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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.
Zhang Lin, In PLoS ONE, 2005
... Polyclonal anti-Notch2, 3, anti-IL-1α antibodies were obtained from Abcam Inc (Cambridge, MA) ...
Papers on Notch2
Black et al., Vancouver, Canada. In Clin Cancer Res, 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.
Osathanon et al., Bangkok, Thailand. In J Periodontal Res, 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.
Spinner et al., Atlanta, United States. In Am J Med Genet A, 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.
Lee et al., Seoul, South Korea. In Oncotarget, 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.
Zanotti et al., United States. In J Biol Chem, 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.
[IgM+IgD+CD27+ B cells in human: an essential role in the protection against encapsulated bacteria].
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.
[Advances in the diagnosis and treatment of Alagille syndrome].
Song et al., Guangzhou, China. In Zhongguo Dang Dai Er Ke Za Zhi, 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.
NOTCH signaling roles in acute myeloid leukemia cell growth and interaction with other stemness-related signals.
Tohda, Tokyo, Japan. In Anticancer Res, 2014
Conversely, knockdown of NOTCH1 and NOTCH2 does not affect the growth of AML cells, whereas it suppresses the growth of T-ALL cells.
Genetic landscape of esophageal squamous cell carcinoma.
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.
Hajdu-Cheney syndrome: a case report with review of literature.
Desai et al., Marmagao, India. In J Radiol Case Rep, 2014
Recent research suggests that it is caused by heterozygous mutation of terminal exon of NOTCH 2. Most characteristic findings include transverse band of acro-osteolysis involving the phalanges of both hands and feet and osteoporosis and deformities involving skull, mandible, spine and other bones.
Hajdu-Cheney syndrome: a review.
Zanotti et al., Farmington, United States. In Orphanet J Rare Dis, 2013
HCS is associated with mutations in exon 34 of NOTCH2 upstream the PEST domain that lead to the creation of a truncated and stable NOTCH2 protein with enhanced NOTCH2 signaling activity.
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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