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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 29 Mar 2014.

Notch 2

Notch2, n-2
This gene encodes a member of the Notch family. Members of this Type 1 transmembrane protein family share structural characteristics including an extracellular domain consisting of multiple epidermal growth factor-like (EGF) repeats, and an intracellular domain consisting of multiple, different domain types. Notch family members play a role in a variety of developmental processes by controlling cell fate decisions. The Notch signaling network is an evolutionarily conserved intercellular signaling pathway which regulates interactions between physically adjacent cells. In Drosophilia, notch interaction with its cell-bound ligands (delta, serrate) establishes an intercellular signaling pathway that plays a key role in development. Homologues of the notch-ligands have also been identified in human, but precise interactions between these ligands and the human notch homologues remain to be determined. This protein is cleaved in the trans-Golgi network, and presented on the cell surface as a heterodimer. This protein functions as a receptor for membrane bound ligands, and may play a role in vascular, renal and hepatic development. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jan 2011] (from NCBI)
Top mentioned proteins: p300, Notch3, JAZF1, HAD, CO-029
Papers using Notch2 antibodies
The role of the vascular endothelial growth factor-Delta-like 4 ligand/Notch4-ephrin B2 cascade in tumor vessel remodeling and endothelial cell functions.
Zhang Lin, In PLoS ONE, 2005
... Polyclonal anti-Notch2, 3, anti-IL-1α antibodies were obtained from Abcam Inc (Cambridge, MA) ...
Papers on Notch2
Notch signaling genes: Myogenic DNA hypomethylation and 5-hydroxymethylcytosine.
Ehrlich et al., Ipswich, United States. In Epigenetics, 26 Apr 2014
Reduced representation bisulfite sequencing (RRBS) indicated significant hypomethylation in myoblasts, myotubes, and skeletal muscle vs. many nonmuscle samples at intragenic or intergenic regions of the following Notch receptor or ligand genes: NOTCH1, NOTCH2, JAG2, and DLL1.
Therapy of Advanced Squamous Cell Carcinoma of the Skin.
Maubec et al., Paris, France. In Curr Treat Options Oncol, 19 Apr 2014
Moreover, there are several new molecular candidate treatment targets for unresectable SCCS including somatic NOTCH1 or NOTCH2 inactivating mutations, ALK1, which could be a good candidate for antiangiogenic therapy and matrix metallopeptidase 7, which enhances proliferation, migration, and invasion of cancer cells.
A Functional Germline Variant in GLI1 Implicates Hedgehog Signaling in Clinical Outcome of Stage II and III Colon Carcinoma Patients.
Gerger et al., Leoben, Austria. In Clin Cancer Res, 15 Apr 2014
Genomic DNA was analyzed for 18 germline polymorphisms in Wnt, Notch, and Hedgehog pathway genes (SFRP, DKK 2 and 3, AXIN2, APC, MYC, TCF7L2, NOTCH2, and GLI1) by TaqMan 5'-exonuclease assays.
NOTCH2 and FLT3 gene mis-splicing are common events in patients with acute myeloid leukemia (AML): new potential targets in AML.
Griffin et al., Boston, United States. In Blood, 26 Mar 2014
Among the most commonly mis-spliced genes (> 70% of AML patients) were two, NOTCH2 and FLT3, genes that encode myeloid cell surface proteins.
Molecular Profiling of HNSCC Cells and Tumors Reveals a Rational Approach to Preclinical Model Selection.
Grandis et al., Pittsburgh, United States. In Mol Cancer Res, 14 Feb 2014
Amplification of eight genes (PIK3CA, EGFR, CCND2, KDM5A, ERBB2, PMS1, FGFR1 and WHSCIL1) and deletion of five genes (CDKN2A, SMAD4, NOTCH2, NRAS and TRIM33) were found in both HNSCC cell lines and tumors.
Mosaic small supernumerary marker chromosome 1 at amniocentesis: prenatal diagnosis, molecular genetic analysis and literature review.
Wang et al., Taipei, Taiwan. In Gene, Nov 2013
We discuss the genotype-phenotype correlation of the involved genes of ALX3, RBM15, NTNG1, SLC25A24, GPSM2, TBX15 and NOTCH2 in this case.
Renal involvement and the role of Notch signalling in Alagille syndrome.
