A, Wara-Aswapati N, Radomska H S, Auron P E, Tenen D G, Sun Z (Jul. 1999). "Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1". Proc. Natl. Acad. Sci. U.S.A. (UNITED STATES) 96 (15): 8705–10. doi:10.1073/pnas.96.15.8705. ISSN 0027-8424. PMID 10411939.  

Further reading

External links

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

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