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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
Alteration in the expression of antioxidant and detoxification genes in Chironomus riparius exposed to zinc oxide nanoparticles.
Chung et al., Seoul, South Korea. In Comp Biochem Physiol B Biochem Mol Biol, 31 Dec 2015
The expression of CuZn superoxide dismutase, manganese superoxide dismutase, catalase, phospholipid hydroperoxide glutathione peroxidase, thioredoxin reductase 1 and delta-3, sigma-4 and epsilon-1 classes of glutathione S-transferases, cytochrome p4509AT2, and heat shock protein 70 were studied using real-time polymerase chain reaction method.
Improved properties of bone and cartilage tissue from 3D inkjet-bioprinted human mesenchymal stem cells by simultaneous deposition and photocrosslinking in PEG-GelMA.
Cui et al., Wuhan, China. In Biotechnol Lett, 30 Nov 2015
Both osteogenic and chondrogenic differentiation as determined by specific gene and protein expression analysis (RUNX2, SP7, DLX5, ALPL, Col1A1, IBSP, BGLAP, SPP1, Col10A1, MMP13, SOX9, Col2A1, ACAN) was improved by PEG-GelMA in comparison to PEG alone.
The Role of FSCN1 in Migration and Invasion of Pituitary Adenomas.
Zhang et al., Beijing, China. In Mol Cell Endocrinol, 29 Nov 2015
In addition, reduction of FSCN1 can obviously down-regulate the level of Notch1 and DLL3.
Dlx5 and Dlx6 control uterine adenogenesis during post-natal maturation: Possible consequences for endometriosis.
Levi et al., Paris, France. In Hum Mol Genet, 28 Nov 2015
UNASSIGNED: Dlx5 and Dlx6 are two closely-associated homeobox genes which code for transcription factors involved in the control of steroidogenesis and reproduction.
Pilot investigation of the molecular discrimination of human osteoblasts from different bone entities.
Nelson et al., Freiburg, Germany. In J Craniomaxillofac Surg, 31 Oct 2015
Gene expression of seven genes (BMP1, CSF-1, TGFBR1, ICAM1, VCAM1, SPP1 and DLX5) was significantly higher in iHOB than in aHOB samples.
A DLL3-targeted antibody-drug conjugate eradicates high-grade pulmonary neuroendocrine tumor-initiating cells in vivo.
Dylla et al., San Francisco, United States. In Sci Transl Med, Sep 2015
Increased expression of delta-like 3 (DLL3) was discovered in SCLC and LCNEC PDX tumors and confirmed in primary SCLC and LCNEC tumors.
Highly efficient in vitro and in vivo delivery of functional RNAs using new versatile MS2-chimeric retrovirus-like particles.
Pagès et al., Tours, France. In Mol Ther Methods Clin Dev, Dec 2014
We could further show that the VLPs were able to activate an osteoblast differentiation pathway by delivering RUNX2- or DLX5-mRNA into primary human bone-marrow mesenchymal-stem cells.
Split-hand/foot malformation - molecular cause and implications in genetic counseling.
Jamsheer et al., Poznań, Poland. In J Appl Genet, Feb 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.
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.
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.
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.
Spondylocostal Dysostosis, Autosomal Recessive
(International Consortium for Vertebral Anomalies and Scoliosis) 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.
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.
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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