Ignet

Gene Information

Gene symbol: TIMP2

Gene name: TIMP metallopeptidase inhibitor 2

HGNC ID: 11821

Synonyms: CSC-21K

Related Genes

#	Gene Symbol	Number of hits
1	DPEP3	1 hits
2	GPM6A	1 hits
3	HAVCR1	1 hits
4	IGF2BP2	1 hits
5	IL10	1 hits
6	IL18	1 hits
7	IL6	1 hits
8	IL8	1 hits
9	INS	1 hits
10	LCN2	1 hits
11	METTL3	1 hits
12	MMP2	1 hits
13	MMP9	1 hits
14	NPHS1	1 hits
15	NPPB	1 hits
16	TNF	1 hits
17	VCAM1	1 hits

Related Sentences

#	PMID	Sentence
1	34995800	METTL3-mediated m⁶A modification of TIMP2 mRNA promotes podocyte injury in diabetic nephropathy.
2	34995800	METTL3-mediated m⁶A modification of TIMP2 mRNA promotes podocyte injury in diabetic nephropathy.
3	34995800	Here, we found that m6A modification was significantly upregulated in the kidney of type 1 and type 2 diabetic mice, which was caused by elevated levels of METTL3.
4	34995800	Here, we found that m6A modification was significantly upregulated in the kidney of type 1 and type 2 diabetic mice, which was caused by elevated levels of METTL3.
5	34995800	Mechanistically, METTL3 modulated Notch signaling via the m6A modification of TIMP2 in an insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)-dependent manner and exerted pro-inflammatory and pro-apoptotic effects.
6	34995800	Mechanistically, METTL3 modulated Notch signaling via the m6A modification of TIMP2 in an insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2)-dependent manner and exerted pro-inflammatory and pro-apoptotic effects.
7	34995800	In summary, this study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN.
8	34995800	In summary, this study suggested that METTL3-mediated m6A modification is an important mechanism of podocyte injury in DN.
9	34995800	Targeting m6A through the writer enzyme METTL3 is a potential approach for the treatment of DN.
10	34995800	Targeting m6A through the writer enzyme METTL3 is a potential approach for the treatment of DN.
11	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.
12	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.
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	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.
16	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.
17	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.
18	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.
19	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.
20	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.
21	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.
22	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.
23	26671966	These biomarkers included 1) podocyte glycoproteins nephrin and podocalyxin, 2) matrix metallopeptidase (MMP)-2 and MMP-9 and their inhibitor tissue inhibitor of metalloproteinase-2, 3) inflammatory molecules and cytokines soluble VCAM-1, TNF-α, soluble TNF receptor receptor-1, IL-6, IL-8, IL-10, and IL-18, and 4) kidney injury biomarkers neutrophil gelatinase-associated lipocalin and kidney injury molecule-1.
24	26671966	These biomarkers included 1) podocyte glycoproteins nephrin and podocalyxin, 2) matrix metallopeptidase (MMP)-2 and MMP-9 and their inhibitor tissue inhibitor of metalloproteinase-2, 3) inflammatory molecules and cytokines soluble VCAM-1, TNF-α, soluble TNF receptor receptor-1, IL-6, IL-8, IL-10, and IL-18, and 4) kidney injury biomarkers neutrophil gelatinase-associated lipocalin and kidney injury molecule-1.
25	26671966	We found that, first, urine levels of nephrin, MMP-2, MMP-9, and kidney injury molecule-1 were significantly higher before delivery in severe preeclampsia than normotensive groups.
26	26671966	We found that, first, urine levels of nephrin, MMP-2, MMP-9, and kidney injury molecule-1 were significantly higher before delivery in severe preeclampsia than normotensive groups.
27	26671966	Second, soluble VCAM-1, soluble TNF receptor-1, and neutrophil gelatinase-associated lipocalin levels were significantly increased in the severe preeclampsia group compared with the normotensive control group before delivery, but levels of these molecules were significantly reduced in postpartum specimens in both groups.
28	26671966	Second, soluble VCAM-1, soluble TNF receptor-1, and neutrophil gelatinase-associated lipocalin levels were significantly increased in the severe preeclampsia group compared with the normotensive control group before delivery, but levels of these molecules were significantly reduced in postpartum specimens in both groups.
29	26671966	Third, IL-6 and IL-8 levels were not different between preeclampsia and normotensive groups but significantly increased in pregnancy complicated with chronic hypertension.
30	26671966	Third, IL-6 and IL-8 levels were not different between preeclampsia and normotensive groups but significantly increased in pregnancy complicated with chronic hypertension.
31	26671966	Finally, tissue inhibitor of metalloproteinase-2 and IL-18 levels were not different among the study groups before delivery but were significantly reduced in postpartum specimens from normotensive controls.
32	26671966	Finally, tissue inhibitor of metalloproteinase-2 and IL-18 levels were not different among the study groups before delivery but were significantly reduced in postpartum specimens from normotensive controls.
33	11909536	In support of this, blockade of MMP-2 activity by injection of TIMP-2 does not perturb circulation but does prevent glomerular assembly.