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Gata2

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Gata2

GATA binding protein 2

PDB rendering based on 1gnf.
Available structures
PDB Ortholog search: PDBe, RCSB
Identifiers
Symbols  ; DCML; IMD21; MONOMAC; NFE1B
External IDs GeneCards:
Orthologs
Species Human Mouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

GATA2 is a human gene which makes a protein called GATA binding protein 2 - 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]

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]

Genetic disorders

Multiple mutations on GATA2 gene have been recently implicated as the cause of primary immunodeficiency in patients with MonoMAC Syndrome, and cases of dendritic cell, monocyte, B NK lymphoid deficiency and leukemia.[11]

Lung cancer

GATA2 has recently been implicated in non-small-cell lung cancer - specifically those tumours that are driven by a faulty Ras protein. Targeting processes that occur downstream of GATA2 signalling with clinically approved drugs had a significant effect in mouse models of the disease.[12]

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.  
  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.  
  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.  
  4. ^ "Entrez Gene: GATA2 GATA binding protein 2". 
  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.  
  6. ^ Ozawa, Y; Towatari M; Tsuzuki S; Hayakawa F; Maeda T; Miyata Y; Tanimoto M; Saito H (October 2001). "Histone deacetylase 3 associates with and represses the transcription factor GATA-2". Blood (United States) 98 (7): 2116–23.  
  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.  
  8. ^ Osada, H; Grutz G; Axelson H; Forster A; Rabbitts T H (October 1995). "Association of erythroid transcription factors: complexes involving the LIM protein RBTN2 and the zinc-finger protein GATA1".  
  9. ^ Tsuzuki, S; Towatari M; Saito H; Enver T (September 2000). "Potentiation of GATA-2 Activity through Interactions with the Promyelocytic Leukemia Protein (PML) and the t(15;17)-Generated PML-Retinoic Acid Receptor α Oncoprotein". Mol. Cell. Biol. (UNITED STATES) 20 (17): 6276–86.  
  10. ^ Zhang, P; Behre G; Pan J; Iwama A; Wara-Aswapati N; Radomska H S; Auron P E; Tenen D G; Sun Z (July 1999). "Negative cross-talk between hematopoietic regulators: GATA proteins repress PU.1".  
  11. ^ Dickinson RE, Griffin H, Bigley V, Reynard LN, Hussain R, Haniffa M, Lakey JH, Rahman T, Wang XN, McGovern N, Pagan S, Cookson S, McDonald D, Chua I, Wallis J, Cant A, Wright M, Keavney B, Chinnery PF, Loughlin J, Hambleton S, Santibanez-Koref M, Collin M (September 2011). "Exome sequencing identifies GATA-2 mutation as the cause of dendritic cell, monocyte, B and NK lymphoid deficiency". Blood 118 (10): 2656–8.  
  12. ^ Kumar, M. S.; Hancock, D. C.; Molina-Arcas, M.; Steckel, M.; East, P.; Diefenbacher, M.; Armenteros-Monterroso, E.; Lassailly, F. O.; Matthews, N.; Nye, E.; Stamp, G.; Behrens, A.; Downward, J. (2012). "The GATA2 Transcriptional Network is Requisite for RAS Oncogene-Driven Non-Small Cell Lung Cancer". Cell 149 (3): 642–655.  

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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