GATA3

The GATA3 gene is located close to the end of the short arm of chromosome 10 at position p14. It consists of 8 exons, and codes for two variants viz., GATA3, variant 1, and GATA3, variant 2.{{cite journal|url=https://www.ncbi.nlm.nih.gov/nuccore/NG_015859.1?&feature=any|title=Homo sapiens GATA binding protein 3 (GATA3) | journal = RefSeqGene on Chromosome - Nucleotide | publisher = National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health |date=2019-05-21 }} Expression of GATA3 may be regulated in part or at times by the antisense RNA, GATA3-AS1, whose gene is located close to the GATA3 gene on the short arm of chromosome 10 at position p14.{{Cite web | url=https://www.ncbi.nlm.nih.gov/gene/399717#summary | title=GATA3-AS1 GATA3 antisense RNA 1 [Homo sapiens (human) | work = Entrez Gene | publisher = National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health }} Various types of mutations including point mutations as well as small- and large-scale deletional mutations cause an autosomal dominant genetic disorder, the Barakat syndrome (also termed hypoparathyroidism, deafness, and renal dysplasia syndrome). The location of GATA3 borders that of other critical sites on chromosome 10, particularly a site located at 10p14-p13. Mutations in this site cause the congenital disorder DiGeorge syndrome/velocardiofacial syndrome complex 2 (or DiGeorge syndrome 2).{{cite web|url=https://www.ncbi.nlm.nih.gov/gtr/conditions/C1832431/|title=DiGeorge syndrome/velocardiofacial syndrome complex 2 - Conditions | work = Genetics Testing Registry (GTR) | publisher = National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health }} Large-scale deletions in GATA3 may span into the DiGeorge syndrome 2 area and thereby cause a complex syndrome with features of the Barakat syndrome combined with some of those of the DiGeorge syndrome 2.{{cite journal | vauthors = Lindstrand A, Malmgren H, Verri A, Benetti E, Eriksson M, Nordgren A, Anderlid BM, Golovleva I, Schoumans J, Blennow E | title = Molecular and clinical characterization of patients with overlapping 10p deletions | journal = American Journal of Medical Genetics. Part A | volume = 152A | issue = 5 | pages = 1233–43 | date = May 2010 | pmid = 20425828 | doi = 10.1002/ajmg.a.33366 | s2cid = 22213304 }} Knockout of both GATA3 genes in mice is fatal: these animals die at embryonic days 11 and 12 due to internal bleeding. They also exhibit gross deformities in the brain and spine as well as aberrations in fetal liver hematopoiesis.{{cite journal | vauthors = Du F, Yuan P, Wang T, Zhao J, Zhao Z, Luo Y, Xu B | title = The Significance and Therapeutic Potential of GATA3 Expression and Mutation in Breast Cancer: A Systematic Review | journal = Medicinal Research Reviews | volume = 35 | issue = 6 | pages = 1300–15 | date = November 2015 | pmid = 26313026 | doi = 10.1002/med.21362 | s2cid = 11668034 }}

GATA3 variant 1 is a linear protein consisting of 444 amino acids. GATA3 variant 2 protein is an identically structured isoform of, but 1 amino acid shorter than, GATA3 variant 1. Differences, if any, in the functions of these two variants have not been reported.{{cite web |url=https://www.ncbi.nlm.nih.gov/nuccore/NM_002051.2|title=Homo sapiens GATA binding protein 3 (GATA3), transcript variant 2, mRN - Nucleotide |date=2019-05-19| publisher = National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health }} With respect to the best studied variant, variant 1, but presumably also variant 2, one of the zinc finger structural motifs, ZNF2, is located at the protein's C-terminus and binds to specific gene promoter DNA sequences to regulate the expression of the genes controlled by these promoters. The other zinc finger, ZNF1, is at the protein's N-terminus and interacts with various nuclear factors, including Zinc finger protein 1 (i.e. ZFPM1, also termed Friends of GATA1 [i.e. FOG-1]) and ZFPM2 (i.e. FOG-2), that modulate GATA3's gene-stimulating actions.{{cite web|url=https://www.ncbi.nlm.nih.gov/protein/50541959|title=trans-acting T-cell-specific transcription factor GATA-3 isoform 1 [Ho - Protein - NCBI | publisher = National Center for Biotechnology Information (NCBI), U.S. National Institutes of Health }}

The GATA3 transcription factor regulates the expression of genes involved in the development of various tissues as well as genes involved in physiological as well as pathological humoral inflammatory and allergic responses.

