Ignet

Gene Information

Gene symbol: NPHS1

Gene name: nephrosis 1, congenital, Finnish type (nephrin)

HGNC ID: 7908

Synonyms: CNF, NPHN

Related Genes

#	Gene Symbol	Number of hits
1	ACE	1 hits
2	ACTN4	1 hits
3	AGT	1 hits
4	CD2	1 hits
5	CD2AP	1 hits
6	CD79A	1 hits
7	CDH3	1 hits
8	KIRREL	1 hits
9	NPHS2	1 hits
10	PRKCA	1 hits
11	PTPRO	1 hits
12	TJP1	1 hits
13	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
2	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
3	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
4	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
5	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
6	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
7	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
8	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
9	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
10	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
11	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
12	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
13	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
14	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
15	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
16	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
17	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
18	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
19	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
20	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
21	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
22	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
23	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
24	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
25	10997929	CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
26	10997929	CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
27	10997929	Mice lacking CD2AP exhibit a congenital nephrotic syndrome characterized by extensive foot process effacement, suggesting that CD2AP-nephrin interactions are critical to maintaining slit diaphragm function.
28	10997929	We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
29	10997929	Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
30	10997929	In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
31	11086029	Reduced filtration surface area in association with these structural changes was confirmed by finding reduced glomerular nephrin content and reduced glomerular filtration rate in Ptpro(-/-) mice.
32	11086029	There was no detectable increase in the urine albumin excretion of Ptpro(-/-) mice.
33	11106563	We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
34	11106563	Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
35	11106563	During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures.
36	11106563	In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
37	11106563	Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
38	11106563	We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
39	11106563	Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
40	11106563	During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures.
41	11106563	In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
42	11106563	Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
43	11106563	We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
44	11106563	Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
45	11106563	During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures.
46	11106563	In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
47	11106563	Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
48	11106563	We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
49	11106563	Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
50	11106563	During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures.
51	11106563	In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
52	11106563	Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
53	11106563	We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
54	11106563	Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
55	11106563	During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures.
56	11106563	In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
57	11106563	Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys.
58	11158218	In proliferative forms of glomerulonephritides (Henoch-Schönlein nephritis, IgA nephropathy, postinfectious and membranoproliferative glomerulonephritis), crescents and sclerotic lesions were negative for nephrin, and mesangial proliferation led to a scattered and sparse staining pattern.
59	11158218	The staining pattern of nephrin was compared to that of ZO-1, a component of the cytoplasmic face of the slit diaphragm.
60	11158218	In proliferative forms of glomerulonephritides (Henoch-Schönlein nephritis, IgA nephropathy, postinfectious and membranoproliferative glomerulonephritis), crescents and sclerotic lesions were negative for nephrin, and mesangial proliferation led to a scattered and sparse staining pattern.
61	11158218	The staining pattern of nephrin was compared to that of ZO-1, a component of the cytoplasmic face of the slit diaphragm.
62	11195047	CD2-associated protein and the kidney.
63	11195047	In particular, two proteins, CD2-associated protein and nephrin, have been identified as critical podocyte proteins that are both required for normal glomerular filtration.
64	11249861	Here, we show that the podocyte-specific markers, glomerular epithelial protein 1 and nephrin, which are normally expressed in capillary loop stage glomeruli in vivo, are also expressed by glomerular figures that form in organ culture.
65	11316852	Blocking angiotensin II synthesis/activity preserves glomerular nephrin in rats with severe nephrosis.
66	11316852	This study used an accelerated model of experimental nephrosis to assess nephrin gene and protein expression in the kidney and the possible modulating effect of drugs that block angiotensin II (AII) synthesis/activity.
