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DLX5 encodes a member of a homeobox transcription factor gene family similiar to the Drosophila distal-less gene.
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Human Polyclonal DLX5 Primary Antibody für ELISA, WB - ABIN451750
Lee, Kim, Kim, Park, Kang, Kyung, Sung, Wozney, Kim, Ryoo: BMP-2-induced Runx2 expression is mediated by Dlx5, and TGF-beta 1 opposes the BMP-2-induced osteoblast differentiation by suppression of Dlx5 expression. in The Journal of biological chemistry 2003
Show all 2 Pubmed References
Human Polyclonal DLX5 Primary Antibody für ICC, IF - ABIN4305382
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
These results indicate activation of DLX5 and RUNX2 (zeige RUNX2 Antikörper) via its distal promoter represents a unique feature of GFs, and is important for ECM (zeige MMRN1 Antikörper) regulation. Down-regulation of these transcription factors in PAFs could be associated with their property to degrade collagen, which may impact on the process of periodontitis.
these findings indicate that, in MSCs, DLX5 is a master regulator of osteogenesis. Furthermore, tanshinone IIA may be valuable for stem cell-based therapies of certain bone diseases.
As a result of disturbed imprinting, the upregulated DLX5 affects trophoblast proliferation in preeclampsia.
These data indicate that certain missense mutations diminish the ability of the Dlx5 homeodomain to recognize and bind target DNAs, and they likely destabilize the formation of functional complexes.
In cells grown on titanium support, DLX5 and RUNX1 (zeige RUNX1 Antikörper) were respectively upregulated (+3.12-fold) and downregulated (-2.14-fold)
Absent expression of the osteoblast-specific maternally imprinted genes, DLX5 and DLX6, causes split hand/split foot malformation type I.
Heterozygous DLX5 nonsense mutation c.G115T(p.E39X) associated with isolated split-hand/foot malformation with reduced penetrance and variable expressivity in two unrelated Polish families.
A novel heterozygous mutation in exon 3 of DLX5 found in the family members with SHFM1 (zeige SHFM1 Antikörper) phenotype.
Genome sequencing of the deletion breakpoints showed that the DLX5 and DLX6 genes are disomic but the putative DYNC1I1 (zeige DYNC1I1 Antikörper) exon 15 and 17 enhancers are deleted.
The duplicated region harbors only DLX5 and DLX6, which are known for their role in SHFM1 (zeige SHFM1 Antikörper).
FGF10 (zeige FGF10 Antikörper) pathway is downregulated in Dlx5(-/-) mice, and activation of FGF10 (zeige FGF10 Antikörper) signaling rescues cranial neural crest cell proliferation and myogenic differentiation.
High DLX5 expression is associated with T-cell lymphomagenesis.
Both transient and stable expression of Necdin (zeige NDN Antikörper) induced osteoblast-specific markers in an osteogenic cell line through formation of a complex with distal-less Homeobox 5 (Dlx5) and Runx2 (zeige RUNX2 Antikörper) promoter activation.
DLX5 and DLX6 reciprocally inhibit BMP/H2-mediated H1 enhancer regulation in mandible embryonic development.
We found that in Dlx5;6 DKO limbs, the AER expresses lower levels of Wnt5a (zeige WNT5A Antikörper), shows scattered beta-catenin (zeige CTNNB1 Antikörper) responsive cells and altered basolateral and planar cell polarity (PCP (zeige BMP1 Antikörper)).
Dlx5 and Dlx6 expression determines uterine architecture and adenogenesis and is needed for implantation
The results presented here indicate that loss of Dlx5 causes a down-modulation of miR (zeige MLXIP Antikörper)-9 and of miR (zeige MLXIP Antikörper)-200-class, which results in the over-expression of the Foxg1 (zeige FOXG1 Antikörper) protein.
Lck (zeige LCK Antikörper)-Dlx5 mice develop T-ALLs that consistently acquire overexpression of Myc (zeige MYC Antikörper) and activation of Akt (zeige AKT1 Antikörper).
Study demonstrated a novel role of miR (zeige MLXIP Antikörper)-124 and Dlx5 in regulating the differentiation of mesenchymal stem cells toward the myogenic lineage, that is, miR (zeige MLXIP Antikörper)-124 inhibits myogenic differentiation partially through targeting Dlx5 expression.
Mash1 (zeige ASCL1 Antikörper) is required for the expression of GAD67 (zeige GAD1 Antikörper) and Dlx5 in taste bud cells.
Retinoic acid treatment leads to a progressive loss of Dlx5 and Dlx6 expression in the first pharyngeal arch.
Imprinting analysis shows that DLX5 is maternally expressed in some organs and tissues but not imprinted in others.
Data indicate that retinoic acid (RA) induces the expression patterns of genes normally expressed in the posterior tooth-forming region, such as pitx2 (zeige PITX2 Antikörper) and dlx2b.
This gene encodes a member of a homeobox transcription factor gene family similiar to the Drosophila distal-less gene. The encoded protein may play a role in bone development and fracture healing. Mutation in this gene, which is located in a tail-to-tail configuration with another member of the family on the long arm of chromosome 7, may be associated with split-hand/split-foot malformation.
distal-less homeo box 5
, homeobox protein DLX-5
, split hand/foot malformation type 1 with sensorineural hearing loss
, homeobox protein DLX-3
, homeobox protein DLL-3
, putative transcription factor DLL3
, distal-less homeobox 5
, distal-less homeobox protein 5
, distal-less homeobox gene 5
, distal-less homeobox protein 2b
, homeobox protein Dlx2b