Ignet

Gene Information

Gene symbol: NOTCH2

Gene name: notch 2

HGNC ID: 7882

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	DLL1	1 hits
3	JAG1	1 hits
4	MAFB	1 hits
5	MIRN98	1 hits
6	NOTCH1	1 hits
7	PLAT	1 hits
8	POFUT1	1 hits
9	RBPJ	1 hits

Related Sentences

#	PMID	Sentence
1	17229764	Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron.
2	17229764	Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process.
3	17229764	Notch1 and Notch2 are detected in the early renal vesicle.
4	17229764	Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors.
5	17229764	The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus.
6	17229764	Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron.
7	17229764	Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process.
8	17229764	Notch1 and Notch2 are detected in the early renal vesicle.
9	17229764	Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors.
10	17229764	The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus.
11	17229764	Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron.
12	17229764	Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process.
13	17229764	Notch1 and Notch2 are detected in the early renal vesicle.
14	17229764	Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors.
15	17229764	The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus.
16	17229764	Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron.
17	17229764	Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process.
18	17229764	Notch1 and Notch2 are detected in the early renal vesicle.
19	17229764	Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors.
20	17229764	The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus.
21	17229764	Notch2, but not Notch1, is required for proximal fate acquisition in the mammalian nephron.
22	17229764	Here we report that Notch2 acts non-redundantly to control the processes of nephron segmentation through an Rbp-J-dependent process.
23	17229764	Notch1 and Notch2 are detected in the early renal vesicle.
24	17229764	Genetic analysis reveals that only Notch2 is required for the differentiation of proximal nephron structures (podocytes and proximal convoluted tubules) despite the presence of activated Notch1 in the nuclei of putative proximal progenitors.
25	17229764	The inability of endogenous Notch1 to compensate for Notch2 deficiency may reflect sub-threshold Notch1 levels in the nucleus.
26	20531454	Here we analyzed the degree of expression and localization of Notch ligands (Jagged1 and Delta1) and activated (cleaved) receptors (Notch1 and Notch2) in healthy human kidneys and in renal biopsies from a wide variety of kidney diseases.
27	20531454	We found that cleaved Notch1, Notch2, and Jagged1 are expressed on podocytes in proteinuric nephropathies and their level of expression correlated with the amount of proteinuria across all disease groups.
28	20531454	Here we analyzed the degree of expression and localization of Notch ligands (Jagged1 and Delta1) and activated (cleaved) receptors (Notch1 and Notch2) in healthy human kidneys and in renal biopsies from a wide variety of kidney diseases.
29	20531454	We found that cleaved Notch1, Notch2, and Jagged1 are expressed on podocytes in proteinuric nephropathies and their level of expression correlated with the amount of proteinuria across all disease groups.
30	23752887	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.
31	23752887	The role of NOTCH2 and JAG1 in formation of proximal nephron structures and podocytes might explain the observed phenotypes of renal dysplasia and proteinuria in patients with Alagille syndrome, and renal tubular acidosis may be the result of JAG1 expression in the collecting ducts.
32	23752887	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.
33	23752887	The role of NOTCH2 and JAG1 in formation of proximal nephron structures and podocytes might explain the observed phenotypes of renal dysplasia and proteinuria in patients with Alagille syndrome, and renal tubular acidosis may be the result of JAG1 expression in the collecting ducts.
34	23806616	Notch2, but not Notch1, plays indispensable roles in kidney organogenesis, and Notch2 haploinsufficiency is associated with Alagille syndrome.
35	23806616	We proposed that proximal nephron fates are regulated by a threshold that requires nearly all available free Notch intracellular domains (NICDs) but could not identify the mechanism that explains why Notch2 (N2) is more important than Notch1 (N1).
36	23806616	Notch2, but not Notch1, plays indispensable roles in kidney organogenesis, and Notch2 haploinsufficiency is associated with Alagille syndrome.
37	23806616	We proposed that proximal nephron fates are regulated by a threshold that requires nearly all available free Notch intracellular domains (NICDs) but could not identify the mechanism that explains why Notch2 (N2) is more important than Notch1 (N1).
