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1. Full Text MiR-18a-5p inhibits endothelial–mesenchymal transition and cardiac fibrosis through the Notch2 pathway
by Geng, Huazhi and Guan, Jun
Biochemical and Biophysical Research Communications, ISSN 0006-291X, 09/2017, Volume 491, Issue 2, pp. 329 - 336
Hyperglycemia plays a crucial role in the pathogenesis of diabetic complications; however, the mechanisms underlying diabetic cardiac fibrosis remain unclear.... 
MicroRNA | EndMT | Notch2 | Fibrosis | High glucose | TARGET | CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | MICRORNAS | DIABETIC CARDIOMYOPATHY | BIOPHYSICS | ALAGILLE-SYNDROME | EXPRESSION | Dependovirus - genetics | Cadherins - metabolism | Genetic Vectors - administration & dosage | Humans | Aortic Valve - drug effects | Diabetes Mellitus, Experimental - genetics | Male | MicroRNAs - metabolism | Diabetes Mellitus, Experimental - chemically induced | Cadherins - genetics | Endomyocardial Fibrosis - prevention & control | Dependovirus - metabolism | Genetic Vectors - chemistry | Signal Transduction | Endothelial Cells - metabolism | Genetic Vectors - metabolism | Glucose - pharmacology | Heart Ventricles - metabolism | MicroRNAs - genetics | Calcium-Binding Proteins - genetics | Platelet Endothelial Cell Adhesion Molecule-1 - genetics | Streptozocin | Vimentin - metabolism | Actins - metabolism | Receptor, Notch2 - genetics | Actins - genetics | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Vimentin - genetics | Epithelial-Mesenchymal Transition | Diabetic Cardiomyopathies - prevention & control | Endomyocardial Fibrosis - genetics | Endomyocardial Fibrosis - chemically induced | Endomyocardial Fibrosis - pathology | Diabetes Mellitus, Experimental - metabolism | Heart Ventricles - pathology | Calcium-Binding Proteins - metabolism | Cell Line | Mice, Inbred C57BL | Gene Expression Regulation | Receptor, Notch2 - metabolism | Aortic Valve - cytology | Aortic Valve - metabolism | Fibronectins - metabolism | Diabetic Cardiomyopathies - genetics | Animals | Endothelial Cells - cytology | Diabetes Mellitus, Experimental - pathology | Diabetic Cardiomyopathies - pathology | Fibronectins - genetics | Diabetic Cardiomyopathies - chemically induced | Endothelial Cells - drug effects | Fibronectins | Hyperglycemia | Stem cells | Glucose | Muscle proteins | Dextrose | Endothelium | Index Medicus
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2. Full Text NOTCH2 mutations in Alagille syndrome
by Kamath, Binita Maya and Bauer, Robert C and Loomes, Kathleen M and Chao, Grace and Gerfen, Jennifer and Hutchinson, Anne and Hardikar, Winita and Hirschfield, Gideon and Jara, Paloma and Krantz, Ian D and Lapunzina, Pablo and Leonard, Laura and Ling, Simon and Ng, Vicky Lee and Hoang, Phuc Le and Piccoli, David A and Spinner, Nancy Bettina
Journal of Medical Genetics, ISSN 0022-2593, 02/2012, Volume 49, Issue 2, pp. 138 - 144
BackgroundAlagille syndrome (ALGS) is a dominant, multisystem disorder caused by mutations in the Jagged1 (JAG1) ligand in 94% of patients, and in the NOTCH2... 