GATA3 belongs to the GATA family of transcription factors. Gene-deletion studies in mice indicate that Gata3 (mouse gene equivalent to GATA3) is critical for the embryonic development and/or function of various cell types (e.g. fat cells, neural crest cells, lymphocytes) and tissues (e.g. kidney, liver, brain, spinal cord, mammary gland). Studies in humans implicate GATA3 in the following:

• 1) GATA3 is required for the development of the parathyroid gland, sensory components of the auditory system, and the kidney in animals and humans. It may also contribute to the development of the vagina and uterus in humans.
• 2) In humans, GATA3 is required for the development and/or function of innate lymphoid cells (ILCs), particularly Group 2 ILCs as well as for the development of T helper cells,(Th cells), particularly Th2 cells. Group 2 ILCs and Th2 cells, and thereby GATA3, are critical for the development of allergic and humoral immune responses in humans. Comparable studies in animals implicate GATA3 in the development of lymphocytes that mediate allergic and humoral immunity as well as allergic and humoral immune responses.{{cite journal | vauthors = Zhu J | title = GATA3 Regulates the Development and Functions of Innate Lymphoid Cell Subsets at Multiple Stages | journal = Frontiers in Immunology | volume = 8 | pages = 1571 | date = 2017 | pmid = 29184556 | pmc = 5694433 | doi = 10.3389/fimmu.2017.01571 | doi-access = free }}
• 3) GATA3 promotes the secretion of IL-4, IL-5, and IL-13 from Th2 cells in humans and has similar actions on comparable mouse lymphocytes. All three of these interleukins serve to promote allergic responses,{{cite journal | vauthors = Yagi R, Zhu J, Paul WE | title = An updated view on transcription factor GATA3-mediated regulation of Th1 and Th2 cell differentiation Z| journal = International Immunology | volume = 23 | issue = 7 | pages = 415–20 | date = Jul 2011 | pmid = 21632975 | doi = 10.1093/intimm/dxr029 | pmc=3123974}}
• 4) GATA3 induces the maturation of precursor cells into breast epithelial cells and maintains these cells in their mature state in mice and possibly humans.{{cite journal | vauthors = Kouros-Mehr H, Slorach EM, Sternlicht MD, Werb Z | title = GATA-3 maintains the differentiation of the luminal cell fate in the mammary gland | journal = Cell | volume = 127 | issue = 5 | pages = 1041–55 | date = Dec 2006 | pmid = 17129787 | pmc = 2646406 | doi = 10.1016/j.cell.2006.09.048 }}{{cite journal | vauthors = Asch-Kendrick R, Cimino-Mathews A | title = The role of GATA3 in breast carcinomas: a review | journal = Human Pathology | volume = 48 | pages = 37–47 | date = February 2016 | pmid = 26772397 | doi = 10.1016/j.humpath.2015.09.035 }}
• 5) In mice, GATA3 is responsible for the normal development of various tissues including the skin, fat cells, the thymus, and the nervous system.{{cite journal | vauthors = Ho IC, Pai SY | title = GATA-3 - not just for Th2 cells anymore | journal = Cellular & Molecular Immunology | volume = 4 | issue = 1 | pages = 15–29 | date = February 2007 | pmid = 17349208 }}

Inactivating mutations in one of the two parental GATA3 genes cause the congenital disorder of hypoparathyroidism with sensorineural deafness and kidney malformations, i.e. the Barakat syndrome. This rare syndrome may occur in families or as a new mutation in an individual from a family with no history of the disorder. Mutations in GATA3 cause variable degrees of hypoparathyroidism, deafness, and kidney disease birth defects because of 1) individual differences in the penetrance of the mutation, 2) a sporadic, and as yet unexplained, association with malformation of uterus and vagina, and 3) mutations which extend beyond the GATA3 gene into chromosomal areas where mutations are responsible for developing other types of abnormalities which are characteristics of the DeGeorge syndrome 2. The Barakat syndrome is due to a haploinsufficiency in GATA3 levels, i.e. levels of the transcription factor that are insufficient for the normal development of the cited tissues during embryogenesis.

