Nkx3-2 cDNA ORF clone, Mus musculus(house mouse)

Pancreatic Pericytes Support Beta-Cell Function in a Tcf7l2-Dependent Manner.
Sakhneny L, Rachi E, Epshtein A, Guez HC, Wald-Altman S, Lisnyansky M, Khalifa-Malka L, Hazan A, Baer D, Priel A, Weil M, Landsman L
Diabetes(2017 Dec)

Neonatal pancreatic pericytes support ?-cell proliferation.
Epshtein A, Rachi E, Sakhneny L, Mizrachi S, Baer D, Landsman L
Molecular metabolism6(10)1330-1338(2017 Oct)

that cartilage-specific and Cre-dependent Nkx3.2 overexpression in mice results in significant postnatal dwarfism in endochondral skeletons
Title: Cartilage-Specific and Cre-Dependent Nkx3.2 Overexpression In Vivo Causes Skeletal Dwarfism by Delaying Cartilage Hypertrophy.

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.
Title: Nkx3.2 promotes primary chondrogenic differentiation by upregulating Col2a1 transcription.

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.
Title: Interplay of Nkx3.2, Sox9 and Pax3 regulates chondrogenic differentiation of muscle progenitor cells.

These results demonstrated that Nkx3.2-dependent suppression of Runx2 was a crucial factor in hypoxia-dependent maintenance of chondrocyte identity.
Title: Nkx3.2-induced suppression of Runx2 is a crucial mediator of hypoxia-dependent maintenance of chondrocyte phenotypes.

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.
Title: Exogenous signal-independent nuclear IkappaB kinase activation triggered by Nkx3.2 enables constitutive nuclear degradation of IkappaB-alpha in chondrocytes.