VASCULAR ANOMALIES | JAG1 MUTATIONS | HAJDU-CHENEY-SYNDROME | MORBIDITY | ARTERIOHEPATIC DYSPLASIA | DISEASE | GENETICS & HEREDITY | DISORDER | POLYCYSTIC KIDNEY SYNDROME | HYPERTENSION | HUMAN JAGGED1 | Cell Line | Gene Expression | Genetic Association Studies | Signal Transduction | Humans | Receptor, Notch2 - metabolism | Receptor, Notch2 - genetics | Alagille Syndrome - genetics | Phenotype | Animals | DNA Mutational Analysis | Facies | HEK293 Cells | Mice | Mutation
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3. Full Text Notch2 Receptor Signaling Controls Functional Differentiation of Dendritic Cells in the Spleen and Intestine
by Lewis, Kanako L and Caton, Michele L and Bogunovic, Milena and Greter, Melanie and Grajkowska, Lucja T and Ng, Dennis and Klinakis, Apostolos and Charo, Israel F and Jung, Steffen and Gommerman, Jennifer L and Ivanov, Ivaylo I and Liu, Kang and Merad, Miriam and Reizis, Boris
Immunity, ISSN 1074-7613, 2011, Volume 35, Issue 5, pp. 780 - 791
Dendritic cells (DCs) in tissues and lymphoid organs comprise distinct functional subsets that differentiate in situ from circulating progenitors.... 
REGULATOR | RESPONSES | HOMEOSTASIS | PATHWAY | MOUSE | SUBSETS | GENERATION | MICE | IMMUNOLOGY | EXPRESSION | Immunoglobulin J Recombination Signal Sequence-Binding Protein - metabolism | Spleen - immunology | Signal Transduction | Dendritic Cells - immunology | Mice, Inbred C57BL | Cells, Cultured | Receptor, Notch2 - metabolism | Male | Mice, Transgenic | Gene Expression Profiling | Intestines - metabolism | Intestines - immunology | fms-Like Tyrosine Kinase 3 - genetics | Cell Differentiation - immunology | Phenotype | Animals | Spleen - metabolism | Gene Expression Regulation, Developmental | Female | Dendritic Cells - cytology | Mice | Dendritic Cells - metabolism | Dendritic cells | T cells | Genes | Spleen | Ligands | Software | Gene expression | Rodents
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4. Full Text The coding genome of splenic marginal zone lymphoma: Activation of NOTCH2 and other pathways regulating marginal zone development
by Rossi, Davide and Trifonov, Vladimir and Fangazio, Marco and Bruscaggin, Alessio and Rasi, Silvia and Spina, Valeria and Monti, Sara and Vaisitti, Tiziana and Arruga, Francesca and Famà, Rosella and Ciardullo, Carmela and Greco, Mariangela and Cresta, Stefania and Piranda, Daniela and Holmes, Antony and Fabbri, Giulia and Messina, Monica and Rinaldi, Andrea and Wang, Jiguang and Agostinelli, Claudio and Piccaluga, Pier Paolo and Lucioni, Marco and Tabbò, Fabrizio and Serra, Roberto and Franceschetti, Silvia and Deambrogi, Clara and Daniele, Giulia and Gattei, Valter and Marasca, Roberto and Facchetti, Fabio and Arcaini, Luca and Inghirami, Giorgio and Bertoni, Francesco and Pileri, Stefano A and Deaglio, Silvia and Foà, Robin and Dalla-Favera, Riccardo and Pasqualucci, Laura and Rabadan, Raul and Gaidano, Gianluca
Journal of Experimental Medicine, ISSN 0022-1007, 08/2012, Volume 209, Issue 9, pp. 1537 - 1551
Splenic marginal zone lymphoma (SMZL) is a B cell malignancy of unknown pathogenesis, and thus an orphan of targeted therapies. By integrating whole-exome... 