Rosenblum et al., Toronto, Canada. In Nat Rev Nephrol, Jul 2013
Alagille syndrome is an autosomal dominant disorder with variable multisystem organ involvement that is caused by mutations in one of two genes in the Notch signalling pathway, JAG1 or NOTCH2.
Notch signaling in skeletal health and disease.
Canalis et al., Hartford, United States. In Eur J Endocrinol, Jun 2013
Inactivating mutations of the Notch ligand JAG1 or of NOTCH2 are associated with Alagille syndrome, and activating mutations in NOTCH2 are associated with Hajdu-Cheney syndrome (HCS).
Notch signaling and bone remodeling.
Long et al., Saint Louis, United States. In Curr Osteoporos Rep, Jun 2013
The recent discovery of activating NOTCH2 mutations as the cause of Hajdu-Cheney syndrome has highlighted the significance of Notch signaling in human bone physiology.
The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development.
Gaidano et al., Novara, Italy. In J Exp Med, 2012
Mutations in NOTCH2, a gene required for marginal-zone B cell development, represent the most frequent lesion in splenic marginal zone lymphoma
Whole-genome sequencing identifies recurrent somatic NOTCH2 mutations in splenic marginal zone lymphoma.
Elenitoba-Johnson et al., Ann Arbor, United States. In J Exp Med, 2012
NOTCH2 mutations play a role in the pathogenesis and progression of the splenic marginal zone lymphoma and are associated with a poor prognosis.
Profiling immunohistochemical expression of NOTCH1-3, JAGGED1, cMET, and phospho-MAPK in 100 carcinomas of unknown primary.
Pavlidis et al., Thessaloníki, Greece. In Clin Exp Metastasis, 2012
immunohistochemical analysis of NOTCH1-3, JAGGED1, cMET, and phospho-MAPK in 100 carcinomas of unknown primary
Conditional deletion of Notch1 and Notch2 genes in excitatory neurons of postnatal forebrain does not cause neurodegeneration or reduction of Notch mRNAs and proteins.
Shen et al., Boston, United States. In J Biol Chem, 2012
Notch1 and Notch2 are not involved in the age-related neurodegeneration caused by loss of presenilin or gamma-secretase
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.
Notch2 and Notch3 function together to regulate vascular smooth muscle development.
Lilly et al., Columbus, United States. In Plos One, 2011
In vitro analysis show that both Notch2 and Notch3 robustly activate smooth muscle differentiation genes, and Notch3, but not Notch2 is a target of Notch signaling
Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis.
Le Caignec et al., Nantes, France. In Nat Genet, 2011
sequenced the exomes of six unrelated individuals with Hajdu-Cheney syndrome and identified heterozygous nonsense and frameshift mutations in NOTCH2 in five of them
Mutations in NOTCH2 cause Hajdu-Cheney syndrome, a disorder of severe and progressive bone loss.
Trembath et al., London, United Kingdom. In Nat Genet, 2011
Hajdu-Cheney syndrome mutations are predicted to lead to the premature truncation of NOTCH2 with either disruption or loss of the C-terminal proline-glutamate-serine-threonine-rich proteolytic recognition sequence.
A multistage genome-wide association study in breast cancer identifies two new risk alleles at 1p11.2 and 14q24.1 (RAD51L1).
Hunter et al., Bethesda, United States. In Nat Genet, 2009
(rs11249433; P = 6.74 x 10(-10) adjusted genotype test, 2 degrees of freedom) resides in a large linkage disequilibrium block neighboring NOTCH2 and FCGR1B; this signal was stronger for estrogen-receptor-positive tumors.
Clinical risk factors, DNA variants, and the development of type 2 diabetes.
Groop et al., Malmö, Sweden. In N Engl J Med, 2008
Variants in 11 genes (TCF7L2, PPARG, FTO, KCNJ11, NOTCH2, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX) were significantly associated with the risk of type 2 diabetes independently of clinical risk factors; variants in 8 of these genes were associated with impaired beta-cell function.
Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes.
Altshuler et al., Oxford, United Kingdom. In Nat Genet, 2008
We detected at least six previously unknown loci with robust evidence for association, including the JAZF1 (P = 5.0 x 10(-14)), CDC123-CAMK1D (P = 1.2 x 10(-10)), TSPAN8-LGR5 (P = 1.1 x 10(-9)), THADA (P = 1.1 x 10(-9)), ADAMTS9 (P = 1.2 x 10(-8)) and NOTCH2 (P = 4.1 x 10(-8)) gene regions.
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