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    Nkx3-2 NK3 homeobox 2 [ Mus musculus (house mouse) ]

    Gene ID: 12020, updated on 18-Sep-2024

    GeneRIFs: Gene References Into Functions

    GeneRIFPubMed TitleDate
    Suppression of Osteoarthritis progression by post-natal Induction of Nkx3.2.

    Suppression of Osteoarthritis progression by post-natal Induction of Nkx3.2.
    Oh HK, Park M, Choi SW, Jeong DU, Kim BJ, Kim JA, Choi HJ, Lee J, Cho Y, Kim JH, Seong JK, Choi BH, Min BH, Kim DW.

    11/22/2021
    these results suggest that Nkx3.2-mediated HIF regulation may allow cartilage-specific avascularity under hypoxic conditions during endochondral skeleton development.

    Nkx3.2 induces oxygen concentration-independent and lysosome-dependent degradation of HIF-1α to modulate hypoxic responses in chondrocytes.
    Im S, Kim DW.

    03/10/2018
    that cartilage-specific and Cre-dependent Nkx3.2 overexpression in mice results in significant postnatal dwarfism in endochondral skeletons

    Cartilage-Specific and Cre-Dependent Nkx3.2 Overexpression In Vivo Causes Skeletal Dwarfism by Delaying Cartilage Hypertrophy.
    Jeong DU, Choi JY, Kim DW.

    05/13/2017
    Nkx3.2 promotes primary chondrogenesis by two mechanisms: Direct and Sox9-independent upregulation of Col2a1 transcription and upregulation of Sox9 mRNA expression under positive feedback system.

    Nkx3.2 promotes primary chondrogenic differentiation by upregulating Col2a1 transcription.
    Kawato Y, Hirao M, Ebina K, Shi K, Hashimoto J, Honjo Y, Yoshikawa H, Myoui A., Free PMC Article

    12/29/2012
    the balance of Pax3, Nkx3.2 and Sox9 may act as a molecular switch during the chondrogenic differentiation of muscle progenitor cells, which may be important for fracture healing.

    Interplay of Nkx3.2, Sox9 and Pax3 regulates chondrogenic differentiation of muscle progenitor cells.
    Cairns DM, Liu R, Sen M, Canner JP, Schindeler A, Little DG, Zeng L., Free PMC Article

    11/17/2012
    These results demonstrated that Nkx3.2-dependent suppression of Runx2 was a crucial factor in hypoxia-dependent maintenance of chondrocyte identity.

    Nkx3.2-induced suppression of Runx2 is a crucial mediator of hypoxia-dependent maintenance of chondrocyte phenotypes.
    Kawato Y, Hirao M, Ebina K, Tamai N, Shi K, Hashimoto J, Yoshikawa H, Myoui A.

    01/28/2012
    Data show that IkappaB kinase beta (IKKbeta) can be activated in the nucleus by Nkx3.2 in the absence of exogenous IKK-activating signals, allowing constitutive nuclear degradation of IkappaB-alpha.

    Exogenous signal-independent nuclear IkappaB kinase activation triggered by Nkx3.2 enables constitutive nuclear degradation of IkappaB-alpha in chondrocytes.
    Yong Y, Choi SW, Choi HJ, Nam HW, Kim JA, Jeong DU, Kim DY, Kim YS, Kim DW., Free PMC Article

    10/8/2011
    Results reveal that the molecular pathway modulated by Bapx1 links two major regulators in chondrogenesis, Sox9 and Runx2, to coordinate skeletal formation.

    Sox9 directly promotes Bapx1 gene expression to repress Runx2 in chondrocytes.
    Yamashita S, Andoh M, Ueno-Kudoh H, Sato T, Miyaki S, Asahara H., Free PMC Article

    01/21/2010
    A regulatory mutation, (-519G-->A) within the neu1 promoter generates a consensus binding site for Nkx3 family transcription repressors.

    A point mutation in the neu1 promoter recruits an ectopic repressor, Nkx3.2 and results in a mouse model of sialidase deficiency.
    Champigny MJ, Mitchell M, Fox-Robichaud A, Trigatti BL, Igdoura SA.

    01/21/2010
    Nkx3.2 has a critical role in the induction of somitic chondrogenesis

    Characterization of Nkx3.2 DNA binding specificity and its requirement for somitic chondrogenesis.
    Kim DW, Kempf H, Chen RE, Lassar AB.

    01/21/2010
    Bapx1 plays a crucial organizing role effecting position and separation of the spleen and pancreas to prevent metaplastic transformation

    Spleen versus pancreas: strict control of organ interrelationship revealed by analyses of Bapx1-/- mice.
    Asayesh A, Sharpe J, Watson RP, Hecksher-Sørensen J, Hastie ND, Hill RE, Ahlgren U., Free PMC Article

    01/21/2010
    in the Bapx1 mutant embryo, Fgf10 expression is downregulated and the dorsal pancreas remains at the midline

    The splanchnic mesodermal plate directs spleen and pancreatic laterality, and is regulated by Bapx1/Nkx3.2.
    Hecksher-Sørensen J, Watson RP, Lettice LA, Serup P, Eley L, De Angelis C, Ahlgren U, Hill RE.

    01/21/2010
    Nkx3.2 represses expression of the chondrocyte maturation factor Runx2, and Runx2 mis-expression can rescue the Nkx3.2-induced blockade of chondrocyte maturation.

    Nkx3.2/Bapx1 acts as a negative regulator of chondrocyte maturation.
    Provot S, Kempf H, Murtaugh LC, Chung UI, Kim DW, Chyung J, Kronenberg HM, Lassar AB.

    01/21/2010
    Pax1 and Pax9 can transactivate regulatory sequences in the Bapx1 promoter to induce chondrogenic differentiation in the sclerotome.

    Pax1 and Pax9 activate Bapx1 to induce chondrogenic differentiation in the sclerotome.
    Rodrigo I, Hill RE, Balling R, Münsterberg A, Imai K.

    01/21/2010
    Targeted disruption of the Nkx3.2 (Bapx1) gene in mice results in limited defects of chondrocranial bones and the axial skeleton, particularly pronounced in cervical vertebrae.

    Transcription factors Nkx3.1 and Nkx3.2 (Bapx1) play an overlapping role in sclerotomal development of the mouse.
    Herbrand H, Pabst O, Hill R, Arnold HH.

    01/21/2010
    Data show that Meox1 activates the Bapx1 promoter in a dose-dependent manner and that this activity is enhanced in the presence of Pax1 and/or Pax9.

    Meox homeodomain proteins are required for Bapx1 expression in the sclerotome and activate its transcription by direct binding to its promoter.
    Rodrigo I, Bovolenta P, Mankoo BS, Imai K., Free PMC Article

    01/21/2010
    Bapx1 overexpression generates limb anteroposterior patterning defects including induction of Shh signaling and ectopic activation of functions downstream of Shh signaling into the anterior region of the autopod.

    Bapx1 homeobox gene gain-of-function mice show preaxial polydactyly and activated Shh signaling in the developing limb.
    Tribioli C, Lufkin T.

    01/21/2010
    Nkx3.2 supports chondrocyte survival by constitutively activating RelA.

    Constitutive RelA activation mediated by Nkx3.2 controls chondrocyte viability.
    Park M, Yong Y, Choi SW, Kim JH, Lee JE, Kim DW.

    01/21/2010
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