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PMID |
Sentence |
1 |
15343382
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Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathways.
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2 |
15343382
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Using conditionally immortalized podocytes after differentiation, we found that infection of podocytes with nef increased Src kinase activity and signal transducer and activator of transcription 3 (Stat3) phosphorylation and activated the Ras-c-Raf-MAPK1,2 pathway.
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3 |
15343382
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A dominant negative mutant of Src abolished the Nef effect, whereas inhibition of MAPK1,2 or dominant negative Stat3 reduced Nef effects partially.
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4 |
15343382
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Nef stimulates proliferation of glomerular podocytes through activation of Src-dependent Stat3 and MAPK1,2 pathways.
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5 |
15343382
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Using conditionally immortalized podocytes after differentiation, we found that infection of podocytes with nef increased Src kinase activity and signal transducer and activator of transcription 3 (Stat3) phosphorylation and activated the Ras-c-Raf-MAPK1,2 pathway.
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6 |
15343382
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A dominant negative mutant of Src abolished the Nef effect, whereas inhibition of MAPK1,2 or dominant negative Stat3 reduced Nef effects partially.
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7 |
17570932
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The mechanism by which Nef induces podocyte proliferation and dedifferentiation has been traced to its ability to activate several signaling pathways including Src-Stat3 and ras-raf-MAPK1, 2.
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8 |
18443354
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Compared with controls, immunohistochemistry revealed that kidneys from HIV-1-transgenic mice (Tg26) and from patients with HIVAN had greater expression of both VEGF and its transcriptional regulator, hypoxia-inducible factor 2alpha (HIF-2alpha).
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9 |
18443354
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Similarly, mRNA and protein levels of VEGF and HIF-2alpha were increased in HIV-infected podocytes in vitro, and this transcriptional upregulation was found to be stimulated by the HIV viral protein Nef in a Src kinase-and Stat3-dependent manner.
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10 |
18443354
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HIV-1 also upregulated VEGFR2 and its co-receptor neuropilin-1 and suppressed the expression of semaphorin 3a in the podocyte.
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11 |
18443354
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Exogenous VEGF stimulated proliferation and de-differentiation of podocytes, which are features of collapsing FSGS, and VEGFR2 neutralizing antibodies reversed these features in podocytes infected with HIV-1 or isolated from Tg26 mice.
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12 |
18443354
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In conclusion, HIV-1 induces VEGF and VEGFR2 expression in podocytes, and this may be a critical step in the pathogenesis of HIVAN.
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13 |
22067944
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We showed that during renal I/R, RAGE ligands HMGB1 and S100B are expressed.
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14 |
31727625
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Using luciferase reporter assays, we did not observe activation of the NOTCH4 promoter with the HIV protein Nef in podocytes.
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15 |
31727625
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Further, we observed upregulated expression of a gamma secretase complex protein, presenilin 1, but not Notch4, in podocytes infected with an HIV-1 expression construct.
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16 |
31727625
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Consistent with the diminished inflammation, kidneys from Notch4d1/Tg26+ mice also showed a significant decrease in expression of the inflammatory cytokine transcripts Il-6 and Ccl2, as well as the master inflammatory transcription factor NF-κB (Nfkb1 transcripts and p65 protein).
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