Revision 1

#24642Store at -20C

1 Kit

(5 x 20 microliters)

Cell Signaling Technology

Orders: 877-616-CELL (2355) [email protected]

Support: 877-678-TECH (8324)

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3 Trask LaneDanversMassachusetts01923USA
For Research Use Only. Not for Use in Diagnostic Procedures.
Product Includes Product # Quantity Mol. Wt Isotype/Source
GATA-1 (D52H6) XP® Rabbit mAb 3535 20 µl 43 kDa Rabbit IgG
GATA-2 (E9T6F) Rabbit mAb 79802 20 µl 51 kDa Rabbit IgG
GATA-3 (D13C9) XP® Rabbit mAb 5852 20 µl 48 kDa Rabbit IgG
GATA-4 (D3A3M) Rabbit mAb 36966 20 µl 55 kDa Rabbit IgG
GATA-6 (D61E4) XP® Rabbit mAb 5851 20 µl 55 kDa Rabbit IgG
Anti-rabbit IgG, HRP-linked Antibody 7074 100 µl Goat 

Please visit for individual component applications, species cross-reactivity, dilutions, protocols, and additional product information.


The GATA Transcription Factor Antibody Sampler Kit provides an economical means of evaluating total levels of GATA family proteins. The kit includes enough antibodies to perform two western blot experiments with each primary antibody.


Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibodies.


GATA proteins comprise a group of transcription factors that are related by the presence of conserved zinc finger DNA-binding domains, which bind directly to the nucleotide sequence core element GATA (1-3). There are six vertebrate GATA proteins, designated GATA-1 to GATA-6 (3). Although they are commonly divided as hematopoietic (GATA-1-3) or cardiac (GATA-4-6) factors, GATA proteins are expressed in a wide variety of tissue and play critical roles in embryonic development and organ differentiation (4). GATA-1 is the founding member of the GATA family and is required for erythroid and megakaryocytic cell development (5,6). Mutations in the corresponding GATA-1 gene are linked to many human diseases, including acute megakaryoblastic leukemia in Down Syndrome children (DS-AMKL), X-linked thrombocytopenia, and gray platelet syndrome (7-10). GATA-2 is widely expressed and plays an essential role in many developmental processes (11). Studies on GATA-2 knockout mice indicate that this protein is required in hematopoiesis (12). GATA-2 also inhibits the differentiation of white and brown adipocytes and has been shown to suppress the proliferation of neuronal progenitor cells (13-15). GATA-3 is a critical regulator of development and is expressed in both hematopoietic and non-hematopoietic tissues, including the kidney, skin, mammary gland, and central nervous system (16-19). GATA-3 knockout mouse embryos die between E11 and E12 due to growth retardation and deformities in the brain and spinal cord (20). The function of GATA-3 has also been extensively studied in T cell development and has been shown to be a downstream target of Notch in Notch-mediated differentiation of TH2 cells (21,22). GATA-4 is crucial for cardiomyocyte differentiation, and not surprisingly, mutations in the GATA-4 gene are implicated in many cardiac diseases, such as tetralogy of Fallot, familial and sporadic dilated cardiomyopathy, and atrial septal defect (23-27). GATA-4 and GATA-6 together maintain intestinal epithelial structure by regulating enterocyte gene expression (28). They also have overlapping roles in steroidogenesis and genital ridge formation during gonadal development (29). GATA-6 plays a critical role in endoderm development and is essential for the development of the heart, gut, and other organs (30-32). Knockout of GATA-6 is embryonic lethal due to defects in the formation of the heart tube and a failure to develop extraembryonic endoderm (30).

  1. Ko, L.J. and Engel, J.D. (1993) Mol Cell Biol 13, 4011-22.
  2. Merika, M. and Orkin, S.H. (1993) Mol Cell Biol 13, 3999-4010.
  3. Lowry, J.A. and Atchley, W.R. (2000) J Mol Evol 50, 103-15.
  4. Tremblay, M. et al. (2018) Development 145, dev164384. doi: 10.1242/dev.164384.
  5. Pevny, L. et al. (1991) Nature 349, 257-60.
  6. Fujiwara, Y. et al. (1996) Proc Natl Acad Sci USA 93, 12355-8.
  7. Wechsler, J. et al. (2002) Nat Genet 32, 148-52.
  8. Cantor, A.B. (2005) Int J Hematol 81, 378-84.
  9. Mehaffey, M.G. et al. (2001) Blood 98, 2681-8.
  10. Tubman, V.N. et al. (2007) Blood 109, 3297-9.
  11. Tong, Q. et al. (2003) Drug News Perspect 16, 585-8.
  12. Tsai, F.Y. et al. (1994) Nature 371, 221-6.
  13. Tong, Q. et al. (2005) Mol Cell Biol 25, 706-15.
  14. Tsai, J. et al. (2005) EMBO Rep 6, 879-84.
  15. El Wakil, A. et al. (2006) Development 133, 2155-65.
  16. Debacker, C. et al. (1999) Mech Dev 85, 183-7.
  17. Grote, D. et al. (2008) PLoS Genet 4, e1000316.
  18. Kaufman, C.K. et al. (2003) Genes Dev 17, 2108-22.
  19. Kouros-Mehr, H. et al. (2006) Cell 127, 1041-55.
  20. Pandolfi, P.P. et al. (1995) Nat Genet 11, 40-4.
  21. Ho, I.C. et al. (2009) Nat Rev Immunol 9, 125-35.
  22. Amsen, D. et al. (2007) Immunity 27, 89-99.
  23. Gan, L. et al. (2014) Gene Expr Patterns 16, 8-22.
  24. Yang, Y.Q. et al. (2013) Hum Mutat 34, 1662-71.
  25. Li, R.G. et al. (2013) Biochem Biophys Res Commun 439, 591-6.
  26. Li, J. et al. (2014) Gene 548, 174-81.
  27. Mohan, R.A. et al. (2014) Am J Med Genet A 164A, 2732-8.
  28. Walker, E.M. et al. (2014) Dev Biol 392, 283-94.
  29. LaVoie, H.A. (2014) Biol Reprod 91, 38.
  30. Cai, K.Q. et al. (2008) Dev Dyn 237, 2820-9.
  31. Charron, F. and Nemer, M. (1999) Semin Cell Dev Biol 10, 85-91.
  32. Haveri, H. et al. (2008) BMC Gastroenterol 8, 9.

Background References

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