MEDICINE, RESEARCH & EXPERIMENTAL | B-CELL LYMPHOMA | HAJDU-CHENEY-SYNDROME | ACUTE LYMPHOBLASTIC-LEUKEMIA | GENES | TRANSCRIPTIONAL REPRESSION | CHRONIC LYMPHOCYTIC-LEUKEMIA | VILLOUS LYMPHOCYTES | SWAP-70 CONTROLS | OF-FUNCTION MUTATIONS | IMMUNOLOGY | SOMATIC MUTATIONS | Lymphoma, B-Cell - metabolism | Signal Transduction | Humans | Splenic Neoplasms - genetics | Gene Expression Regulation, Neoplastic | Receptor, Notch2 - metabolism | Chromatin Assembly and Disassembly | Receptor, Notch2 - genetics | Lymphoma, B-Cell - genetics | Homeodomain Proteins - genetics | Exome | Splenic Neoplasms - pathology | NF-kappa B - genetics | Lymphoma, B-Cell - pathology | Splenic Neoplasms - metabolism | Polymorphism, Single Nucleotide | B-Lymphocytes - pathology | Mutation | Nuclear Proteins - genetics | Receptor, Notch1 - genetics | B-Lymphocytes - metabolism | 304
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5. Full Text Mutations in NOTCH2 cause Hajdu-Cheney syndrome, a disorder of severe and progressive bone loss
by Simpson, Michael A and Irving, Melita D and Asilmaz, Esra and Gray, Mary J and Dafou, Dimitra and Elmslie, Frances V and Mansour, Sahar and Holder, Sue E and Brain, Caroline E and Burton, Barbara K and Kim, Katherine H and Pauli, Richard M and Aftimos, Salim and Stewart, Helen and Kim, Chong Ae and Holder-Espinasse, Muriel and Robertson, Stephen P and Drake, William M and Trembath, Richard C
Nature Genetics, ISSN 1061-4036, 2011, Volume 43, Issue 4, pp. 303 - 305
We used an exome-sequencing strategy and identified an allelic series of NOTCH2 mutations in Hajdu-Cheney syndrome, an autosomal dominant multisystem disorder... 
GENETICS & HEREDITY | Exons | Humans | DNA, Complementary - genetics | Mutant Proteins - genetics | Receptor, Notch2 - metabolism | Male | Mutant Proteins - metabolism | Receptor, Notch2 - genetics | Hajdu-Cheney Syndrome - metabolism | Hajdu-Cheney Syndrome - genetics | Hajdu-Cheney Syndrome - pathology | Protein Sorting Signals - genetics | DNA Mutational Analysis | Pedigree | Base Sequence | Alleles | Female | Mutation | Osteoporosis | Somatotropin | Care and treatment | Gene mutations | Physiological aspects | Genetic aspects | Research | Osteolysis | Health aspects | Risk factors | Studies | Medical research | Bone density | Genes
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6. Full Text Whole-genome sequencing identifies recurrent somatic NOTCH2 mutations in splenic marginal zone lymphoma
by Kiel, Mark J and Velusamy, Thirunavukkarasu and Betz, Bryan L and Zhao, Lili and Weigelin, Helmut G and Chiang, Mark Y and Huebner-Chan, David R and Bailey, Nathanael G and Yang, David T and Bhagat, Govind and Miranda, Roberto N and Bahler, David W and Jeffrey Medeiros, L and Lim, Megan S and Elenitoba-Johnson, Kojo S.J
Journal of Experimental Medicine, ISSN 0022-1007, 08/2012, Volume 209, Issue 9, pp. 1553 - 1565
Splenic marginal zone lymphoma (SMZL), the most common primary lymphoma of spleen, is poorly understood at the genetic level. In this study, using whole-genome... 
B-CELLS | INACTIVATION | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | SEL-10 | PATHWAY | CODING GENOME | SQUAMOUS-CELL CARCINOMA | DISORDER | CHRONIC LYMPHOCYTIC-LEUKEMIA | OF-FUNCTION MUTATIONS | IMMUNOLOGY | Protein Structure, Tertiary | Lymphoma, B-Cell - mortality | Humans | Lymphoma, B-Cell - diagnosis | Middle Aged | Splenic Neoplasms - genetics | Receptor, Notch2 - metabolism | Male | Receptor, Notch2 - genetics | Survival Rate | Splenic Neoplasms - diagnosis | Lymphoma, B-Cell - genetics | Sequence Analysis, DNA | Splenic Neoplasms - mortality | Female | Aged | Mutation | Genome, Human | 304
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7. Full Text C8orf4 negatively regulates self-renewal of liver cancer stem cells via suppression of NOTCH2 signalling
by Zhu, Pingping and Wang, Yanying and Du, Ying and He, Lei and Huang, Guanling and Zhang, Geng and Yan, Xinlong and Fan, Zusen
Nature Communications, ISSN 2041-1723, 05/2015, Volume 6, Issue 1, p. 7122
Liver cancer stem cells (CSCs) harbour self-renewal and differentiation properties, accounting for chemotherapy resistance and recurrence. However, the... 
