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NKX3-2 encodes a member of the NK family of homeobox-containing proteins. Additionally we are shipping NK3 Homeobox 2 Antibodies (57) and and many more products for this protein.
Showing 5 out of 5 products:
Bapx1-endothelin 1 (show EDN1 Proteins) effector, patterns jaw joint
NKL (show GLIS2 Proteins) homeobox (show Lbx1 Proteins) gene NKX2-5 (show NKX2-5 Proteins) was activated by NKX3-2 in CCRF-CEM and by FOXG1 (show FOXG1 Proteins) in PEER, representing mutually inhibitory activators of this translocated oncogene (show RAB1A Proteins).
post-translational modification of Nkx3.2 employing HDAC9 (show HDAC9 Proteins)-PIASy (show PIAS4 Proteins)-RNF4 (show RNF4 Proteins) axis plays a crucial role in controlling chondrocyte viability and hypertrophic maturation during skeletal development in vertebrates.
Bapx1 indicates poor prognosis for gastric cancer patients by promoting tumor migration and invasion via TGF-beta (show TGFB1 Proteins)-induced epithelial-mesenchymal transition.
PI3K (show PIK3CA Proteins)-mediated suppression of Nkx3.2 in chondrocytes plays a role in the control of cartilage hypertrophy during skeletal development in vertebrates.
Our findings indicate that BAPX-1/NKX-3.2 is a molecular switch that is involved in controlling the hypertrophic phenotype of the postdevelopmental (OA) articular chondrocyte.
Ihh (show IHH Proteins)-induced Nkx3.2 degradation requires Wnt5a (show WNT5A Proteins), which is capable of triggering Nkx3.2 degradation
Data show that IkappaB kinase (show CHUK Proteins) beta (IKKbeta (show IKBKB Proteins)) can be activated in the nucleus by Nkx3.2 in the absence of exogenous IKK (show CHUK Proteins)-activating signals, allowing constitutive nuclear degradation of IkappaB-alpha (show NFKBIA Proteins).
NKX3-2 plays an important role in endochondral ossification of both the axial and appendicular skeleton in humans
Data show that Meox1 (show MEOX1 Proteins) activates the Bapx1 promoter in a dose-dependent manner and that this activity is enhanced in the presence of Pax1 (show PAX1 Proteins) and/or Pax9 (show PAX9 Proteins).
these results suggest that Nkx3.2-mediated HIF regulation may allow cartilage-specific avascularity under hypoxic conditions during endochondral skeleton development.
that cartilage-specific and Cre-dependent Nkx3.2 overexpression in mice results in significant postnatal dwarfism in endochondral skeletons
Nkx3.2 promotes primary chondrogenesis by two mechanisms: Direct and Sox9 (show SOX9 Proteins)-independent upregulation of Col2a1 (show COL2A1 Proteins) transcription and upregulation of Sox9 (show SOX9 Proteins) mRNA expression under positive feedback system.
the balance of Pax3 (show PAX3 Proteins), Nkx3.2 and Sox9 (show SOX9 Proteins) may act as a molecular switch during the chondrogenic differentiation of muscle progenitor cells, which may be important for fracture healing.
These results demonstrated that Nkx3.2-dependent suppression of Runx2 (show RUNX2 Proteins) was a crucial factor in hypoxia-dependent maintenance of chondrocyte identity.
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.
Pax1 (show PAX1 Proteins) and Pax9 (show PAX9 Proteins) can transactivate regulatory sequences in the Bapx1 promoter to induce chondrogenic differentiation in the sclerotome.
Nkx3.2 has a critical role in the induction of somitic chondrogenesis
This gene encodes a member of the NK family of homeobox-containing proteins. The encoded protein may play a role in skeletal development.
NK3 homeobox 2
, bagpipe homeobox homolog 1
, homeobox protein Nkx-3.2
, bagpipe homeobox protein homolog 1
, NK class homeoprotein Nkx-3.2
, homeobox protein NK-3 homolog B
, bagpipe homeobox gene 1 homolog
, homeodomain protein Nkx-3.2