Jarid2 (jumonji, AT rich interactive domain 2) is a protein coding gene that functions as a putativetranscription factor. Distinguished as anuclear protein necessary for mouseembryogenesis, Jarid2 is a member of the jumonji family that contains a DNA binding domain known as theAT-rich interaction domain (ARID).[7][8][9][10]In vitro studies of Jarid2 reveal that ARID along with other functional domains are involved in DNA binding, nuclear localization,transcriptional repression,[11] and recruitment of Polycomb-repressive complex 2 (PRC2).[12][13] Intracellular mechanisms underlying these interactions remain largely unknown.
In search of developmentally important genes, Jarid2 has previously been identified bygene trap technology as an important factor necessary fororgan development.[7][11][14] During mouse organogenesis, Jarid2 is involved in the formation of theneural tube and development of the liver, spleen, thymus and cardiovascular system.[15][16] Continuous Jarid2 expression in the tissues of the heart, highlight its presiding role in the development of both the embryonic and the adult heart.[7] Mutant models of Jarid2 embryos show severe heart malformations, ventricular septal defects,noncompaction of the ventricular wall, andatrial enlargement.[7] Homozygous mutants of Jarid2 are found to die soon after birth.[7] Overexpression of the mouse Jarid2 gene has been reported to represscardiomyocyte proliferation through it close interaction with retinoblastoma protein (Rb), a master cell cycle regulator.[11][14][17] Retinoblastoma-binding protein-2 and the human SMCX protein share regions of homology between mice and humans.[5]
^Takahashi M, Kojima M, Nakajima K, Suzuki-Migishima R, Motegi Y, Yokoyama M, Takeuchi, T (2004). "Cardiac abnormalities cause early lethality of jumonji mutant mice".Biochemical and Biophysical Research Communications.324 (4):1319–23.Bibcode:2004BBRC..324.1319T.doi:10.1016/j.bbrc.2004.09.203.PMID15504358.
^Toyoda M, Kojima M, Takeuchi T (2000). "Jumonji is a nuclear protein that participates in the negative regulation of cell growth".Biochemical and Biophysical Research Communications.274 (2):332–6.Bibcode:2000BBRC..274..332T.doi:10.1006/bbrc.2000.3138.PMID10913339.
^abcKlassen SS, Rabkin SW (2008). "Nitric oxide induces gene expression of jumonji and retinoblastoma 2 protein while reducing expression of atrial natriuretic peptide precursor type B in cardiomyocytes".Folia Biologica.54 (2):65–70.doi:10.14712/fb2008054020065.PMID18498724.
^Motoyama J, Kitajima K, Kojima M, Kondo S, Takeuchi T (1997). "Organogenesis of the liver, thymus and spleen is affected in jumonji mutant mice".Mechanisms of Development.66 (1–2):27–37.doi:10.1016/s0925-4773(97)00082-8.PMID9376320.S2CID6531281.
Volcik KA, Zhu H, Finnell RH, et al. (2004). "Evaluation of the jumonji gene and risk for spina bifida and congenital heart defects".Am. J. Med. Genet. A.126 (2):215–7.doi:10.1002/ajmg.a.20574.PMID15057990.S2CID221248186.
Pedrosa E, Ye K, Nolan KA, et al. (2007). "Positive association of schizophrenia to JARID2 gene".Am. J. Med. Genet. B Neuropsychiatr. Genet.144 (1):45–51.doi:10.1002/ajmg.b.30386.PMID16967465.S2CID25560999.