TARGET | HEPATOCELLULAR-CARCINOMA | GENE | INTEGRATION | TC-1 | PATHWAY | MULTIDISCIPLINARY SCIENCES | GROWTH | IDENTIFICATION | TUMOR-INITIATING CELLS | PREDICTION | Protein Structure, Tertiary | Neoplasm Transplantation | Neoplastic Stem Cells - cytology | Prognosis | Signal Transduction | Humans | Neoplasm Proteins - physiology | Receptor, Notch2 - metabolism | Transcriptome | Cytoplasm - metabolism | Male | Receptor, Notch2 - genetics | Animals | Gene Deletion | HEK293 Cells | Liver Neoplasms - metabolism | Cell Line, Tumor | Mice | Mice, Inbred BALB C | Active Transport, Cell Nucleus | Green Fluorescent Proteins - chemistry | Neoplasm Proteins - genetics | Carcinoma, Hepatocellular - metabolism
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8. Full Text NOTCH2 Mutations Cause Alagille Syndrome, a Heterogeneous Disorder of the Notch Signaling Pathway
by McDaniell, Ryan and Warthen, Daniel M and Sanchez-Lara, Pedro A and Pai, Athma and Krantz, Ian D and Piccoli, David A and Spinner, Nancy B
The American Journal of Human Genetics, ISSN 0002-9297, 2006, Volume 79, Issue 1, pp. 169 - 173
Alagille syndrome (AGS) is caused by mutations in the gene for the Notch signaling pathway ligand Jagged1 ( ), which are found in 94% of patients. To identify... 
HEART | DEFECTS | GENE | ARTERIOHEPATIC DYSPLASIA | GENETICS & HEREDITY | RECEPTOR | LIGAND | EXPRESSION | HUMAN JAGGED1 | Alagille Syndrome - genetics | Signal Transduction | Pedigree | Humans | Receptor, Notch2 - metabolism | Female | Male | Receptor, Notch2 - genetics | Mutation | Genetic aspects | Diagnosis | Research | Gene mutations | Alagille syndrome | Report
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9. Full Text Notch2 is required for progression of pancreatic intraepithelial neoplasia and development of pancreatic ductal adenocarcinoma
by Pawel K. Mazur and Henrik Einwächter and Marcel Lee and Bence Sipos and Hassan Nakhai and Roland Rad and Ursula Zimber-Strobl and Lothar J. Strobl and Freddy Radtke and Günter Klöppel and Roland M. Schmid and Jens T. Siveke and Elliott Kieff
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2010, Volume 107, Issue 30, pp. 13438 - 13443
Pancreatic cancer is one of the most fatal malignancies lacking effective therapies. Notch signaling is a key regulator of cell fate specification and... 
