Ignet

Gene Information

Gene symbol: NOTCH1

Gene name: notch 1

HGNC ID: 7881

Related Genes

#	Gene Symbol	Number of hits
1	AKT1	1 hits
2	ANPEP	1 hits
3	APOB	1 hits
4	BECN1	1 hits
5	CASP3	1 hits
6	CD28	1 hits
7	CD34	1 hits
8	CD40	1 hits
9	CD44	1 hits
10	CDC34	1 hits
11	CDKN2A	1 hits
12	DNMT3A	1 hits
13	DNMT3B	1 hits
14	EPOR	1 hits
15	EZH2	1 hits
16	FGF10	1 hits
17	FOXO1	1 hits
18	FRAP1	1 hits
19	GSK3B	1 hits
20	HES1	1 hits
21	HEY1	1 hits
22	HEY2	1 hits
23	IGF1R	1 hits
24	ING1	1 hits
25	INS	1 hits
26	JAG1	1 hits
27	JAG2	1 hits
28	MIRNLET7B	1 hits
29	MSX2	1 hits
30	MYC	1 hits
31	NANOG	1 hits
32	NEDD4	1 hits
33	NOTCH2	1 hits
34	PARP1	1 hits
35	POU5F1	1 hits
36	PPARG	1 hits
37	PPARGC1A	1 hits
38	RBPJ	1 hits
39	SCD	1 hits
40	SIRT1	1 hits
41	SLC37A4	1 hits
42	SMAD4	1 hits
43	TACSTD1	1 hits
44	TNFRSF11B	1 hits
45	TP53	1 hits
46	TRDMT1	1 hits
47	UCP2	1 hits
48	UCP3	1 hits
49	VEGFA	1 hits
50	ZMPSTE24	1 hits

