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DLX5 encodes a member of a homeobox transcription factor gene family similiar to the Drosophila distal-less gene. De plus, nous expédions Distal-Less Homeobox 5 Kits (15) et Distal-Less Homeobox 5 Protéines (8) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal DLX5 Primary Antibody pour 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. dans The Journal of biological chemistry 2003
Show all 2 Pubmed References
Human Polyclonal DLX5 Primary Antibody pour 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. dans Nature methods 2013
Our results in mice suggest that long-range DLX5 enhancer elements located in the human SLC25A13 (Montrer slc25a13 Anticorps) gene may underlie the sensorineural hearing loss that is sometimes associated with SHFM1 (Montrer SHFM1 Anticorps).
These results indicate activation of DLX5 and RUNX2 (Montrer RUNX2 Anticorps) via its distal promoter represents a unique feature of GFs, and is important for ECM (Montrer MMRN1 Anticorps) 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 (Montrer RUNX1 Anticorps) 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 (Montrer SHFM1 Anticorps) phenotype.
Genome sequencing of the deletion breakpoints showed that the DLX5 and DLX6 genes are disomic but the putative DYNC1I1 (Montrer DYNC1I1 Anticorps) exon 15 and 17 enhancers are deleted.
T-614 promotes osteoblastic differentiation by increasing the expression of Osterix (Montrer SP7 Anticorps) and Dlx5.
Results indicate that Dlx5 and Runx2 (Montrer RUNX2 Anticorps) are critical factors for the upregulated Osterix (Montrer SP7 Anticorps) expression in shPP2A cells, which is considered to be important for the accelerated osteoblast differentiation in these cells.
FGF10 (Montrer FGF10 Anticorps) pathway is downregulated in Dlx5(-/-) mice, and activation of FGF10 (Montrer FGF10 Anticorps) 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 (Montrer NDN Anticorps) induced osteoblast-specific markers in an osteogenic cell line through formation of a complex with distal-less Homeobox 5 (Dlx5) and Runx2 (Montrer RUNX2 Anticorps) 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 (Montrer WNT5A Anticorps), shows scattered beta-catenin (Montrer CTNNB1 Anticorps) responsive cells and altered basolateral and planar cell polarity (PCP (Montrer BMP1 Anticorps)).
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 (Montrer MLXIP Anticorps)-9 and of miR (Montrer MLXIP Anticorps)-200-class, which results in the over-expression of the Foxg1 (Montrer FOXG1 Anticorps) protein.
Lck (Montrer LCK Anticorps)-Dlx5 mice develop T-ALLs that consistently acquire overexpression of Myc (Montrer MYC Anticorps) and activation of Akt (Montrer AKT1 Anticorps).
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 (Montrer PITX2 Anticorps) 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