Ignet

Gene Information

Gene symbol: ADAM10

Gene name: ADAM metallopeptidase domain 10

HGNC ID: 188

Synonyms: kuz, MADM, HsT18717, CD156c

Related Genes

#	Gene Symbol	Number of hits
1	ACTN4	1 hits
2	CXCL16	1 hits
3	DPEP3	1 hits

Related Sentences

#	PMID	Sentence
1	24752304	oxLDL-induced lipid accumulation in glomerular podocytes: role of IFN-γ, CXCL16, and ADAM10.
2	24752304	Moreover, the effects of CXCL16 antibody, IFN-γ, and ADAM10 inhibitor on oxLDL intake and CXCL16 expression were also explored to elucidate the regulatory factors of lipid accumulation in podocytes.
3	24752304	oxLDL-induced lipid accumulation in glomerular podocytes: role of IFN-γ, CXCL16, and ADAM10.
4	24752304	Moreover, the effects of CXCL16 antibody, IFN-γ, and ADAM10 inhibitor on oxLDL intake and CXCL16 expression were also explored to elucidate the regulatory factors of lipid accumulation in podocytes.
5	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
6	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.
7	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
8	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
9	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
10	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
11	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
12	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
13	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
14	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
15	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.
16	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
17	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
18	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
19	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
20	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
21	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
22	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
23	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
24	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.
25	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
26	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
27	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
28	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
29	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
30	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
31	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
32	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
33	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.
34	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
35	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
36	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
37	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
38	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
39	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
40	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
41	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
42	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.
43	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
44	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
45	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
46	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
47	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
48	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
49	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
50	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
51	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.
52	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
53	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
54	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
55	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
56	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
57	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
58	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
59	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
60	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.
61	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
62	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
63	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
64	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
65	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
66	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
67	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
68	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
69	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.
70	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
71	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
72	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
73	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
74	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
75	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
76	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.
77	32705248	oxLDL promotes podocyte migration by regulating CXCL16, ADAM10 and ACTN4.
78	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.
79	32705248	CXCL16 and ADAM10 expression levels in oxLDL‑treated podocytes were measured via reverse transcription‑quantitative PCR and western blotting.
80	32705248	CXCL16 or ADAM10 overexpression and knockdown assays were conducted.
81	32705248	The results indicated that oxLDL stimulation increased ADAM10 and CXCL16 expression levels, and enhanced podocyte migration compared with the control group.
82	32705248	Moreover, CXCL16 and ADAM10 overexpression significantly increased podocyte migration and the expression of actinin‑α4 (ACTN4) compared with the control groups.
83	32705248	By contrast, CXCL16 and ADAM10 knockdown significantly reduced podocyte migration and the expression of ACTN4 compared with the control groups.
84	32705248	The results suggested that oxLDL promoted podocyte migration by regulating CXCL16 and ADAM10 expression, as well as by modulating the actin cytoskeleton.
85	32705248	Therefore, CXCL16 and ADAM10 may serve as novel therapeutic targets for primary nephrotic syndrome in children.