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this study revealed that HOXB9 (show HOXB9 Proteins), HOXB13 (show HOXB13 Proteins), and HOXD13 were upregulated and may play important roles in laryngeal squamous cell carcinoma (LSCC). Moreover, HOXB9 (show HOXB9 Proteins) may serve as a novel marker of poor prognosis and a potential therapeutic target in LSCC patients.
The results suggest that the c.917G>A (p.R306Q) mutation in the HOXD13 gene, may be responsible for syndactyly type Ic in this family.
Knock down of the dickkopf (show DKK1 Proteins) WNT (show WNT2 Proteins) signaling pathway inhibitor 2 (DKK2 (show DKK2 Proteins)) resulted in a significant suppression of HOXD10 (show HOXD10 Proteins), HOXD11 (show HOXD11 Proteins) and HOXD13 while over-expression of DKK2 (show DKK2 Proteins) and stimulation with factors of the WNT (show WNT2 Proteins) signaling pathway.
a novel mutation causing truncation of HOXD13 protein was successfully identified as being associated with an atypical non-syndromic SPD phenotype in our study.
down-regulation of HOXD13 might be a potentially useful prognostic marker for patients with breast cancer.
A homozygous HOXD13 missense mutation causes a severe form of synpolydactyly with metacarpal to carpal transformation.
HOXD13 methylation is a common event in primary breast cancer and is associated with poor survival of breast cancer patients.
A 27 bp expansion mutation in exon 1 of HOXD13 was associated with autosomal dominant synpolydactyly in a Chinese family.
Linkage analysis of the syndactyly type 1 subtype c (SD1-c) phenotype based on two Chinese families with 3/4 fingers syndactyly shows that two missense mutations in codon 306 of HOXD13 underlie SD1-c.
Identification of a novel c.659G>C (p.Gly220Ala) mutation outside the HOXD13 homeodomain responsible for synpolydactyly in a Chinese family.
we report on the genome-wide profiling of HOXA13 (show HOXA13 Proteins) and HOXD13 in vivo binding and changes of the transcriptome and chromatin state in the transition from the early to the late-distal limb developmental program, as well as in Hoxa13 (show HOXA13 Proteins)(-/-); Hoxd13(-/-) limbs.
The age-associated accumulation of somatic mutations that occurs in the Nup98 (show NUP98 Proteins)-HOXD13 (NHD13) mouse model of leukemia progression was significantly elevated by co-expression of a PKR (show EIF2AK2 Proteins) transgene.
Shox2 (show SHOX2 Proteins) expression restricted to the proximal limb along with Hoxd9 (show HOXD9 Proteins) and Hoxa11 (show HOXA11 Proteins) expression, juxtaposing the distal expression of Hoxa13 (show HOXA13 Proteins) and Hoxd13.
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b (show CDKN2B Proteins)) collaborates with oncogene (show RAB1A Proteins) fusion protein Nup98 (show NUP98 Proteins)-HoxD13 transgene in the development of predominantly myeloid neoplasms.
study elucidated the mechanism underlying a novel missense mutation in HOXD13 (Q317K) associated with a complex hand and foot malformation phenotype; results show that the mutation results in a shift in the binding profile of the mutant toward a bicoid/PITX1 (show PITX1 Proteins) motif
providing synpolydactyly limb explant cultures with cells expressing either HOXD13 or WNT5A (show WNT5A Proteins) led to a non-cell autonomous partial rescue of cell polarity the perichondral region and restored the expression of perichondral markers.
a slight and transient deregulation of Hoxd13 expression can readily affect the relative lengths of limb segments during development
findings show that expression of NUP98 (show NUP98 Proteins)-HOXD13 impairs class switch recombination and reduces the antibody-mediated immune response, in addition to its role in leukemia
Mice expressing both the FLT3 (show FLT3 Proteins)/ITD and Nup98 (show NUP98 Proteins)-HoxD13 (NHD13) fusion gene developed acute myeloid leukemia (show BCL11A Proteins) with 100% penetrance
Data show that cis (show CISH Proteins)-regulatory elements driving Hoxd gene expression in distal limbs are present in fish.
This gene belongs to the homeobox family of genes. The homeobox genes encode a highly conserved family of transcription factors that play an important role in morphogenesis in all multicellular organisms. Mammals possess four similar homeobox gene clusters, HOXA, HOXB, HOXC and HOXD, located on different chromosomes, consisting of 9 to 11 genes arranged in tandem. This gene is one of several homeobox HOXD genes located in a cluster on chromosome 2. Deletions that remove the entire HOXD gene cluster or the 5' end of this cluster have been associated with severe limb and genital abnormalities. Mutations in this particular gene cause synpolydactyly.
, homeobox protein Hox-4.8
, homeobox protein Hox-4G
, homeobox protein Hox-D13
, homeobox protein hoxd13
, homeobox D13
, homeo box 4I
, homeo box D13
, homeobox protein Hox-4I
, homeobox gene D-13
, LOW QUALITY PROTEIN: homeobox protein Hox-D13