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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Jan 2016.

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, galectin-1, CAN
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.
Supplier
Zhang Lin, In PLoS ONE, 2005
... Polyclonal anti-Notch2, 3, anti-IL-1α antibodies were obtained from Abcam Inc (Cambridge, MA) ...
Papers on Notch2
NOTCH1, TP53, and MAP2K1 Mutations in Splenic Diffuse Red Pulp Small B-cell Lymphoma Are Associated With Progressive Disease.
New
Campo et al., London, United Kingdom. In Am J Surg Pathol, 29 Feb 2016
No mutations were found in NOTCH2 or MYD88.
NOT ALL NOTCH IS CREATED EQUAL: THE ONCOGENIC ROLE OF NOTCH2 IN BLADDER CANCER AND ITS IMPLICATIONS FOR TARGETED THERAPY.
New
Black et al., Vancouver, Canada. In Clin Cancer Res, 14 Feb 2016
Here we hypothesized that NOTCH2 is an oncogene suitable for therapeutic targeting in BC.
Jagged1 inhibits osteoprotegerin expression by human periodontal ligament cells.
New
Osathanon et al., Bangkok, Thailand. In J Periodontal Res, 11 Feb 2016
Lentiviral small hairpin RNA particles against NOTCH2 were employed to inhibit NOTCH2 expression.
Compound heterozygous mutations in NEK8 in siblings with end-stage renal disease with hepatic and cardiac anomalies.
New
Spinner et al., Atlanta, United States. In Am J Med Genet A, 24 Jan 2016
UNASSIGNED: We studied two brothers who presented in the newborn period with cardiac, renal, and hepatic anomalies that were initially suggestive of ALGS, although no mutations in JAG1 or NOTCH2 were identified.
PKCδ activated by c-MET enhances infiltration of human glioblastoma cells through NOTCH2 signaling.
New
Lee et al., Seoul, South Korea. In Oncotarget, 17 Jan 2016
Notably, PKCδ enhanced Tyr418 phosphorylation of the non-receptor tyrosine kinase SRC, which in turn activated STAT3 and subsequent NOTCH2 signaling, ultimately leading to GBM cell invasiveness.
Hajdu Cheney Mouse Mutants Exhibit Osteopenia, Increased Osteoclastogenesis and Bone Resorption.
New
Zanotti et al., United States. In J Biol Chem, 01 Jan 2016
Hajdu Cheney Syndrome, a disease characterized by osteoporosis and fractures, is associated with NOTCH2 mutations resulting in a truncated stable protein and gain-of-function.
Discordant clinical phenotype in monozygotic twins with Alagille syndrome: Possible influence of non-genetic factors.
New
Spinner et al., Nagano, Japan. In Am J Med Genet A, Nov 2015
Alagille syndrome is typically the result of germline mutations in JAG1 or NOTCH2 and is one of several human diseases caused by Notch signaling abnormalities.
Alagille syndrome and a JAG1 mutation: 41 cases of experience at a single center.
New
Noh et al., Seoul, South Korea. In Korean J Pediatr, Oct 2015
Mutations in the Notch signaling pathway, such as in JAG1 and NOTCH2, play a key role in embryonic development.
Capillaroscopic findings in a case of Hajdu-Cheney syndrome.
New
Rednic et al., Cluj-Napoca / Kolozsvár, Romania. In Osteoporos Int, Oct 2015
Hajdu-Cheney syndrome (HCS) is a very rare connective tissue disease characterized by osteoporosis, early dentition loss and a particular phenotype as a result of enhanced NOTCH2 signaling.
Whole exome sequencing of microdissected splenic marginal zone lymphoma: a study to discover novel tumor-specific mutations.
Hansmann et al., Frankfurt am Main, Germany. In Bmc Cancer, 2014
RESULTS: Overall, 25 nonsynonymous somatic SNVs were identified, including known mutations in the NOTCH2 and MYD88 genes.
Genetic landscape of esophageal squamous cell carcinoma.
Impact
He et al., Beijing, China. In Nat Genet, 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 coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Impact
GeneRIF
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.
Impact
GeneRIF
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).
Impact
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.
Impact
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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