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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 24 Oct 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, HAD, CO-029, JAZF1
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
A microRNA-mediated regulatory loop modulates NOTCH and MYC oncogenic signals in B and T cell malignancies.
Aguiar et al., Graz, Austria. In Leukemia, 14 Nov 2014
MicroRNA-30a, a member of family of microRNAs that are transcriptionally suppressed by MYC, directly binds to and inhibits NOTCH1 and NOTCH2 expression.
Mutational landscape of aggressive cutaneous squamous cell carcinoma.
Frederick et al., Anderson, United States. In Clin Cancer Res, 10 Nov 2014
Three novel candidate tumor suppressors with putative links to cancer or differentiation, NOTCH2, PARD3 and RASA1, were also identified as possible drivers in cSCC.
Genetic landscape of esophageal squamous cell carcinoma.
He et al., Beijing, China. In Nat Genet, 31 Oct 2014
The Hippo and Notch pathways were dysregulated by mutations in FAT1, FAT2, FAT3 or FAT4 (27%) or AJUBA (JUB; 7%) and NOTCH1, NOTCH2 or NOTCH3 (22%) or FBXW7 (5%), respectively.
The cell of origin and subtype of K-Ras-induced lung tumors are modified by Notch and Sox2.
Onaitis et al., Durham, United States. In Genes Dev, 01 Oct 2014
Chromatin immunoprecipitation demonstrates Sox2 binding to NOTCH1 and NOTCH2 regulatory regions.
Transcriptional profile of fibroblasts obtained from the primary site, lymph node and bone marrow of breast cancer patients.
Azevedo Koike Folgueira et al., São Paulo, Brazil. In Genet Mol Biol, 30 Sep 2014
In a biological validation set, NOTCH2 was confirmed to be more expressed in N+ (vs CAF) and ADCY2, HECTD1, HNMT, LOX, MACF1, SLC1A3 and USP16 more expressed in BM (vs CAF).
[Mantle cell lymphoma: Towards a personalized therapeutic strategy?]
García-Marco et al., Madrid, Spain. In Med Clin (barc), Aug 2014
Advances in the biology and pathogenesis of MCL have unveiled several genes involved in deregulation of cell cycle checkpoints and the finding of subclonal populations with specific recurrent mutations (p53, ATM, NOTCH2) with an impact on disease progression and refractoriness to treatment.
Genetic aberrations of signaling pathways in lymphomagenesis: revelations from next generation sequencing studies.
Gaidano et al., Novara, Italy. In Semin Cancer Biol, Dec 2013
mutations of BRAF, MYD88 and NOTCH2), and new targets to be translated into therapeutic interventions (i.e.
The Truncate Mutation of Notch2 Enhances Cell Proliferation through Activating the NF-κB Signal Pathway in the Diffuse Large B-Cell Lymphomas.
Zhou et al., Hangzhou, China. In Plos One, Dec 2013
The Notch2 is a critical membrane receptor for B-cell functions, and also displays various biological roles in lymphoma pathogenesis.
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).
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
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
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.
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
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.
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