High impact information on DLX5

• Endogenous levels of Dlx5 are 3-fold higher in hypertrophic versus non-hypertrophic cells by real-time PCR analysis, and overexpression of Dlx5 in non-hypertrophic chondrocytes activates the proximal Col10a1 promoter 3-fold [1].
• In situ hybridization studies indicated that Dlx5 is expressed in chick calvarial osteoblasts (cCOB) in vivo [2].
• To study the effect of overexpression of Dlx5 on osteoblast differentiation, we infected primary osteoblast cultures from 15-day-old embryonal chicken calvaria with replication competent retroviral vectors [RCASBP(A)] expressing Dlx5 or control replication competent avian splice acceptor brianhightiter polymerase subtype A [RCASBP(A)] [2].
• DLX5 positions the neural crest and preplacode region at the border of the neural plate [3].
• The disruption of cell contacts temporarily delayed onset of gene expression but by 48 h both Msx2 and Dlx5 were expressed [4].

Biological context of DLX5

• In this sequence, a binding site for Dlx5/6 transcription factors (nt -99 to -87) retards a protein specific for hypertrophic chondrocytes in electrophoretic mobility shift assay [1].

Anatomical context of DLX5

• In particular, the developmental expression pattern is characterized by an early appearance of cDlx transcript in the prospective forebrain region of gastrulating embryos [5].
• Our results suggest that Dlx5 plays an important role in inducing calvarial osteoblast differentiation [2].

Other interactions of DLX5

• We report the cloning and expression pattern of the chicken DLX3 gene, a homeobox gene highly related to the DLX5 gene with regard to both the encoded protein structure and the expression pattern [6].

Analytical, diagnostic and therapeutic context of DLX5

• Northern blot analysis and in situ hybridization studies reveal that cDlx expression is developmentally regulated and is tissue specific [5].

References