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Gene Information
Gene symbol: NPPB
Gene name: natriuretic peptide B
HGNC ID: 7940
Related Genes
| # | Gene Symbol | Number of hits |
| 1 | TGFA | 1 hits |
| 2 | TIMP2 | 1 hits |
Related Sentences
| # | PMID | Sentence |
| 1 | 30899395 | To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an in vitro model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)β1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. |
| 2 | 30899395 | BNP treatment considerably induced GSK3β inhibition, marked by inhibitory phosphorylation at the serine 9 residue, and this significantly correlated with the abrogated TIMP2 induction in TGFβ1-injured podocytes. |
| 3 | 30899395 | Moreover, genetic knockout of GSK3β in podocytes is sufficient to attenuate the TGFβ1 induced TIMP2 expression and ECM deposition, reminiscent of the effect of BNP. |
| 4 | 30899395 | Conversely, ectopic expression of a nonphosphorylatable GSK3β mutant abolished the inhibitory effect of BNP on TGFβ1-elicited TIMP2 overexpression and ECM accumulation, signifying an essential role of GSK3β inhibition in mediating the effect of BNP. |
| 5 | 30899395 | To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an in vitro model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)β1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. |
| 6 | 30899395 | BNP treatment considerably induced GSK3β inhibition, marked by inhibitory phosphorylation at the serine 9 residue, and this significantly correlated with the abrogated TIMP2 induction in TGFβ1-injured podocytes. |
| 7 | 30899395 | Moreover, genetic knockout of GSK3β in podocytes is sufficient to attenuate the TGFβ1 induced TIMP2 expression and ECM deposition, reminiscent of the effect of BNP. |
| 8 | 30899395 | Conversely, ectopic expression of a nonphosphorylatable GSK3β mutant abolished the inhibitory effect of BNP on TGFβ1-elicited TIMP2 overexpression and ECM accumulation, signifying an essential role of GSK3β inhibition in mediating the effect of BNP. |
| 9 | 30899395 | To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an in vitro model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)β1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. |
| 10 | 30899395 | BNP treatment considerably induced GSK3β inhibition, marked by inhibitory phosphorylation at the serine 9 residue, and this significantly correlated with the abrogated TIMP2 induction in TGFβ1-injured podocytes. |
| 11 | 30899395 | Moreover, genetic knockout of GSK3β in podocytes is sufficient to attenuate the TGFβ1 induced TIMP2 expression and ECM deposition, reminiscent of the effect of BNP. |
| 12 | 30899395 | Conversely, ectopic expression of a nonphosphorylatable GSK3β mutant abolished the inhibitory effect of BNP on TGFβ1-elicited TIMP2 overexpression and ECM accumulation, signifying an essential role of GSK3β inhibition in mediating the effect of BNP. |
| 13 | 30899395 | To understand the molecular mechanism underlying this renoprotective effect, the efficacy of BNP was examined in an in vitro model of glomerular sclerosis by exposing glomerular podocytes to transforming growth factor (TGF)β1-containing media that recapitulates the profibrogenic milieu in chronic glomerular disease. |
| 14 | 30899395 | BNP treatment considerably induced GSK3β inhibition, marked by inhibitory phosphorylation at the serine 9 residue, and this significantly correlated with the abrogated TIMP2 induction in TGFβ1-injured podocytes. |
| 15 | 30899395 | Moreover, genetic knockout of GSK3β in podocytes is sufficient to attenuate the TGFβ1 induced TIMP2 expression and ECM deposition, reminiscent of the effect of BNP. |
| 16 | 30899395 | Conversely, ectopic expression of a nonphosphorylatable GSK3β mutant abolished the inhibitory effect of BNP on TGFβ1-elicited TIMP2 overexpression and ECM accumulation, signifying an essential role of GSK3β inhibition in mediating the effect of BNP. |