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Human Polyclonal HOXD13 Primary Antibody pour ELISA, IHC - ABIN4319735
Cantile, Franco, Tschan, Baumhoer, Zlobec, Schiavo, Forte, Bihl, Liguori, Botti, Tornillo, Karamitopoulou-Diamantis, Terracciano, Cillo: HOX D13 expression across 79 tumor tissue types. dans International journal of cancer 2009
this study revealed that HOXB9, HOXB13, and HOXD13 were upregulated and may play important roles in laryngeal squamous cell carcinoma (LSCC). Moreover, HOXB9 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 WNT signaling pathway inhibitor 2 (DKK2) resulted in a significant suppression of HOXD10, HOXD11 and HOXD13 while over-expression of DKK2 and stimulation with factors of the WNT 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.
A genome-wide array-comparative genomic hybridization (aCGH) analysis revealed global chromosomal aberration in MWCNTs-treated clones, predominantly at chromosome 2q31-32, where the potential oncogenes HOXD9 and HOXD13 are located
Data indicate increased levels of reactive oxygen species (ROS) were detected in bone marrow nucleated cells (BMNC) that express CD71 in in NUP98-HOXD13 (NHD13) transgenic mice, a murine model for myelodysplastic syndromes (MDS).
Molecular characteristics of a HOXD13 synpolydactyly 1 nonsense mutation in a Chinese family.
findings show that expression of NUP98-HOXD13 impairs class switch recombination and reduces the antibody-mediated immune response, in addition to its role in leukemia
Misexpression of HOXD13(G11A) in the developing chick limb phenocopied the human SPD phenotype
This finding expands the phenotypic spectrum associated with HOXD13 mutations and advances our understanding of human limb development.
Correlation between Synpolydactyly and alanine expansion in HOXD13.
HOXD13 gene mutation was responsible for the synpolydactyly (SPD) phenotype in this family.
results show the first nonsense mutation in the HOXD13 gene underlying a severe form of SPD in the homozygous state, and a milder form of SPD with approximately 50% penetrance in the heterozygous state.
a duplication mutation, c. 186-212dup, in exon 1 of the HOXD13 gene in the affected individuals in a Chinese family with unusual clinical manifestations of synpolydactyly
we report on the genome-wide profiling of HOXA13 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(-/-); Hoxd13(-/-) limbs.
The age-associated accumulation of somatic mutations that occurs in the Nup98-HOXD13 (NHD13) mouse model of leukemia progression was significantly elevated by co-expression of a PKR transgene.
Shox2 expression restricted to the proximal limb along with Hoxd9 and Hoxa11 expression, juxtaposing the distal expression of Hoxa13 and Hoxd13.
Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene fusion protein Nup98-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 motif
providing synpolydactyly limb explant cultures with cells expressing either HOXD13 or WNT5A 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
expression of NHD13 fusion gene resulted in impaired NHEJ-mediated DNA break repair.
Anterior-posterior differences in HoxD chromatin topology in limb development.
Mice expressing both the FLT3/ITD and Nup98-HoxD13 (NHD13) fusion gene developed acute myeloid leukemia with 100% penetrance
Data show that cis-regulatory elements driving Hoxd gene expression in distal limbs are present in fish.
Data show that the intergenic region between Evx2 and Hoxd13 behaves as a boundary element that functions differentially in space and time, specifically in the development of limbs, genital bud, and brain.
Genetic analysis of the Dyc mutant revealed a trinucleotide expansion in the polyalanine-encoding region of the Hoxd13 gene resulting in a 7-alanine expansion, responsible for fork stalling and template switching.
The synpolydactyly homolog (spdh) mutation in the mouse -- a defect in patterning and growth of limb cartilage elements
genes compete for a remote enhancer that recognizes the locus in a polar fashion, with a preference for 5' extremity; modifications in either number or topography of Hoxd loci induced regulatory reallocations affecting both number and morphology of digits
NUP98-HOXD13 promoted growth and impaired differentiation of hematopoietic progenitor cells; transplantation of bone marrow cells cotransduced with NUP98-HOXD13 and the HOX cofactor Meis1 rapidly caused lethal and transplantable acute myeloid leukemia
early posterior restriction of Hox gene products sets up an anterior-posterior prepattern, which determines the localized activation of Shh; this signal is then translated into digit morphological asymmetry by promoting the late expression of Hoxd genes
EphA7 is a direct downstream target of Hoxd13 and Hoxa13 during limb development
a HOXD13 homeodomain is not necessary for posterior prevalence in mouse limb development
results support the idea that modulation of 5'Hoxd gene expression, by acquisition of novel enhancer elements, offered the substrate for the evolution of fins and the origin of tetrapod limbs
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