Ignet

Gene Information

Gene symbol: NRP1

Gene name: neuropilin 1

HGNC ID: 8004

Synonyms: NRP, VEGF165R, CD304

Related Genes

#	Gene Symbol	Number of hits
1	CD40	1 hits
2	CDKN1B	1 hits
3	DICER1	1 hits
4	EPO	1 hits
5	FLT1	1 hits
6	HLA-B	1 hits
7	IKZF2	1 hits
8	KDR	1 hits
9	PDGFA	1 hits
10	PDGFC	1 hits
11	PGF	1 hits
12	PSMD9	1 hits
13	RBL2	1 hits
14	THBS1	1 hits
15	VEGFA	1 hits
16	VEGFB	1 hits

Related Sentences

#	PMID	Sentence
1	10845581	Coexpression of VEGF receptors VEGF-R2 and neuropilin-1 in proliferative diabetic retinopathy.
2	11297552	Platelet-derived growth factor C (PDGF-C), a novel growth factor that binds to PDGF alpha and beta receptor.
3	11297552	We have characterized platelet-derived growth factor (PDGF) C, a novel growth factor belonging to the PDGF family.
4	11297552	PDGF-C is a multidomain protein with the N-terminal region homologous to the extracellular CUB domain of neuropilin-1, and the C-terminal region consists of a growth factor domain (GFD) with homology to vascular endothelial growth factor (25%) and PDGF A-chain (23%).
5	11297552	Competition binding and immunoprecipitation studies on cells bearing both PDGF alpha and beta receptors reveal a high affinity binding of recombinant GFD (PDGF-CC) to PDGF receptor-alpha homodimers and PDGF receptor-alpha/beta heterodimers.
6	11297552	Together, these studies describe a third member of the PDGF family (PDGF-C) as a potent mitogen for cells of mesenchymal origin in in vitro and in vivo systems with a binding pattern similar to PDGF-AB.
7	16816123	For example, levels of proangiogenic VEGF-A, VEGF-B, neuropilin-1, VEGFR-1, and VEGFR-2 were reduced and the levels of antiangiogenic thrombospondin-1 and retinoblastoma like-2 were increased.
8	17402563	We found that retinal vascular cells have a characteristic pattern in VEGF receptor expression, which causes vascular pathology more frequently in the retina than in other organs.
9	17402563	Neuropilin 1 (NRP 1), which enhances VEGF receptor function, is abundantly expressed in the retinal endothelial cells and is upregulated by VEGF itself and by hypoxia to regulate a positive feedback mechanism in retinal neovascularization.
10	17402563	Finally, we found that erythropoietin is an ischemia-induced angiogenic factor that acts independently and as potently as VEGF in proliferative diabetic retinopathy (PDR).
11	18725525	Dicer-deficient T reg lineage cells failed to remain stable, as a subset of cells down-regulated the T reg cell-specific transcription factor FoxP3, whereas the majority expressed altered levels of multiple genes and proteins (including Neuropilin 1, glucocorticoid-induced tumor necrosis factor receptor, and cytotoxic T lymphocyte antigen 4) associated with the T reg cell fingerprint.
12	18725525	In fact, a significant percentage of the T reg lineage cells took on a T helper cell memory phenotype including increased levels of CD127, interleukin 4, and interferon gamma.
13	19782046	We previously showed that EOC cells employ an autocrine VEGF/VEGFR2 signaling loop.
14	19782046	Glucose (but not pyruvate) deprivation induced significant increase in VEGF transcription and secretion, but a rapid reduction in VEGFR2 protein synthesis and glycosylation, combined with a reduction in co-receptor neuropilin-1 (NRP-1) protein levels.
15	19782046	In contrast, mRNA for KDR and NRP-1 was increased upon glucose depletion suggesting a mechanism of feed back upon protein reduction.
16	19782046	The addition of the proteosome inhibitor epoxomycin restored VEGFR2 under glucose free conditions, suggesting degradation as the main mechanism of VEGFR2 reduction and transcriptional activation through the unfolded protein response (UPR) which was activated in glucose-starved cells through the upregulation of the Endoplasmic reticulum chaperon GRP-78.
17	19782046	Our finding that glucose can regulate VEGF/VEGFR2 levels suggests that initiation and/or progression of ovarian surface epithelial cells towards a neoplastic phenotype might be modulated by dietary conditions, and that a patient's metabolic status may alter the effectiveness of the known anti-angiogenic therapies.
18	19782046	We previously showed that EOC cells employ an autocrine VEGF/VEGFR2 signaling loop.
19	19782046	Glucose (but not pyruvate) deprivation induced significant increase in VEGF transcription and secretion, but a rapid reduction in VEGFR2 protein synthesis and glycosylation, combined with a reduction in co-receptor neuropilin-1 (NRP-1) protein levels.
