GATA transcription factor

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GATA transcription factors are a family of transcription factors characterized by their ability to bind to the DNA sequence "GATA". [1]

Contents

GATA transcription factors have been correlated to their broader influence on stem cell development. Findings however, have pointed to a more direct influence by GATA transcription factors, as they are salient components in the more concentrated regulation of gene expression. Data points to the roles GATA transcription factors play in stages past early development in endocrine organs. [2]

Despite GATA’s influence on endocrine organs and cell development, they have a complex relation to the development and growth of breast cancer. Its immediate influence is not yet known, its high risk for mutation however, makes determining the immediate influence of paramount importance in battling breast cancer. [3]

Some research that has been done on the GATA transcription factor for its role in the development of breast cancer suggests that a specific GATA transcription factor GATA3 can actually inhibit further growth of breast cancer cells. [4] The complete mechanism in which this happens is still not clear. [4] However, research has suggested that the GATA transcription factor creates an unfavorable chemical environment for the breast cancer tumor cells which inhibits the progression of these cells. [4] One way that has been suggested is that the GATA transcription factor lowers the level of adenosine triphosphate (ATP) in the cell. [4] This creates an unfavorable chemical environment for the breast cancer cells because usually they require high levels of ATP to survive. [4] In addition, research has suggested that there is a specific gene called the TRP1 that is expressed in breast cancer cells and the GATA3 transcription factor plays a role in regulating this gene. [5]

Genes

In humans:

In yeast:

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<span class="mw-page-title-main">GATA3</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">GATA6</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">SIM2</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">ID4</span> Protein-coding gene in humans

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<span class="mw-page-title-main">ZFPM2</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">ZBTB32</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">FOXA1</span> Protein-coding gene in the species Homo sapiens

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<span class="mw-page-title-main">Emberger syndrome</span> Medical condition

The Emberger syndrome is a rare, autosomal dominant, genetic disorder caused by familial or sporadic inactivating mutations in one of the two parental GATA2 genes. The mutation results in a haploinsufficiency in the levels of the gene's product, the GATA2 transcription factor. This transcription factor is critical for the embryonic development, maintenance, and functionality of blood-forming, lympathic-forming, and other tissues. The syndrome includes as its primary symptoms: serious abnormalities of the blood such as the myelodysplastic syndrome and acute myeloid leukemia; lymphedema of the lower limbs, and sensorineural hearing loss. However, the anomalies caused by GATA2 mutations are highly variable with some individuals showing little or no such symptoms even in old age while others exhibit non-malignant types of hematological anomalies; lymphedema in areas besides the lower limbs, little or no hearing loss; or anomalies in other tissues. The syndrome may present with relatively benign signs and/or symptoms and then progress rapidly or slowly to the myelodysplastic syndrome and/or acute myeloid leukemia. Alternatively, it may present with one of the latter two life-threatening disorders.

GATA2 deficiency is a grouping of several disorders caused by common defect, namely, familial or sporadic inactivating mutations in one of the two parental GATA2 genes. Being the gene haploinsufficient, mutations that cause a reduction in the cellular levels of the gene's product, GATA2, are autosomal dominant. The GATA2 protein is a transcription factor critical for the embryonic development, maintenance, and functionality of blood-forming, lymphatic-forming, and other tissue-forming stem cells. In consequence of these mutations, cellular levels of GATA2 are deficient and individuals develop over time hematological, immunological, lymphatic, or other presentations that may begin as apparently benign abnormalities but commonly progress to severe organ failure, opportunistic infections, virus infection-induced cancers, the myelodysplastic syndrome, and/or leukemia. GATA2 deficiency is a life-threatening and precancerous condition.

References

  1. Ko LJ, Engel JD (July 1993). "DNA-binding specificities of the GATA transcription factor family". Molecular and Cellular Biology. 13 (7): 4011–4022. doi:10.1128/mcb.13.7.4011. PMC   359950 . PMID   8321208.
  2. Viger RS, Guittot SM, Anttonen M, Wilson DB, Heikinheimo M (April 2008). "Role of the GATA family of transcription factors in endocrine development, function, and disease". Molecular Endocrinology. 22 (4): 781–798. doi: 10.1210/me.2007-0513 . PMC   2276466 . PMID   18174356.
  3. Du F, Yuan P, Wang T, Zhao J, Zhao Z, Luo Y, Xu B (November 2015). "The Significance and Therapeutic Potential of GATA3 Expression and Mutation in Breast Cancer: A Systematic Review". Medicinal Research Reviews. 35 (6): 1300–1315. doi:10.1002/med.21362. PMID   26313026. S2CID   11668034.
  4. 1 2 3 4 5 Li M, Qi Y, Chen M, Wang Z, Zeng D, Xiao Y, et al. (2019). "GATA Binding Protein 3 Boosts Extracellular ATP Hydrolysis and Inhibits Metastasis of Breast Cancer by Up-regulating Ectonucleoside Triphosphate Diphosphohydrolase 3". International Journal of Biological Sciences. 15 (12): 2522–2537. doi:10.7150/ijbs.35563. PMC   6854379 . PMID   31754326.
  5. Chen JQ, Bao Y, Lee J, Murray JL, Litton JK, Xiao L, et al. (October 2013). "Prognostic value of the trichorhinophalangeal syndrome-1 (TRPS-1), a GATA family transcription factor, in early-stage breast cancer". Annals of Oncology. 24 (10): 2534–2542. doi:10.1093/annonc/mdt190. PMC   3784330 . PMID   23729783.