Acinar cells | Developmental biology | Cell lines | Pancreatic cells | Mice | Lesions | Carcinogenesis | Pancreatic neoplasms | Tumors | Notch receptors | K-Ras | Genetically engineered mice | Myc | Pancreatic cancer | Notch | ACTIVATION | MULTIDISCIPLINARY SCIENCES | MOUSE | C-MYC | ADULT MICE | CANCER | EPITHELIAL-MESENCHYMAL TRANSITION | pancreatic cancer | SIGNALING PATHWAY | GROWTH | ACINAR-CELLS | EXPRESSION | genetically engineered mice | Immunohistochemistry | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Male | Receptor, Notch2 - genetics | Gene Expression Profiling | Carcinoma, Pancreatic Ductal - genetics | Adenocarcinoma - metabolism | Carcinoma in Situ - genetics | Female | Adenocarcinoma - genetics | Proto-Oncogene Proteins p21(ras) - metabolism | Signal Transduction | Carcinoma in Situ - pathology | Pancreatic Neoplasms - pathology | Kaplan-Meier Estimate | Receptor, Notch2 - metabolism | Pancreas - pathology | Pancreatic Neoplasms - genetics | Pancreas - metabolism | Receptor, Notch1 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Carcinoma, Pancreatic Ductal - pathology | Proto-Oncogene Proteins c-myc - metabolism | Blotting, Western | Disease Progression | Mice, Knockout | Animals | Cell Line, Tumor | Proto-Oncogene Proteins c-myc - genetics | Carcinoma in Situ - metabolism | Receptor, Notch1 - genetics | Biological Sciences
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10. Full Text Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis
by Isidor, Bertrand and Lindenbaum, Pierre and Pichon, Olivier and Bézieau, Stéphane and Dina, Christian and Jacquemont, Sébastien and Martin-Coignard, Dominique and Thauvin-Robinet, Christel and Le Merrer, Martine and Mandel, Jean-Louis and David, Albert and Faivre, Laurence and Cormier-Daire, Valérie and Redon, Richard and Le Caignec, Cédric
Nature Genetics, ISSN 1061-4036, 02/2011, Volume 43, Issue 4, pp. 306 - 308
Hajdu-Cheney syndrome is a rare autosomal dominant skeletal disorder with facial anomalies, osteoporosis and acro-osteolysis. We sequenced the exomes of six... 
OSTEOBLAST DIFFERENTIATION | ALAGILLE-SYNDROME | SIGNALING PATHWAY | GENETICS & HEREDITY | Rare Diseases - genetics | Frameshift Mutation | Exons | Humans | Middle Aged | Child, Preschool | Molecular Sequence Data | Male | Receptor, Notch2 - genetics | Hajdu-Cheney Syndrome - metabolism | Young Adult | Base Sequence | Adult | Female | Rare Diseases - pathology | Rare Diseases - metabolism | Amino Acid Sequence | Signal Transduction | Receptor, Notch2 - metabolism | Codon, Nonsense | DNA - genetics | Hajdu-Cheney Syndrome - genetics | Hajdu-Cheney Syndrome - pathology | Pedigree | Adolescent | Heterozygote | Mutation | Somatotropin | Osteoporosis | Care and treatment | Physiological aspects | Congenital heart disease | Genetic aspects | Research | Risk factors | Proteins | Genetics | Bone density
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11. Full Text Notch2 governs the rate of generation of mouse long- and short-term repopulating stem cells
by Varnum-Finney, Barbara and Halasz, Lia M and Sun, Mingyi and Gridley, Thomas and Radtke, Freddy and Bernstein, Irwin D
Journal of Clinical Investigation, ISSN 0021-9738, 03/2011, Volume 121, Issue 3, pp. 1207 - 1216
HSCs either self-renew or differentiate to give rise to multipotent cells whose progeny provide blood cell precursors. However, surprisingly little is known... 
PROGENITOR CELLS | B-CELLS | DELTA1 | MEDICINE, RESEARCH & EXPERIMENTAL | B1B CELLS | SIDE POPULATION | IN-VIVO | SELF-RENEWAL | JAGGED1 | FATE | PRECURSORS | Signal Transduction | Bone Marrow Cells - cytology | Cells, Cultured | Receptor, Notch2 - metabolism | Mice, Transgenic | Stem Cells - cytology | Receptor, Notch1 - metabolism | Regeneration | Animals | Microscopy, Fluorescence - methods | Ligands | Cell Differentiation | Mice | Physiological aspects | Cellular signal transduction | Research | Cell differentiation | Stem cells
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12. Full Text Liver‐specific inactivation of Notch2, but not Notch1, compromises intrahepatic bile duct development in mice
by Geisler, Fabian and Nagl, Florian and Mazur, Pawel K and Lee, Marcel and Zimber‐Strobl, Ursula and Strobl, Lothar J and Radtke, Freddy and Schmid, Roland M and Siveke, Jens T
Hepatology, ISSN 0270-9139, 08/2008, Volume 48, Issue 2, pp. 607 - 616
The Notch pathway is an evolutionary conserved, intercellular signaling pathway that plays an important role in cell fate specification and the embryonic... 