20	19782046	In contrast, mRNA for KDR and NRP-1 was increased upon glucose depletion suggesting a mechanism of feed back upon protein reduction.
21	19782046	The addition of the proteosome inhibitor epoxomycin restored VEGFR2 under glucose free conditions, suggesting degradation as the main mechanism of VEGFR2 reduction and transcriptional activation through the unfolded protein response (UPR) which was activated in glucose-starved cells through the upregulation of the Endoplasmic reticulum chaperon GRP-78.
22	19782046	Our finding that glucose can regulate VEGF/VEGFR2 levels suggests that initiation and/or progression of ovarian surface epithelial cells towards a neoplastic phenotype might be modulated by dietary conditions, and that a patient's metabolic status may alter the effectiveness of the known anti-angiogenic therapies.
23	20228789	This regulation was mediated by VEGF receptor 1 and neuropilin 1 expressed by the endothelium.
24	21056561	Placental growth factor-2 (PlGF-2) exhibits neurotrophic activity in dorsal root ganglion (DRG) neurons through the neuropilin-1 (NP-1) receptor in vitro.
25	21056561	In addition, we overexpressed PlGF-1, an isoform of PlGF that does not bind NP-1.
26	21056561	These findings suggest that PlGF-2 electro-gene therapy can significantly ameliorate sensory deficits (i.e. hypoalgesia) in diabetic mice through NP-1 in DRG and peripheral nerves.
27	21056561	Placental growth factor-2 (PlGF-2) exhibits neurotrophic activity in dorsal root ganglion (DRG) neurons through the neuropilin-1 (NP-1) receptor in vitro.
28	21056561	In addition, we overexpressed PlGF-1, an isoform of PlGF that does not bind NP-1.
29	21056561	These findings suggest that PlGF-2 electro-gene therapy can significantly ameliorate sensory deficits (i.e. hypoalgesia) in diabetic mice through NP-1 in DRG and peripheral nerves.
30	21056561	Placental growth factor-2 (PlGF-2) exhibits neurotrophic activity in dorsal root ganglion (DRG) neurons through the neuropilin-1 (NP-1) receptor in vitro.
31	21056561	In addition, we overexpressed PlGF-1, an isoform of PlGF that does not bind NP-1.
32	21056561	These findings suggest that PlGF-2 electro-gene therapy can significantly ameliorate sensory deficits (i.e. hypoalgesia) in diabetic mice through NP-1 in DRG and peripheral nerves.
33	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
34	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
35	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
36	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
37	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
38	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
39	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
40	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
41	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
42	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
43	23825071	The pathophysiology of AGE-challenged podocytes, such as hypertrophy, apoptosis, and reduced cell migration, is closely related to the induction of the cell cycle inhibitor p27(Kip1) and to the inhibition of neuropilin 1 (NRP1).
44	23825071	We have previously demonstrated that treatment with erythropoietin is associated with protective effects for podocytes in vitro. db/db mice with overt DN aged 15-16 wk were treated with either placebo, epoetin-β, or continuous erythropoietin receptor activator (CERA) for 2 wk. db/db mice compared with nondiabetic db/m control mice revealed the expected increases in body weight, blood glucose, albumin-to-creatinine ratio, and AGE accumulation.
45	23825071	However, the albumin-to-creatinine ratio was significantly lower in db/db mice treated with epoetin-β or CERA.
46	23825071	Induction of p27(Kip1) and suppression of NRP1 were significantly reduced in the epoetin-β treatment group versus the CERA treatment group.
47	23825071	Together, independently from hematopoetic effects, epoetin-β or CERA treatment was associated with protective changes in DN, especially that NRP1 and p27(Kip1) expressions as well as numbers of podocytes returned to normal levels.
48	23966994	We describe the recent discovery of unique cell surface markers and transcription factors (including Neuropilin-1 and Helios) that can be used to distinguish tTreg and pTreg subsets in vivo.