Related Sentences

#	PMID	Sentence
1	12181058	To assess whether the cells with EPO inducement could respond at this point to G-CSF signal, or vice versa, the EPO-stimulated population was re-grown with G-CSF, constituting 95.2% myeloid, of 5075-fold, cells after 14 d of re-culture.
2	12181058	Conversely, reculture of the G-CSF-stimulated population with EPO resulted in a 4083-fold growth with 81.4% erythroid cells.
3	12181058	Analysis of primitive markers, CD34 and Notch1, or lineage markers, EPO-R and CD13, by single-cell reverse transcription polymerase chain reaction showed that individual colonies of 2-16 cells contained at least one CD34-positive cell with expression ofNotch1 and co-expression of EPO-R and CD13 appeared on either CD34-positive or CD34-negative cells.
4	14651921	In the pancreas, mesenchymal FGF10 is required to maintain the Pdx1-expressing epithelial progenitor cell population, and in the absence of FGF10 signaling, these cells fail to proliferate.
5	14651921	A hyperplastic pancreas consisting of undifferentiated cells expressing Pdx1, Nkx6.1, and cell adhesion markers normally characterizing early pancreatic progenitor cells resulted.
6	14651921	The FGF10-positive pancreatic cells expressed Notch1 and Notch2, the Notch-ligand genes Jagged1 and Jagged2, as well as the Notch target gene Hes1.
7	15084270	Coligation of Notch 1 together with TCR and CD28 resulted in a dramatic inhibition of T cell activation, proliferation, and cytokine production.
8	15084270	This effect was dependent on presenilin activity and induced the expression of HES-1, suggestive of Notch 1 signaling.
9	15084270	Biochemical analysis demonstrated an inhibition of AKT and GSK3beta phosphorylation following Notch 1 engagement while other biochemical signals such as TCR and ERK phosphorylation remained intact.
10	15084270	Coligation of Notch 1 together with TCR and CD28 resulted in a dramatic inhibition of T cell activation, proliferation, and cytokine production.
11	15084270	This effect was dependent on presenilin activity and induced the expression of HES-1, suggestive of Notch 1 signaling.
12	15084270	Biochemical analysis demonstrated an inhibition of AKT and GSK3beta phosphorylation following Notch 1 engagement while other biochemical signals such as TCR and ERK phosphorylation remained intact.
13	15084270	Coligation of Notch 1 together with TCR and CD28 resulted in a dramatic inhibition of T cell activation, proliferation, and cytokine production.
14	15084270	This effect was dependent on presenilin activity and induced the expression of HES-1, suggestive of Notch 1 signaling.
15	15084270	Biochemical analysis demonstrated an inhibition of AKT and GSK3beta phosphorylation following Notch 1 engagement while other biochemical signals such as TCR and ERK phosphorylation remained intact.
16	17003479	We demonstrate that under these experimental conditions the exocrine acinar cells lose their differentiated characteristics: expression of the acinar transcription factors p48/Ptf1alpha and Mist1 is decreased or lost, whereas expression of the embryonic transcription factor Pdx1 is increased.
17	17003479	The receptors Notch1 and Notch2, members of the DSL family of Notch ligands, and the target genes in the Notch-signaling pathway Hes1, Hey1, and Hey2 become strongly up-regulated.
18	17003479	This effect seems to be Hes1-independent and mainly coincides with decreased Hey1 and Hey2 mRNA expression.
19	17172638	The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension.
20	17172638	There are no focused studies in muscle on the ubiquitin ligase Nedd4.
21	17172638	This increase was strongly correlated with decreased Notch1 expression, a known target of Nedd4 in other cell types.
22	17172638	Overexpression of dominant negative Nedd4 in soleus muscles completely reversed the unloading-induced decrease of Notch1 expression, indicating that Nedd4 is required for Notch1 inactivation.
23	17172638	Overexpression of wild-type Nedd4 in soleus muscles of weight bearing rats caused a decrease in Notch1 protein, indicating that Nedd4 is sufficient for Notch1 down-regulation.
24	17172638	To further show that Notch1 is a Nedd4 substrate in muscle, conditional overexpression of Nedd4 in C2C12 myotubes induced ubiquitination of Notch1.
25	17172638	This is the first finding of a Nedd4 substrate in muscle and of an ubiquitin ligase, the activity of which distinguishes disuse from cachexia atrophy.
26	17172638	The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension.
27	17172638	There are no focused studies in muscle on the ubiquitin ligase Nedd4.
28	17172638	This increase was strongly correlated with decreased Notch1 expression, a known target of Nedd4 in other cell types.
29	17172638	Overexpression of dominant negative Nedd4 in soleus muscles completely reversed the unloading-induced decrease of Notch1 expression, indicating that Nedd4 is required for Notch1 inactivation.
30	17172638	Overexpression of wild-type Nedd4 in soleus muscles of weight bearing rats caused a decrease in Notch1 protein, indicating that Nedd4 is sufficient for Notch1 down-regulation.
31	17172638	To further show that Notch1 is a Nedd4 substrate in muscle, conditional overexpression of Nedd4 in C2C12 myotubes induced ubiquitination of Notch1.
32	17172638	This is the first finding of a Nedd4 substrate in muscle and of an ubiquitin ligase, the activity of which distinguishes disuse from cachexia atrophy.
33	17172638	The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension.
34	17172638	There are no focused studies in muscle on the ubiquitin ligase Nedd4.
35	17172638	This increase was strongly correlated with decreased Notch1 expression, a known target of Nedd4 in other cell types.
36	17172638	Overexpression of dominant negative Nedd4 in soleus muscles completely reversed the unloading-induced decrease of Notch1 expression, indicating that Nedd4 is required for Notch1 inactivation.
37	17172638	Overexpression of wild-type Nedd4 in soleus muscles of weight bearing rats caused a decrease in Notch1 protein, indicating that Nedd4 is sufficient for Notch1 down-regulation.