Mouse studies indicate that inhibiting the expression of GATA3 using antisense RNA methods suppresses allergic inflammation. The protein is overexpressed in the afflicted tissues of individuals with various forms of allergy including asthma, rhinitis, nasal polyps, and atopic eczema. This suggests that it may have a role in promoting these disorders.{{cite journal | vauthors = Bachert C, Zhang L, Gevaert P | title = Current and future treatment options for adult chronic rhinosinusitis: Focus on nasal polyposis | journal = The Journal of Allergy and Clinical Immunology | volume = 136 | issue = 6 | pages = 1431–1440 | date = December 2015 | pmid = 26654192 | doi = 10.1016/j.jaci.2015.10.010 }} In a phase IIA clinical study of individuals suffering allergen-induced asthma, inhalation of Deoxyribozyme ST010, which specifically inactivates GATA3 messenger RNA, for 28 days reduced early and late immune lung responses to inhaled allergen. The clinical benefit of inhibiting GATA3 in this disorder is thought to be due to interfering with the function of Group 2 ILCs and Th2 cells by, for example, reducing their production of IL-4, IL-13, and especially IL-5. Reduction in these eosinophil-stimulating interleukins, it is postulated, reduces this cells ability to promote allergic reactivity and responses.{{cite journal | vauthors = Garn H, Renz H | title = GATA-3-specific DNAzyme - A novel approach for stratified asthma therapy | journal = European Journal of Immunology | volume = 47 | issue = 1 | pages = 22–30 | date = January 2017 | pmid = 27910098 | doi = 10.1002/eji.201646450 | doi-access = free }} For similar reasons, this treatment might also prove to be clinical useful for treating other allergic disorders.

GATA3 is one of the three genes mutated in >10% of breast cancers (Cancer Genome Atlas).{{cite journal | vauthors = Koboldt DC, Fulton RS, McLellan MD | title = Comprehensive molecular portraits of human breast tumours | journal = Nature | volume = 490 | issue = 7418 | pages = 61–70 | date = Oct 2012 | pmid = 23000897 | pmc = 3465532 | doi = 10.1038/nature11412 | bibcode = 2012Natur.490...61T }} Studies in mice indicate that the gene is critical for the normal development of breast tissue and directly regulates luminal cell (i.e. cells lining mammary ducts) differentiation in experimentally induced breast cancer.{{cite journal | vauthors = Kouros-Mehr H, Bechis SK, Slorach EM, Littlepage LE, Egeblad M, Ewald AJ, Pai SY, Ho IC, Werb Z | title = GATA-3 links tumor differentiation and dissemination in a luminal breast cancer model | journal = Cancer Cell | volume = 13 | issue = 2 | pages = 141–52 | date = Feb 2008 | pmid = 18242514 | pmc = 2262951 | doi = 10.1016/j.ccr.2008.01.011 }} Analytic studies of human breast cancer tissues suggest that GATA3 is required for specific type of low risk breast cancer (i.e. luminal A), is integral to the expression of estrogen receptor alpha, and (in estrogen receptor negative/androgen receptor positive cancers) androgen receptor signaling.{{cite journal | vauthors = Wilson BJ, Giguère V | title = Meta-analysis of human cancer microarrays reveals GATA3 is integral to the estrogen receptor alpha pathway | journal = Molecular Cancer | volume = 7 | pages = 49 | year = 2008 | pmid = 18533032 | pmc = 2430971 | doi = 10.1186/1476-4598-7-49 | doi-access = free }}{{cite journal | vauthors = Dydensborg AB, Rose AA, Wilson BJ, Grote D, Paquet M, Giguère V, Siegel PM, Bouchard M | title = GATA3 inhibits breast cancer growth and pulmonary breast cancer metastasis | journal = Oncogene | volume = 28 | issue = 29 | pages = 2634–42 | date = Jul 2009 | pmid = 19483726 | doi = 10.1038/onc.2009.126| s2cid = 2923763 | doi-access = }}{{cite journal | vauthors = Sanga S, Broom BM, Cristini V, Edgerton ME | title = Gene expression meta-analysis supports existence of molecular apocrine breast cancer with a role for androgen receptor and implies interactions with ErbB family | journal = BMC Medical Genomics | volume = 2 | pages = 59 | year = 2009 | pmid = 19747394 | pmc = 2753593 | doi = 10.1186/1755-8794-2-59 | doi-access = free }} These studies suggest that GATA3 is involved in the development of at least certain types of breast cancer in humans. However, there is disagreement on this, with some studies suggesting that the expression of the GATA3 acts to inhibit and other studies suggesting that it acts to promote the development, growth, and/or spread of this cancer. Further studies are needed to elucidate the role, if any, of GATA3 in the development of breast cancer.

