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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: CAN, ACID, delta4, delta1, Dlx6
Papers using Dlx5 antibodies
Design and validation of a tool for neurite tracing and analysis in fluorescence microscopy images
Supplier
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 methylation profiling identifies novel methylated genes in neuroblastoma tumors.
New
Carén et al., Göteborg, Sweden. In Epigenetics, Feb 2016
The genes with the highest number of hypermethylated CpG sites in INRG M tumors are TERT, PCDHGA4, DLX5, and DLX6-AS1.
CD200 expression in human cultured bone marrow mesenchymal stem cells is induced by pro-osteogenic and pro-inflammatory cues.
New
Deschaseaux et al., Tours, France. In J Cell Mol Med, Feb 2016
After sorting, measurement of lineage markers showed that the osteoblastic genes RUNX2 and DLX5 were up-regulated in CD200(pos) cells compared to CD200(neg) fraction.
Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
New
van Wijnen et al., Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
Comparison of molecular profiles of human mesenchymal stem cells derived from bone marrow, umbilical cord blood, placenta and adipose tissue.
New
Kim et al., Seoul, South Korea. In Int J Mol Med, Jan 2016
The gene expression profiles of stemness-related genes [octamer-binding transcription factor 4 (OCT4), sex determining region Y-box (SOX)2, MYC, Krüppel-like factor 4 (KLF4), NANOG, LIN28 and REX1] and lineage‑related and differentiation stage-related genes [B4GALNT1 (GM2/GS2 synthase), inhibin, beta A (INHBA), distal-less homeobox 5 (DLX5), runt-related transcription factor 2 (RUNX2), proliferator‑activated receptor gamma (PPARG), CCAAT/enhancer-binding protein alpha (C/EBPA), bone morphogenetic protein 7 (BMP7) and SOX9] were compared using RT-PCR.
The apical ectodermal ridge of the mouse model of ectrodactyly Dlx5;Dlx6-/- shows altered stratification and cell polarity, which are restored by exogenous Wnt5a ligand.
New
Merlo et al., Torino, Italy. In Hum Mol Genet, Jan 2016
Type-1 SHFM is linked to deletions/rearrangements of the DLX5-DLX6 locus and point mutations in the DLX5 gene.
Quinomycin A targets Notch signaling pathway in pancreatic cancer stem cells.
New
Subramaniam et al., Kansas City, United States. In Oncotarget, Jan 2016
Furthermore, levels of Notch 1-4 receptors, their ligands Jagged1, Jagged2, DLL1, DLL3, DLL4 and the downstream target protein Hes-1 were reduced.
Characterization of the osteogenic potential of mesenchymal stem cells from human periodontal ligament based on cell surface markers.
Hong et al., Los Angeles, United States. In Int J Oral Sci, 2014
CD271(+) DMSCs demonstrated the greatest osteogenic potential with strong induction of osteogenic markers such as DLX5, RUNX2, and BGLAP.
Split-hand/foot malformation - molecular cause and implications in genetic counseling.
Review
Jamsheer et al., Poznań, Poland. In J Appl Genet, 2014
In addition, three genes, i.e., TP63, WNT10B, and DLX5 are known to carry point mutations in patients affected by SHFM.
Possible roles of DLK1 in the Notch pathway during development and disease.
Review
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.
Notch signaling in human development and disease.
Review
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.
Rapp-Hodgkin syndrome and SHFM1 patients: delineating the p63-Dlx5/Dlx6 pathway.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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].
GeneRIF
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.
GeneRIF
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.
Spondylocostal Dysostosis, Autosomal Recessive
Review
Young et al., Seattle, United States. In Unknown Journal, 2009
Subtypes are defined by identification of two mutant alleles in any one of the four genes in which mutations are known to cause autosomal recessive (AR) SCDO: DLL3, MESP2, LFNG, and HES7.
Defective somitogenesis and abnormal vertebral segmentation in man.
Review
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.
Molecular subclasses of high-grade glioma predict prognosis, delineate a pattern of disease progression, and resemble stages in neurogenesis.
Impact
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.
Impact
GeneRIF
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.
Impact
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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