38	24526233	Activation of Notch1 and Notch2 has been recently implicated in human glomerular diseases.
39	24526233	In vitro, the specific knockdown of Notch2 increases apoptosis in damaged podocytes, while Notch2 agonistic antibodies enhance activation of Akt and protect damaged podocytes from apoptosis.
40	24526233	Treatment with triciribine, an inhibitor of Akt pathway, abolishes the protective effect of the Notch2 agonistic antibody.
41	24526233	Activation of Notch1 and Notch2 has been recently implicated in human glomerular diseases.
42	24526233	In vitro, the specific knockdown of Notch2 increases apoptosis in damaged podocytes, while Notch2 agonistic antibodies enhance activation of Akt and protect damaged podocytes from apoptosis.
43	24526233	Treatment with triciribine, an inhibitor of Akt pathway, abolishes the protective effect of the Notch2 agonistic antibody.
44	24526233	Activation of Notch1 and Notch2 has been recently implicated in human glomerular diseases.
45	24526233	In vitro, the specific knockdown of Notch2 increases apoptosis in damaged podocytes, while Notch2 agonistic antibodies enhance activation of Akt and protect damaged podocytes from apoptosis.
46	24526233	Treatment with triciribine, an inhibitor of Akt pathway, abolishes the protective effect of the Notch2 agonistic antibody.
47	24722438	In this study, we generated transgenic mice that overexpress Mafb in podocytes using the nephrin promoter/enhancer.
48	24722438	Moreover, hyperglycemia-induced downregulation of Nephrin was mitigated in diabetic Mafb transgenic mice, and reporter assay results suggested that Mafb regulates Nephrin directly.
49	24722438	Finally, Notch2 expression increased in diabetic glomeruli, and this effect was enhanced in diabetic Mafb transgenic glomeruli.
50	26293507	Notch1 and Notch2 in Podocytes Play Differential Roles During Diabetic Nephropathy Development.
51	26293507	Here, we report that conditional deletion of Notch1 in podocytes using NPHS2(cre)Notch1(flox/flox) animals resulted in marked amelioration of DKD.
52	26293507	Deletion of Notch1 in podocytes also resulted in an increase in Notch2 expression, indicating an interaction between the receptors.
53	26293507	At the same time, transgenic overexpression of Notch2 in podocytes did not induce phenotypic changes, while constitutive expression of Notch1 caused rapid development of albuminuria and glomerulosclerosis.
54	26293507	Notch1 and Notch2 in Podocytes Play Differential Roles During Diabetic Nephropathy Development.
55	26293507	Here, we report that conditional deletion of Notch1 in podocytes using NPHS2(cre)Notch1(flox/flox) animals resulted in marked amelioration of DKD.
56	26293507	Deletion of Notch1 in podocytes also resulted in an increase in Notch2 expression, indicating an interaction between the receptors.
57	26293507	At the same time, transgenic overexpression of Notch2 in podocytes did not induce phenotypic changes, while constitutive expression of Notch1 caused rapid development of albuminuria and glomerulosclerosis.
58	26293507	Notch1 and Notch2 in Podocytes Play Differential Roles During Diabetic Nephropathy Development.
59	26293507	Here, we report that conditional deletion of Notch1 in podocytes using NPHS2(cre)Notch1(flox/flox) animals resulted in marked amelioration of DKD.
60	26293507	Deletion of Notch1 in podocytes also resulted in an increase in Notch2 expression, indicating an interaction between the receptors.
61	26293507	At the same time, transgenic overexpression of Notch2 in podocytes did not induce phenotypic changes, while constitutive expression of Notch1 caused rapid development of albuminuria and glomerulosclerosis.
62	27185860	We examined the renal phenotype of newborn compound mutant mice carrying only one allele of Par1a or Par1b.
63	27185860	Furthermore, Par1a/b mutants expressed low levels of renal Notch ligand Jag1, activated Notch2, and Notch effecter Hes1.
64	32509213	Pofut1 gene encodes a O-fucosyltransferase that adds fucose to the serine/threonine residue in the sequence of C²XXXX(S/T)C³ of EGF-like domain in a protein.
65	32509213	O-fucosylation has been shown to be required for some EGF-like domain-containing proteins to function, e.g., Notch1, and POFUT1 deficiency could affect cellular function and cause diseases.
66	32509213	To understand why POFUT1 is dispensable for podocytes, we searched mouse podocyte essential gene candidates (as determined by single-cell RNA-seq) and found only two POFUT1 substrates, NOTCH2 and tPA.
67	34649592	CDKN2B-AS1 participates in high glucose-induced apoptosis and fibrosis via NOTCH2 through functioning as a miR-98-5p decoy in human podocytes and renal tubular cells.