Immuocytochemical analysis of GATA3 protein in breast cells is a valuable marker for diagnosing primary breast cancer, being tested as positive in up to 94% of cases. It is especially valuable for estrogen receptor positive breast cancers but is less sensitive (435-66% elevated), although still more valuable than many other markers, for diagnosing triple-negative breast cancers. This analysis is widely used as a clinically valuable marker for breast cancer.{{cite journal | vauthors = Liu H, Shi J, Wilkerson ML, Lin F | title = Immunohistochemical evaluation of GATA3 expression in tumors and normal tissues: a useful immunomarker for breast and urothelial carcinomas | journal = American Journal of Clinical Pathology | volume = 138 | issue = 1 | pages = 57–64 | date = July 2012 | pmid = 22706858 | doi = 10.1309/AJCP5UAFMSA9ZQBZ | doi-access = free }}{{cite journal | vauthors = Peng Y, Butt YM, Chen B, Zhang X, Tang P | title = Update on Immunohistochemical Analysis in Breast Lesions | journal = Archives of Pathology & Laboratory Medicine | volume = 141 | issue = 8 | pages = 1033–1051 | date = August 2017 | pmid = 28574279 | doi = 10.5858/arpa.2016-0482-RA | doi-access = free }}

Similar to breast tumors, the role of GATA3 in the genesis of other tumor types is unclear but detection of its transcription factor product may be diagnostically useful. Immuocytochemical analysis of GATA3 protein is considered a valuable marker for certain types of urinary bladder and urethral cancers as well as for parathyroid gland tumors (cancerous or benign), Single series reports suggest that this analysis might also be of value for diagnosing salivary gland tumors, salivary duct carcinomas, mammary analog secretory carcinomas, benign ovarian Brenner tumors, benign Walthard cell rests, and paragangliomas.{{cite journal | vauthors = Inamura K | title = Bladder Cancer: New Insights into Its Molecular Pathology | journal = Cancers | volume = 10 | issue = 4 | pages = 100| date = April 2018 | pmid = 29614760 | pmc = 5923355 | doi = 10.3390/cancers10040100 | doi-access = free }}

GATA3 has been shown to interact with the following transcription factor regulators: ZFPM1 and ZFPM2; LMO1;{{cite journal | vauthors = Ono Y, Fukuhara N, Yoshie O | title = TAL1 and LIM-only proteins synergistically induce retinaldehyde dehydrogenase 2 expression in T-cell acute lymphoblastic leukemia by acting as cofactors for GATA3 | journal = Molecular and Cellular Biology | volume = 18 | issue = 12 | pages = 6939–50 | date = Dec 1998 | pmid = 9819382 | pmc = 109277 | doi = 10.1128/MCB.18.12.6939}}{{cite journal | vauthors = Ono Y, Fukuhara N, Yoshie O | title = Transcriptional activity of TAL1 in T cell acute lymphoblastic leukemia (T-ALL) requires RBTN1 or -2 and induces TALLA1, a highly specific tumor marker of T-ALL | journal = The Journal of Biological Chemistry | volume = 272 | issue = 7 | pages = 4576–81 | date = Feb 1997 | pmid = 9020185 | doi = 10.1074/jbc.272.7.4576 | doi-access = free }} and FOXA1.{{cite journal | vauthors = Albergaria A, Paredes J, Sousa B, Milanezi F, Carneiro V, Bastos J, Costa S, Vieira D, Lopes N, Lam EW, Lunet N, Schmitt F | title = Expression of FOXA1 and GATA-3 in breast cancer: the prognostic significance in hormone receptor-negative tumours | journal = Breast Cancer Research | volume = 11 | issue = 3 | pages = R40 | year = 2009 | pmid = 19549328 | pmc = 2716509 | doi = 10.1186/bcr2327 | doi-access = free }} These regulators may promote or inhibit GATA3 in stimulating the expression of its target genes.

