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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 25 Aug 2015.

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, CAN, galectin-1
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
NOTCH2 signaling confers immature morphology and aggressiveness in human hepatocellular carcinoma cells.
New
Lee et al., Kōchi, Japan. In Oncol Rep, 04 Sep 2015
Since NOTCH2, yet not NOTCH1 has been shown essential for murine hepatogenesis, NOTCH2 rather than NOTCH1 may be more relevant to human hepatocarcinogenesis; however, no previous studies have supported this hypothesis.
A very rare cause of acro-osteolysis: Hajdu-Cheney syndrome.
New
Allanore et al., Paris, France. In Joint Bone Spine, 13 Aug 2015
Molecular analysis confirmed the diagnosis with the identification of a mutation in the NOTCH2 gene.
[Mantle cell lymphoma: Towards a personalized therapeutic strategy?].
Review
New
García-Marco et al., Madrid, Spain. In Med Clin (barc), 22 Jul 2015
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.
[IgM+IgD+CD27+ B cells in human: an essential role in the protection against encapsulated bacteria].
New
Descatoire et al., Paris, France. In Med Sci (paris), Jun 2015
The identification of a human MZB cell precursor with NOTCH2-dependent differentiation properties further argue in favor of the existence of a MZB cell lineage in humans, like in rodents.
A novel genomic signature reclassifies an oral cancer subtype.
New
Rabbitts et al., Riyadh, Saudi Arabia. In Int J Cancer, Jun 2015
Exome sequencing showed that OVC samples lacked mutations in genes commonly associated with OSCC (TP53, NOTCH1, NOTCH2, CDKN2A and FAT1).
Cross talk between EBV and telomerase: the role of TERT and NOTCH2 in the switch of latent/lytic cycle of the virus.
New
De Rossi et al., Padova, Italy. In Cell Death Dis, Dec 2014
BATF, a transcription factor activated by NOTCH2, the major NOTCH family member in B cells, negatively affects the expression of BZLF1, the master regulator of viral lytic cycle.
NOTCH signaling roles in acute myeloid leukemia cell growth and interaction with other stemness-related signals.
Review
New
Tohda, Tokyo, Japan. In Anticancer Res, Nov 2014
Conversely, knockdown of NOTCH1 and NOTCH2 does not affect the growth of AML cells, whereas it suppresses the growth of T-ALL cells.
[Advances in the diagnosis and treatment of Alagille syndrome].
Review
New
Song et al., Guangzhou, China. In Zhongguo Dang Dai Er Ke Za Zhi, Nov 2014
In this disease, the Notch signalling pathway is impaired due to mutation in JAG1 (ALGS type 1) or NOTCH2 (ALGS type 2) gene, affecting multiple organs or systems such as liver, heart, eyes, vertebrate and face.
Genetic landscape of esophageal squamous cell carcinoma.
New
Impact
He et al., Beijing, China. In Nat Genet, 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.
Therapy of advanced squamous cell carcinoma of the skin.
Review
New
Maubec et al., Paris, France. In Curr Treat Options Oncol, Jun 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.
Mosaic small supernumerary marker chromosome 1 at amniocentesis: prenatal diagnosis, molecular genetic analysis and literature review.
Review
Wang et al., Taipei, Taiwan. In Gene, 2013
We discuss the genotype-phenotype correlation of the involved genes of ALX3, RBM15, NTNG1, SLC25A24, GPSM2, TBX15 and NOTCH2 in this case.
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
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.
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
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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