CELLS | BILIARY TREE | ALAGILLE-SYNDROME | GENE | PROLIFERATION | DIFFERENTIATION | MUTATIONS | MOUSE HEPATOCYTES | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | HUMAN JAGGED1 | Animals, Newborn | Severity of Illness Index | Bile Ducts, Intrahepatic - pathology | Liver - pathology | Liver - metabolism | Receptor, Notch2 - metabolism | Hepatocytes - pathology | Mice, Transgenic | Receptor, Notch2 - genetics | Gene Dosage | Bile Ducts, Intrahepatic - growth & development | Receptor, Notch1 - metabolism | Liver - growth & development | Mice, Knockout | Animals | Bile Ducts, Intrahepatic - metabolism | Fibrosis | Bile Ducts, Intrahepatic - abnormalities | Mice | Receptor, Notch1 - genetics
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13. Full Text Regulated Proteolysis of NOTCH2 and NOTCH3 Receptors by ADAM10 and Presenilins
by Groot, Arjan J and Habets, Roger and Yahyanejad, Sanaz and Hodin, Caroline M and Reiss, Karina and Saftig, Paul and Theys, Jan and Vooijs, Marc
Molecular and Cellular Biology, ISSN 0270-7306, 08/2014, Volume 34, Issue 15, pp. 2822 - 2832
In mammals, there are four NOTCH receptors and five Delta-Jagged-type ligands regulating many aspects of embryonic development and adult tissue homeostasis.... 
GROWTH-FACTOR RECEPTOR | STEM-CELLS | ACTIVATION | SIGNALING PATHWAY | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | NECROSIS-FACTOR-ALPHA | MUTATIONS | CLEAVAGE | AORTIC-VALVE DISEASE | INTRACELLULAR DOMAIN | CELL BIOLOGY | ADAM17 Protein | Cell Line | NIH 3T3 Cells | Receptors, Notch - metabolism | Humans | Receptor, Notch2 - metabolism | Presenilin-2 - metabolism | Metalloproteases - metabolism | ADAM Proteins - metabolism | Amyloid Precursor Protein Secretases - metabolism | Animals | Proteolysis | Presenilin-1 - metabolism | HEK293 Cells | Membrane Proteins - metabolism | Mice
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14. Full Text Notch2 controls non-autonomous Wnt-signalling in chronic lymphocytic leukaemia
by Mangolini, Maurizio and Götte, Frederik and Moore, Andrew and Ammon, Tim and Oelsner, Madlen and Lutzny-Geier, Gloria and Klein-Hitpass, Ludger and Williamson, James C and Lehner, Paul J and Dürig, Jan and Möllmann, Michael and Rásó-Barnett, Lívia and Hughes, Katherine and Santoro, Antonella and Méndez-Ferrer, Simón and Oostendorp, Robert A. J and Zimber-Strobl, Ursula and Peschel, Christian and Hodson, Daniel J and Schmidt-Supprian, Marc and Ringshausen, Ingo
Nature Communications, ISSN 2041-1723, 12/2018, Volume 9, Issue 1, pp. 3839 - 17
The Wnt signalling pathway, one of the core de-regulated pathways in chronic lymphocytic leukaemia (CLL), is activated in only a subset of patients through... 
ACTIVATION | CLL | PATHWAY | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | IN-VIVO | DISEASE | MOUSE | STROMAL CELLS | CANCER | BETA | Cell Line | Animals | Receptor Cross-Talk | Humans | Leukemia, Lymphocytic, Chronic, B-Cell - metabolism | Receptor, Notch2 - metabolism | Mice | Mesenchymal Stem Cells - metabolism | beta Catenin - metabolism | Bone Marrow Cells - metabolism | Wnt Signaling Pathway | Cellular Reprogramming | Chronic lymphatic leukemia | Cell survival | Wnt protein | Mesenchyme | Leukemia | Activation | Pharmacology | Cadherin | Survival | β-catenin | Complement component C1q | Signaling | Signal transduction | Cell activation | N-Cadherin | Lymphocytes B | Stromal cells | Inhibition | Mutation | Tumors
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