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Gene Review

NKX2-2  -  NK2 homeobox 2

Homo sapiens

Synonyms: Homeobox protein NK-2 homolog B, Homeobox protein Nkx-2.2, NKX2.2, NKX2B
 
 
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Disease relevance of NKX2-2

 

High impact information on NKX2-2

  • To assess the possibility that the NK2-SD may contribute to DNA-binding specificity, we used a PCR-based approach to identify a consensus DNA-binding sequences for Nkx2.2, an NK-2 family member involved in pancreas and central nervous system development [2].
  • FoxA2, Nkx2.2, and PDX-1 regulate islet beta-cell-specific mafA expression through conserved sequences located between base pairs -8118 and -7750 upstream from the transcription start site [3].
  • Consistent with a role in transcription, small interfering RNA-mediated knockdown of PDX-1 led to decreased mafA mRNA production in INS-1-derived beta-cell lines (832/13 and 832/3), while MafA expression was undetected in the pancreatic epithelium of Nkx2.2 null animals [3].
  • The nkx2.2 gene has two noncoding alternative first exons (exons 1a and 1b) [4].
  • To better understand how Neurogenin3 directs endocrine differentiation, we examined the mechanisms by which Neurogenin3 regulates the promoters of three transcription factor genes expressed in endocrine precursor cells: the nkx2.2 gene, the PAX4 gene, and the NEUROG3 gene, the human gene encoding Neurogenin3 itself [5].
 

Biological context of NKX2-2

  • Both identified NLSs act cooperatively in mediating complete nuclear transport of Nkx2.2 [6].
  • Electrophoretic mobility shift assays demonstrate that homeodomain transcription factors PDX1 and Nkx2.2 can bind to the sequence element located at -800 base pairs [7].
  • Identification and characterization of an Nkx2.2 enhancer reveals that expression is directly regulated by positive Shh-Gli signaling and negative Tcf repressor activity [8].
 

Anatomical context of NKX2-2

  • Such overlap was never observed for other regional transcription factors that define neighboring forebrain domains in the developing brain, such as Nkx2.1 (medial ganglionic eminence), Nkx2.2 (pallidal and diencephalic progenitors) or Pax6 (dorsal telencephalic progenitors) [9].
  • In this report, we show that specification of oligodendrocyte precursors (OLPs) from ventral Nkx2.2-expressing neural progenitors occurs precisely when these progenitors stop generating neurons, indicating that the mechanism of the neuronal/oligodendroglial switch is a common feature of ventral OLP specification [10].
  • Here, we show that Wnt pathway inhibitors regulate the threshold response of a ventral Shh target gene, Nkx2.2, to establish its restricted expression in the ventral spinal cord [8].
 

Other interactions of NKX2-2

  • Thus, it involved enhanced expression of the oligodendrogenic transcription factors Olig1, Olig2, and Nkx2.2 and diminished expression of Id2, an inhibitor of oligodendrogenic differentiation [11].
  • We found that cells expressing Olig2, Nkx2.2, and NG2 were enriched among virus-infected, GFP-positive (GFP+) cells [12].
  • Neurogenin3 bound to and effectively activated transcription through the nkx2.2 and PAX4 E boxes [5].
 

Analytical, diagnostic and therapeutic context of NKX2-2

  • Important regulators of beta-cell formation and function, PDX-1, FoxA2, and Nkx2.2, were shown to specifically bind to region 3 in vivo using the chromatin immunoprecipitation assay [3].

References

  1. Expression profiling of EWS/FLI identifies NKX2.2 as a critical target gene in Ewing's sarcoma. Smith, R., Owen, L.A., Trem, D.J., Wong, J.S., Whangbo, J.S., Golub, T.R., Lessnick, S.L. Cancer Cell (2006) [Pubmed]
  2. Intramolecular control of transcriptional activity by the NK2-specific domain in NK-2 homeodomain proteins. Watada, H., Mirmira, R.G., Kalamaras, J., German, M.S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  3. FoxA2, Nkx2.2, and PDX-1 regulate islet beta-cell-specific mafA expression through conserved sequences located between base pairs -8118 and -7750 upstream from the transcription start site. Raum, J.C., Gerrish, K., Artner, I., Henderson, E., Guo, M., Sussel, L., Schisler, J.C., Newgard, C.B., Stein, R. Mol. Cell. Biol. (2006) [Pubmed]
  4. Distinct gene expression programs function in progenitor and mature islet cells. Watada, H., Scheel, D.W., Leung, J., German, M.S. J. Biol. Chem. (2003) [Pubmed]
  5. Neurogenin3 activates the islet differentiation program while repressing its own expression. Smith, S.B., Watada, H., German, M.S. Mol. Endocrinol. (2004) [Pubmed]
  6. The homeodomain of Nkx2.2 carries two cooperatively acting nuclear localization signals. Hessabi, B., Schmidt, I., Walther, R. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  7. Transcriptional and translational regulation of beta-cell differentiation factor Nkx6.1. Watada, H., Mirmira, R.G., Leung, J., German, M.S. J. Biol. Chem. (2000) [Pubmed]
  8. Wnt signaling inhibitors regulate the transcriptional response to morphogenetic Shh-Gli signaling in the neural tube. Lei, Q., Jeong, Y., Misra, K., Li, S., Zelman, A.K., Epstein, D.J., Matise, M.P. Dev. Cell (2006) [Pubmed]
  9. Transplanted dopamine neurons derived from primate ES cells preferentially innervate DARPP-32 striatal progenitors within the graft. Ferrari, D., Sanchez-Pernaute, R., Lee, H., Studer, L., Isacson, O. Eur. J. Neurosci. (2006) [Pubmed]
  10. Ventral neural progenitors switch toward an oligodendroglial fate in response to increased Sonic hedgehog (Shh) activity: involvement of Sulfatase 1 in modulating Shh signaling in the ventral spinal cord. Danesin, C., Agius, E., Escalas, N., Ai, X., Emerson, C., Cochard, P., Soula, C. J. Neurosci. (2006) [Pubmed]
  11. Mesenchymal stem cells instruct oligodendrogenic fate decision on adult neural stem cells. Rivera, F.J., Couillard-Despres, S., Pedre, X., Ploetz, S., Caioni, M., Lois, C., Bogdahn, U., Aigner, L. Stem Cells (2006) [Pubmed]
  12. Growth factor treatment and genetic manipulation stimulate neurogenesis and oligodendrogenesis by endogenous neural progenitors in the injured adult spinal cord. Ohori, Y., Yamamoto, S., Nagao, M., Sugimori, M., Yamamoto, N., Nakamura, K., Nakafuku, M. J. Neurosci. (2006) [Pubmed]
 
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