Ignet

Gene Information

Gene symbol: DPEP3

Gene name: dipeptidase 3

HGNC ID: 23029

Related Genes

#	Gene Symbol	Number of hits
1	ADAM10	1 hits
2	BSG	1 hits
3	CXCL16	1 hits
4	HAVCR1	1 hits
5	IL10	1 hits
6	IL18	1 hits
7	IL6	1 hits
8	IL8	1 hits
9	LCN2	1 hits
10	MME	1 hits
11	MMP2	1 hits
12	MMP9	1 hits
13	NPHS1	1 hits
14	TGFA	1 hits
15	TIMP2	1 hits
16	TNF	1 hits
17	VCAM1	1 hits

Related Sentences

#	PMID	Sentence
1	19827739	Neprilysin (NEP, CD10, CALLA-common acute lymphoblastic leukaemia antigen, neutral endopeptidase, enkephalinase) is a zinc-dependent metallopeptidase, which is the first podocytic antigen, which has been shown to induce human membranous glomerulonephritis (GN).
2	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.
3	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.
4	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.
5	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.
6	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.
7	31014956	Bsg silencing in cultured podocytes exposed to transforming growth factor-β suppressed focal adhesion rearrangement and cellular motility via the activation of β₁ integrin-focal adhesion kinase-matrix metallopeptidase signaling.
8	31014956	In addition, induction of vascular endothelial growth factor and endothelin-1, which are implicated in podocyte-to-endothelial cross-communication, was lower in the supernatants of cultured Bsg-silenced podocytes stimulated with transforming growth factor-β.
9	31014956	The current study thus suggests that Bsg silencing via suppression of β₁ integrin-focal adhesion kinase-matrix metallopeptidase signaling may be an attractive therapeutic strategy for the maintenance of podocytes in patients with proteinuric kidney diseases.
10	31014956	Bsg silencing in cultured podocytes exposed to transforming growth factor-β suppressed focal adhesion rearrangement and cellular motility via the activation of β₁ integrin-focal adhesion kinase-matrix metallopeptidase signaling.
11	31014956	In addition, induction of vascular endothelial growth factor and endothelin-1, which are implicated in podocyte-to-endothelial cross-communication, was lower in the supernatants of cultured Bsg-silenced podocytes stimulated with transforming growth factor-β.
12	31014956	The current study thus suggests that Bsg silencing via suppression of β₁ integrin-focal adhesion kinase-matrix metallopeptidase signaling may be an attractive therapeutic strategy for the maintenance of podocytes in patients with proteinuric kidney diseases.
13	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
14	32705248	The present study investigated the role of CXC motif chemokine ligand 16 (CXCL16) and ADAM metallopeptidase domain 10 (ADAM10) in oxidized low‑density lipoprotein (oxLDL)‑stimualted podocytes and the underlying mechanisms.
15	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
16	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
17	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
18	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
19	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
20	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
21	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.