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Delta-like 3

Dlx5, Delta3, DLL3
This gene encodes a member of the delta protein ligand family. This family functions as Notch ligands that are characterized by a DSL domain, EGF repeats, and a transmembrane domain. Mutations in this gene cause autosomal recessive spondylocostal dysostosis 1. Two transcript variants encoding distinct isoforms have been identified for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CAN, delta4, delta1, fibrillin-1
Papers using Dlx5 antibodies
Design and validation of a tool for neurite tracing and analysis in fluorescence microscopy images
Chao Moses V. et al., In Nature neuroscience, 2003
... Time-pregnant Sprague-Dawley rats, CD1 mice (Charles River Laboratories), Dlx5/6-Flpe and RCE:FRT transgenic mice ...
Papers on Dlx5
Genome-wide DNA methylation study identifies significant epigenomic changes in osteoarthritic cartilage.
Sawalha et al., Oklahoma City, United States. In Arthritis Rheumatol, 31 Oct 2014
We found differential methylation in genes with prior links to OA, including RUNX1, RUNX2, DLX5, FURIN, HTRA1, FGFR2, NFATC1, SNCAIP, and COL11A2.
The bone marrow stromal compartment in multiple myeloma patients retains capability for osteogenic differentiation in vitro: defining the stromal defect in myeloma.
Yong et al., London, United Kingdom. In Br J Haematol, 31 Oct 2014
Adherent cultures from MM BM are able to differentiate into osteoblasts, as indicated by the early upregulation of RUNX2, SP7, AXIN2 and DLX5, and the production of alkaline phosphatase and calcium.
Heterozygous DLX5 nonsense mutation associated with isolated split-hand/foot malformation with reduced penetrance and variable expressivity in two unrelated families.
Jamsheer et al., Poznań, Poland. In Birth Defects Res A Clin Mol Teratol, 05 Oct 2014
SHFM1 is usually inherited as an autosomal dominant trait with reduced penetrance, although recessive inheritance has been described for a single family carrying a homozygous DLX5 missense variant.
DLX3 regulates bone mass by targeting genes supporting osteoblast differentiation and mineral homeostasis in vivo.
Morasso et al., Bethesda, United States. In Cell Death Differ, 30 Sep 2014
Using RNA sequencing and chromatin immunoprecipitation-Seq analyses, we demonstrate that DLX3 regulates transcription factors crucial for bone formation such as Dlx5, Dlx6, Runx2 and Sp7 as well as genes important to mineral deposition (Ibsp, Enpp1, Mepe) and bone turnover (Opg).
Novel daidzein analogs enhance osteogenic activity of bone marrow-derived mesenchymal stem cells and adipose-derived stromal/stem cells through estrogen receptor dependent and independent mechanisms.
Bunnell et al., In Stem Cell Res Ther, 28 Sep 2014
The analysis of lineage specific gene expression demonstrated increased expression of key osteogenic genes (RUNX2, c-FOS, SPARC, DLX5, SPP1, COL1A1, IGF1, SOST, and DMP1) and earlier induction of these lineage specific genes, following treatment with 2g or 2l, relative to vehicle-treated cells.
Expression of SP7, RUNX1, DLX5, and CTNNB1 in human mesenchymal stem cells cultured on xenogeneic bone substitute as compared with machined titanium.
Covani et al., Pisa, Italy. In Implant Dent, Aug 2014
RNA quantification for genes DLX5, CTNNB1, RUNX1, and SP7 was assessed by quantitative real-time polymerase chain reaction.
Deletions of exons with regulatory activity at the DYNC1I1 locus are associated with split-hand/split-foot malformation: array CGH screening of 134 unrelated families.
Spielmann et al., In Orphanet J Rare Dis, Dec 2013
Exons 15 and 17 of DYNC1I1 are known to act as tissue specific limb enhancers of DLX5/6, two genes that have been shown to be associated with SHFM in mice.
Notch signaling in human development and disease.
Spinner et al., Philadelphia, United States. In Semin Cell Dev Biol, 2012
Notch associated disorders include the autosomal dominant, multi-system, Alagille syndrome caused by mutations in both a ligand (Jagged1 (JAG1)) and receptor (NOTCH2) and autosomal recessive spondylocostal dysostosis, caused by mutations in a ligand (Delta-like-3 (DLL3)), as well as several other members of the Notch signaling pathway.