67	11316852	In summary, progressive renal injury was associated with downregulation of nephrin gene that was totally prevented by angiotensin-converting enzyme inhibitor and AII receptor blocker, suggesting that renoprotection afforded by drugs that interfere with AII synthesis/activity was related to an effect on nephrin assembly.
68	11316852	Blocking angiotensin II synthesis/activity preserves glomerular nephrin in rats with severe nephrosis.
69	11316852	This study used an accelerated model of experimental nephrosis to assess nephrin gene and protein expression in the kidney and the possible modulating effect of drugs that block angiotensin II (AII) synthesis/activity.
70	11316852	In summary, progressive renal injury was associated with downregulation of nephrin gene that was totally prevented by angiotensin-converting enzyme inhibitor and AII receptor blocker, suggesting that renoprotection afforded by drugs that interfere with AII synthesis/activity was related to an effect on nephrin assembly.
71	11316852	Blocking angiotensin II synthesis/activity preserves glomerular nephrin in rats with severe nephrosis.
72	11316852	This study used an accelerated model of experimental nephrosis to assess nephrin gene and protein expression in the kidney and the possible modulating effect of drugs that block angiotensin II (AII) synthesis/activity.
73	11316852	In summary, progressive renal injury was associated with downregulation of nephrin gene that was totally prevented by angiotensin-converting enzyme inhibitor and AII receptor blocker, suggesting that renoprotection afforded by drugs that interfere with AII synthesis/activity was related to an effect on nephrin assembly.
74	11337370	Aggregated but not disaggregated human IgG(4), plasmalemmal insertion of membrane attack complex of complement, tumor necrosis factor-alpha, and puromycin, induced the shedding of nephrin with a loss of surface expression.
75	11411021	Nephrin mRNA regulation by protein kinase C.
76	11416156	Proteinuria and perinatal lethality in mice lacking NEPH1, a novel protein with homology to NEPHRIN.
77	11416156	Based on similarity to NEPHRIN and abundant expression in kidney, this protein was designated NEPH1 and embryonic stem cells containing the retroviral insertion in the Neph1 locus were used to generate mutant mice.
78	11416156	These findings suggest that NEPH1, like NEPHRIN, may play an important role in maintaining the structure of the filtration barrier that prevents proteins from freely entering the glomerular urinary space.
79	11416156	Proteinuria and perinatal lethality in mice lacking NEPH1, a novel protein with homology to NEPHRIN.
80	11416156	Based on similarity to NEPHRIN and abundant expression in kidney, this protein was designated NEPH1 and embryonic stem cells containing the retroviral insertion in the Neph1 locus were used to generate mutant mice.
81	11416156	These findings suggest that NEPH1, like NEPHRIN, may play an important role in maintaining the structure of the filtration barrier that prevents proteins from freely entering the glomerular urinary space.
82	11416156	Proteinuria and perinatal lethality in mice lacking NEPH1, a novel protein with homology to NEPHRIN.
83	11416156	Based on similarity to NEPHRIN and abundant expression in kidney, this protein was designated NEPH1 and embryonic stem cells containing the retroviral insertion in the Neph1 locus were used to generate mutant mice.
84	11416156	These findings suggest that NEPH1, like NEPHRIN, may play an important role in maintaining the structure of the filtration barrier that prevents proteins from freely entering the glomerular urinary space.
85	11458036	However, more recent studies on nephrin, a key component of the slit diaphragm, as well as the podocyte and slit diaphragm-associated intracellular proteins, CD2-associated protein, podocin and alpha-actinin-4, have emphasized the role of the slit diaphragm as a central size-selective filtration barrier.
86	11562357	Interaction with podocin facilitates nephrin signaling.
87	11562357	Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
88	11562357	In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes.
89	11562357	Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin.
90	11562357	Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria.
91	11562357	Interaction with podocin facilitates nephrin signaling.
92	11562357	Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
93	11562357	In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes.
94	11562357	Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin.
95	11562357	Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria.
96	11562357	Interaction with podocin facilitates nephrin signaling.
97	11562357	Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
98	11562357	In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes.
99	11562357	Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin.
100	11562357	Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria.
101	11562357	Interaction with podocin facilitates nephrin signaling.
102	11562357	Mutations of NPHS1 or NPHS2, the genes encoding for the glomerular podocyte proteins nephrin and podocin, cause steroid-resistant proteinuria.
103	11562357	In addition, mice lacking CD2-associated protein (CD2AP) develop a nephrotic syndrome that resembles NPHS mutations suggesting that all three proteins are essential for the integrity of glomerular podocytes.
104	11562357	Nephrin-induced signaling is greatly enhanced by podocin, which binds to the cytoplasmic tail of nephrin.
105	11562357	Mutational analysis suggests that abnormal or inefficient signaling through the nephrin-podocin complex contributes to the development of podocyte dysfunction and proteinuria.
106	11701993	The identification of nephrin, a component of the slit diaphragm, and the intracellular slit diaphragm associated proteins CD2AP and podocin has demonstrated the existence of proteins that directly contribute to a functional kidney filter.