• GATA transcription factors

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• {{cite journal | vauthors = Naylor MJ, Ormandy CJ | title = Gata-3 and mammary cell fate | journal = Breast Cancer Research | volume = 9 | issue = 2 | pages = 302 | year = 2007 | pmid = 17381824 | pmc = 1868924 | doi = 10.1186/bcr1661 | doi-access = free }}
• {{cite journal | vauthors = Ho IC, Vorhees P, Marin N, Oakley BK, Tsai SF, Orkin SH, Leiden JM | title = Human GATA-3: a lineage-restricted transcription factor that regulates the expression of the T cell receptor alpha gene | journal = The EMBO Journal | volume = 10 | issue = 5 | pages = 1187–92 | date = May 1991 | pmid = 1827068 | pmc = 452772 | doi = 10.1002/j.1460-2075.1991.tb08059.x}}
• {{cite journal | vauthors = Marine J, Winoto A | title = The human enhancer-binding protein Gata3 binds to several T-cell receptor regulatory elements | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 88 | issue = 16 | pages = 7284–8 | date = Aug 1991 | pmid = 1871134 | pmc = 52279 | doi = 10.1073/pnas.88.16.7284 | bibcode = 1991PNAS...88.7284M | doi-access = free }}
• {{cite journal | vauthors = Ko LJ, Yamamoto M, Leonard MW, George KM, Ting P, Engel JD | title = Murine and human T-lymphocyte GATA-3 factors mediate transcription through a cis-regulatory element within the human T-cell receptor delta gene enhancer | journal = Molecular and Cellular Biology | volume = 11 | issue = 5 | pages = 2778–84 | date = May 1991 | pmid = 2017177 | pmc = 360054 | doi = 10.1128/mcb.11.5.2778}}
• {{cite journal | vauthors = Siegel MD, Zhang DH, Ray P, Ray A | title = Activation of the interleukin-5 promoter by cAMP in murine EL-4 cells requires the GATA-3 and CLE0 elements | journal = The Journal of Biological Chemistry | volume = 270 | issue = 41 | pages = 24548–55 | date = Oct 1995 | pmid = 7592673 | doi = 10.1074/jbc.270.41.24548 | doi-access = free }}
• {{cite journal | vauthors = Labastie MC, Bories D, Chabret C, Grégoire JM, Chrétien S, Roméo PH | title = Structure and expression of the human GATA3 gene | journal = Genomics | volume = 21 | issue = 1 | pages = 1–6 | date = May 1994 | pmid = 8088776 | doi = 10.1006/geno.1994.1217 }}
• {{cite journal | vauthors = Ono Y, Fukuhara N, Yoshie O | title = Transcriptional activity of TAL1 in T cell acute lymphoblastic leukemia (T-ALL) requires RBTN1 or -2 and induces TALLA1, a highly specific tumor marker of T-ALL | journal = The Journal of Biological Chemistry | volume = 272 | issue = 7 | pages = 4576–81 | date = Feb 1997 | pmid = 9020185 | doi = 10.1074/jbc.272.7.4576 | doi-access = free }}
• {{cite journal | vauthors = Ono Y, Fukuhara N, Yoshie O | title = TAL1 and LIM-only proteins synergistically induce retinaldehyde dehydrogenase 2 expression in T-cell acute lymphoblastic leukemia by acting as cofactors for GATA3 | journal = Molecular and Cellular Biology | volume = 18 | issue = 12 | pages = 6939–50 | date = Dec 1998 | pmid = 9819382 | pmc = 109277 | doi = 10.1128/MCB.18.12.6939}}
• {{cite journal | vauthors = Yang GP, Ross DT, Kuang WW, Brown PO, Weigel RJ | title = Combining SSH and cDNA microarrays for rapid identification of differentially expressed genes | journal = Nucleic Acids Research | volume = 27 | issue = 6 | pages = 1517–23 | date = Mar 1999 | pmid = 10037815 | pmc = 148347 | doi = 10.1093/nar/27.6.1517 }}
• {{cite journal | vauthors = Blumenthal SG, Aichele G, Wirth T, Czernilofsky AP, Nordheim A, Dittmer J | title = Regulation of the human interleukin-5 promoter by Ets transcription factors. Ets1 and Ets2, but not Elf-1, cooperate with GATA3 and HTLV-I Tax1 | journal = The Journal of Biological Chemistry | volume = 274 | issue = 18 | pages = 12910–6 | date = Apr 1999 | pmid = 10212281 | doi = 10.1074/jbc.274.18.12910 | doi-access = free }}