38	17172638	To further show that Notch1 is a Nedd4 substrate in muscle, conditional overexpression of Nedd4 in C2C12 myotubes induced ubiquitination of Notch1.
39	17172638	This is the first finding of a Nedd4 substrate in muscle and of an ubiquitin ligase, the activity of which distinguishes disuse from cachexia atrophy.
40	17172638	The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension.
41	17172638	There are no focused studies in muscle on the ubiquitin ligase Nedd4.
42	17172638	This increase was strongly correlated with decreased Notch1 expression, a known target of Nedd4 in other cell types.
43	17172638	Overexpression of dominant negative Nedd4 in soleus muscles completely reversed the unloading-induced decrease of Notch1 expression, indicating that Nedd4 is required for Notch1 inactivation.
44	17172638	Overexpression of wild-type Nedd4 in soleus muscles of weight bearing rats caused a decrease in Notch1 protein, indicating that Nedd4 is sufficient for Notch1 down-regulation.
45	17172638	To further show that Notch1 is a Nedd4 substrate in muscle, conditional overexpression of Nedd4 in C2C12 myotubes induced ubiquitination of Notch1.
46	17172638	This is the first finding of a Nedd4 substrate in muscle and of an ubiquitin ligase, the activity of which distinguishes disuse from cachexia atrophy.
47	17172638	The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension.
48	17172638	There are no focused studies in muscle on the ubiquitin ligase Nedd4.
49	17172638	This increase was strongly correlated with decreased Notch1 expression, a known target of Nedd4 in other cell types.
50	17172638	Overexpression of dominant negative Nedd4 in soleus muscles completely reversed the unloading-induced decrease of Notch1 expression, indicating that Nedd4 is required for Notch1 inactivation.
51	17172638	Overexpression of wild-type Nedd4 in soleus muscles of weight bearing rats caused a decrease in Notch1 protein, indicating that Nedd4 is sufficient for Notch1 down-regulation.
52	17172638	To further show that Notch1 is a Nedd4 substrate in muscle, conditional overexpression of Nedd4 in C2C12 myotubes induced ubiquitination of Notch1.
53	17172638	This is the first finding of a Nedd4 substrate in muscle and of an ubiquitin ligase, the activity of which distinguishes disuse from cachexia atrophy.
54	19680556	We re-sequenced all exons, intron-exon boundaries and selected conserved non-coding sequences of candidate genes involved in aging-related processes, including dietary restriction (PPARG, PPARGC1A, SIRT1, SIRT3, UCP2, UCP3), metabolism (IGF1R, APOB, SCD), autophagy (BECN1, FRAP1), stem cell activation (NOTCH1, DLL1), tumor suppression (TP53, CDKN2A, ING1), DNA methylation (TRDMT1, DNMT3A, DNMT3B) Progeria syndromes (LMNA, ZMPSTE24, KL) and stress response (CRYAB, HSPB2).
55	19901970	The absence of Smad4 in a Pten-mutant background enhanced cell proliferation and triggered transdifferentiation from acinar, centroacinar and islet cells, accompanied by activation of Notch1 signaling.
56	20522599	Modulation of notch-1 signaling alleviates vascular endothelial growth factor-mediated diabetic nephropathy.
57	21494254	With confirmation using RNA and protein analyses, GSI-I blocked nuclear accumulation of cleaved Notch1 and Notch2, and inhibited Notch targets Hey2 and Myc.
58	21804540	Combined haploinsufficiency of FoxO1 and Notch1 markedly raises insulin sensitivity in diet-induced insulin resistance, as does liver-specific knockout of the Notch transcriptional effector Rbp-Jκ.
59	21804540	Conversely, Notch1 gain-of-function promotes insulin resistance in a FoxO1-dependent manner and induces glucose-6-phosphatase expression.
60	21804540	Combined haploinsufficiency of FoxO1 and Notch1 markedly raises insulin sensitivity in diet-induced insulin resistance, as does liver-specific knockout of the Notch transcriptional effector Rbp-Jκ.
61	21804540	Conversely, Notch1 gain-of-function promotes insulin resistance in a FoxO1-dependent manner and induces glucose-6-phosphatase expression.
62	21813561	We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt.
63	21813561	The results of Notch1 overexpression and knockdown indicated that Notch1 signaling participated in the interaction of PARP and p50, and inhibited PARP- and p50-mediated apoptosis directly.
64	21813561	Thus, our study demonstrated that Notch1 signaling protects cells from PARP- and NF-κB-induced apoptosis under high glucose through the activation of Akt.
65	21813561	We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt.
66	21813561	The results of Notch1 overexpression and knockdown indicated that Notch1 signaling participated in the interaction of PARP and p50, and inhibited PARP- and p50-mediated apoptosis directly.
67	21813561	Thus, our study demonstrated that Notch1 signaling protects cells from PARP- and NF-κB-induced apoptosis under high glucose through the activation of Akt.
68	21813561	We found that apoptosis was increased in both STZ-induced diabetic mice and high-glucose-treated HRVECs, which was due to increased activation of PARP, cleaved caspase3, and reduced expression of Notch1 and p-Akt.
69	21813561	The results of Notch1 overexpression and knockdown indicated that Notch1 signaling participated in the interaction of PARP and p50, and inhibited PARP- and p50-mediated apoptosis directly.
70	21813561	Thus, our study demonstrated that Notch1 signaling protects cells from PARP- and NF-κB-induced apoptosis under high glucose through the activation of Akt.
71	22086681	Metformin also decreased the expression of CSC markers,CD44, EpCAM,EZH2, Notch-1, Nanog and Oct4, and caused reexpression of miRNAs (let-7a,let-7b, miR-26a, miR-101, miR-200b, and miR-200c) that are typically lost in pancreatic cancer and especially in pancreatospheres.
72	22086681	We also found that reexpression of miR-26a by transfection led to decreased expression of EZH2 and EpCAM in pancreatic cancer cells.
73	23874840	Osteoprotegerin inhibits calcification of vascular smooth muscle cell via down regulation of the Notch1-RBP-Jκ/Msx2 signaling pathway.