Possible roles of DLK1 in the Notch pathway during development and disease.
Gaemers et al., Amsterdam, Netherlands. In Biochim Biophys Acta, 2012
In mammals, four Notch receptors (NOTCH1-4) and five activating canonical ligands (JAGGED1, JAGGED2, DLL1, DLL3 and DLL4) have been described.
Rapp-Hodgkin syndrome and SHFM1 patients: delineating the p63-Dlx5/Dlx6 pathway.
López-Expósito et al., Murcia, Spain. In Gene, 2012
Two patients that have in common a p63-Dlx5/Dlx6 pathway dysregulation.
Mutations in the Notch pathway alter the patterning of multifidus.
Wilson-Rawls et al., Phoenix, United States. In Anat Rec (hoboken), 2012
Intriguing changes are observed in the cranio-caudal borders of multifidus muscle in mutant Dll3 and Lfng models of idiopathic scoliosis.
Identification of a novel DLX5 mutation in a family with autosomal recessive split hand and foot malformation.
Alkuraya et al., Riyadh, Saudi Arabia. In J Med Genet, 2012
the first intragenic DLX5 mutation in split hand and foot malformation is found; a potential dual role for DLX5 in limb development is suggested
[Changes in the expression of Dlx5, Msx2, and Dlx5/Msx2 in hPDLSCs loaded with cyclic tensile stress].
Zhao et al., Chengdu, China. In Sichuan Da Xue Xue Bao Yi Xue Ban, 2011
Cyclic tensile stress may induce differentiation of periodontal ligament stem cells towards mineralized tissue cells by promoting Dlx5 mRNA expression and decreasing Msx2 expression.
Akt phosphorylates and regulates the function of Dlx5.
Lee et al., Kwangju, South Korea. In Biochem Biophys Res Commun, 2011
These results suggest that Dlx5 is a novel target of Akt and that the activity of Dlx5 could be modulated by a novel mechanism involving Akt during osteoblast differentiation.
The role of Notch in patterning the human vertebral column.
Dunwoodie, Sydney, Australia. In Curr Opin Genet Dev, 2009
More specifically it describes that mutations in genes encoding Notch pathway components (DLL3, MESP2, LFNG and HES7) cause severe congenital vertebral defects in humans.
Defective somitogenesis and abnormal vertebral segmentation in man.
Turnpenny, Exeter, United Kingdom. In Adv Exp Med Biol, 2007
Only a minority of abnormal segmentation phenotypes appear to follow Mendelian inheritance but three genes--DLL3, MESP2 and LNFG--have now been identified for spondylocostal dysostosis (SCD), a spinal malformation characterized by extensive hemivertebrae, trunkal shortening and abnormally aligned ribs with points of fusion.
[Autism, epilepsy and genetics].
Manchado et al., Barcelona, Spain. In Rev Neurol, 2007
CONCLUSIONS: The relation between pervasive developmental disorders and epilepsy, epileptiform activity and subclinical seizures can be explained from a neurobiological point of view, on the one hand, by an imbalance between the excitatory system -glutamate- and the inhibitory system -gamma-aminobutyric acid (GABA)- in key points in the cerebral cortex and, on the other, by means of molecular genetic studies and studies of candidate genes (FOXP2, WNT2, subunits of GABA receptors, neuroligins, ARX, SCN1A, SCN2A, MECP2, CDKL5 and DLX5).
Molecular subclasses of high-grade glioma predict prognosis, delineate a pattern of disease progression, and resemble stages in neurogenesis.
Aldape et al., San Francisco, United States. In Cancer Cell, 2006
A robust two-gene prognostic model utilizing PTEN and DLL3 expression suggests that Akt and Notch signaling are hallmarks of poor prognosis versus better prognosis gliomas, respectively.
Loss of silent-chromatin looping and impaired imprinting of DLX5 in Rett syndrome.
Kohwi-Shigematsu et al., Berkeley, United States. In Nat Genet, 2005
Mecp2 regulates Dlx5 by means of a silent chromatin loop
Mutations in the human delta homologue, DLL3, cause axial skeletal defects in spondylocostal dysostosis.
Turnpenny et al., Exeter, United Kingdom. In Nat Genet, 2000
Dll3 is mutated in the X-ray-induced mouse mutant pudgy (pu), causing a variety of vertebrocostal defects similar to SD phenotypes.
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