• {{cite journal | vauthors = Van Esch H, Groenen P, Nesbit MA, Schuffenhauer S, Lichtner P, Vanderlinden G, Harding B, Beetz R, Bilous RW, Holdaway I, Shaw NJ, Fryns JP, Van de Ven W, Thakker RV, Devriendt K | s2cid = 4327212 | title = GATA3 haplo-insufficiency causes human HDR syndrome | journal = Nature | volume = 406 | issue = 6794 | pages = 419–22 | date = Jul 2000 | pmid = 10935639 | doi = 10.1038/35019088 | bibcode = 2000Natur.406..419V }}
• {{cite journal | vauthors = Hartley JL, Temple GF, Brasch MA | title = DNA cloning using in vitro site-specific recombination | journal = Genome Research | volume = 10 | issue = 11 | pages = 1788–95 | date = Nov 2000 | pmid = 11076863 | pmc = 310948 | doi = 10.1101/gr.143000 }}
• {{cite journal | vauthors = Muroya K, Hasegawa T, Ito Y, Nagai T, Isotani H, Iwata Y, Yamamoto K, Fujimoto S, Seishu S, Fukushima Y, Hasegawa Y, Ogata T | title = GATA3 abnormalities and the phenotypic spectrum of HDR syndrome | journal = Journal of Medical Genetics | volume = 38 | issue = 6 | pages = 374–80 | date = Jun 2001 | pmid = 11389161 | pmc = 1734904 | doi = 10.1136/jmg.38.6.374 }}
• {{cite journal | vauthors = Crawford SE, Qi C, Misra P, Stellmach V, Rao MS, Engel JD, Zhu Y, Reddy JK | title = Defects of the heart, eye, and megakaryocytes in peroxisome proliferator activator receptor-binding protein (PBP) null embryos implicate GATA family of transcription factors | journal = The Journal of Biological Chemistry | volume = 277 | issue = 5 | pages = 3585–92 | date = Feb 2002 | pmid = 11724781 | doi = 10.1074/jbc.M107995200 | doi-access = free }}
• {{cite journal | vauthors = Kieffer LJ, Greally JM, Landres I, Nag S, Nakajima Y, Kohwi-Shigematsu T, Kavathas PB | title = Identification of a candidate regulatory region in the human CD8 gene complex by colocalization of DNase I hypersensitive sites and matrix attachment regions which bind SATB1 and GATA-3 | journal = Journal of Immunology | volume = 168 | issue = 8 | pages = 3915–22 | date = Apr 2002 | pmid = 11937547 | doi = 10.4049/jimmunol.168.8.3915 | doi-access = free }}
• {{cite journal | vauthors = Asnagli H, Afkarian M, Murphy KM | title = Cutting edge: Identification of an alternative GATA-3 promoter directing tissue-specific gene expression in mouse and human | journal = Journal of Immunology | volume = 168 | issue = 9 | pages = 4268–71 | date = May 2002 | pmid = 11970965 | doi = 10.4049/jimmunol.168.9.4268 | doi-access = free }}
• {{cite journal | vauthors = Steenbergen RD, OudeEngberink VE, Kramer D, Schrijnemakers HF, Verheijen RH, Meijer CJ, Snijders PJ | title = Down-regulation of GATA-3 expression during human papillomavirus-mediated immortalization and cervical carcinogenesis | journal = The American Journal of Pathology | volume = 160 | issue = 6 | pages = 1945–51 | date = Jun 2002 | pmid = 12057898 | pmc = 1850837 | doi = 10.1016/S0002-9440(10)61143-1 }}
• {{cite journal | vauthors = Höfer T, Nathansen H, Löhning M, Radbruch A, Heinrich R | title = GATA-3 transcriptional imprinting in Th2 lymphocytes: a mathematical model | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 99 | issue = 14 | pages = 9364–8 | date = Jul 2002 | pmid = 12087127 | pmc = 123146 | doi = 10.1073/pnas.142284699 | bibcode = 2002PNAS...99.9364H | doi-access = free }}
• {{cite journal | vauthors = Karunaratne A, Hargrave M, Poh A, Yamada T | title = GATA proteins identify a novel ventral interneuron subclass in the developing chick spinal cord | journal = Developmental Biology | volume = 249 | issue = 1 | pages = 30–43 | date = Sep 2002 | pmid = 12217316 | doi = 10.1006/dbio.2002.0754 | doi-access = free }}

{{refend}}

• {{MeshName|GATA3+protein,+human}}
• {{FactorBook|GATA3}}

{{Transcription factors|g2}}

Category:Transcription factors