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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 AGT 1 hits
3 CD2 1 hits
4 CD2AP 1 hits
5 CD79A 1 hits
6 CDH3 1 hits
7 PTPRO 1 hits
8 TJP1 1 hits
9 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 CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
3 10997929 CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
4 10997929 CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
5 10997929 CD2AP is expressed with nephrin in developing podocytes and is found widely in mature kidney and elsewhere.
6 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.
7 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.
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 CD2-associated protein (CD2AP) is an adapter molecule that can bind to the cytoplasmic domain of nephrin, a component of the glomerular slit diaphragm.
10 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.
11 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.
12 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.
13 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.
14 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.
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 We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
18 10997929 We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
19 10997929 We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
20 10997929 We have examined the patterns of expression of both CD2AP and nephrin in developing mouse and human kidney.
21 10997929 Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
22 10997929 Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
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 Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
25 10997929 Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared.
26 10997929 In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
27 10997929 In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
28 10997929 In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
29 10997929 In laminin-beta(2) mutant mice exhibiting nephrotic syndrome, CD2AP in glomeruli was aberrantly localized in a primarily punctate pattern.
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 We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
35 11106563 We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
36 11106563 We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
37 11106563 We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys.
38 11106563 Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
39 11106563 Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
40 11106563 Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
41 11106563 Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
42 11106563 Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies.
43 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.
44 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.
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 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.
47 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.
48 11106563 In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
49 11106563 In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
50 11106563 In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
51 11106563 In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
52 11106563 In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area.
53 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.
54 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.
55 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.
56 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.
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 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.
60 11158218 The staining pattern of nephrin was compared to that of ZO-1, a component of the cytoplasmic face of the slit diaphragm.
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 Blocking angiotensin II synthesis/activity preserves glomerular nephrin in rats with severe nephrosis.
67 11316852 Blocking angiotensin II synthesis/activity preserves glomerular nephrin in rats with severe nephrosis.
68 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.
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 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.
71 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.
72 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.
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.