Disease relevance of HOXD10

• One epithelial Wilm's tumor expressed only an aberrant 0.3 kb HOXD10 transcript [1].
• The purpose of this study was to determine the relative expression of HOXD10 in human endometrial adenocarcinomas [2].
• Human HOXD10 gene expression is altered in endometrial carcinoma and varies with the histologic grade of differentiation [2].
• Homeobox D10 induces phenotypic reversion of breast tumor cells in a three-dimensional culture model [3].

High impact information on HOXD10

• Among abdominal-B subfamily members, the mitotic proteolysis of HOXC10 appears unique, since the levels of the paralogous HOXD10 and the related homeoprotein HOXC13 are constant throughout the cell cycle [4].
• HOX4C and HOX4D proteins synthesized in bacteria bind to the same conserved sequence located around position -120, as well as to the TATA box and immediately upstream and downstream nucleotides [5].
• Using cotransfection experiments, we show that this endogenous DNA sequence can mediate transactivation by the HOX4D and HOX4C proteins and that this effect requires the presence of TAAT-related binding sites [6].
• Whole-genome linkage analysis with Affymetrix GeneChip Mapping 10K Array defined a 7-Mb critical region on chromosome 2q31, which led to candidate-gene sequencing of six HOX genes and detection of a single missense mutation, M319K (956T-->A), in the HOXD10 gene [7].
• (vii) We observe an additional trimer class involving non-DNA-bound PBX and DNA-bound MEIS-HOXD9 or MEIS-HOXD10 heterodimers that is enhanced by mutation of the PBX homeodomain [8].

Biological context of HOXD10

• A single missense mutation was identified (M319K, 956T > A) in the homeodomain recognition helix of the HOXD10 gene that segregated with disease in one large British family [9].
• RESULTS: The sequence of the purified HOXD10 product corresponds to the known DNA sequence reported in the National Institute of Health Gene Bank. mRNA expression of HOXD10 relative to beta-tubulin is significantly lower in endometrial carcinomas than in normal endometrium [2].
• This mutation was recently described in a family of Italian descent with CVT and Charcot-Marie-Tooth deformity HOXD10 gene mutations were not identified in any of the other families or sporadic patients with CVT, suggesting that genetic heterogeneity underlies this disorder [9].

Anatomical context of HOXD10

• HOXD10 M319K mutation in a family with isolated congenital vertical talus [9].
• Expression of HOXD10 gene in normal endometrium and endometrial adenocarcinoma [2].
• The three genes, Hoxa10, Hoxc10, and Hoxd10, are all expressed in the lumbar spinal cord and have distinct expression patterns [10].
• To test the hypothesis that restricted expression of Hoxd10 contributes to the attainment of an LS identity, and specifically an LS motoneuron identity, Hoxd10 was ectopically expressed in thoracic segments in chick embryos by means of in ovo electroporation [11].

Associations of HOXD10 with chemical compounds

• The expression of HOXD10 relative to beta-tubulin (internal control) was assessed by densitometric comparison of co-amplified Phosphorus-32 (32P) labeled gene products separated by agarose gel electrophoresis [2].

Other interactions of HOXD10

• These results show that the HOX4D and HOX4C genes are genuine sequence-specific transcription factors and suggest that, as in Drosophila, cross-regulatory interactions between these genes might be essential for their proper expression [6].
• In contrast, HOXD10 and to a lesser degree HOXB9 bound the PPE with high affinities regardless of whether PBX1b was present [12].
• The associated thresholds for gene expression increase sequentially from Hoxd-10 to Hoxd-13 (threshold collinearity) [13].
• Particularly, we determined that for Hoxd10 as a transcriptional activator, both Smad1 and Smad6 opposed its activity [14].

Analytical, diagnostic and therapeutic context of HOXD10

• Direct sequencing of purified HOXD10 polymerase chain reaction product was also performed [2].

References