Ignet

Gene Information

Gene symbol: MYLIP

Gene name: myosin regulatory light chain interacting protein

HGNC ID: 21155

Synonyms: MIR, IDOL

Related Genes

#	Gene Symbol	Number of hits
1	BAX	1 hits
2	BCL2	1 hits
3	CASP3	1 hits
4	CD2AP	1 hits
5	CUL3	1 hits
6	DNMT1	1 hits
7	FOXA1	1 hits
8	FOXC2	1 hits
9	HES1	1 hits
10	HEY1	1 hits
11	KCNQ1OT1	1 hits
12	MIAT	1 hits
13	MIRN107	1 hits
14	MIRN145	1 hits
15	MIRN15B	1 hits
16	NFIC	1 hits
17	NLRP3	1 hits
18	NOTCH1	1 hits
19	TLR4	1 hits
20	VEGFA	1 hits
21	XIST	1 hits

Related Sentences

#	PMID	Sentence
1	35130620	miR-30a-5p promotes glomerular podocyte apoptosis via DNMT1-mediated hypermethylation under hyperhomocysteinemia.
2	35130620	miR-30a-5p promotes glomerular podocyte apoptosis via DNMT1-mediated hypermethylation under hyperhomocysteinemia.
3	35130620	miR-30a-5p promotes glomerular podocyte apoptosis via DNMT1-mediated hypermethylation under hyperhomocysteinemia.
4	35130620	We found that elevated Hcy downregulates miR-30a-5p expression in the mice and Hcy-treated podocytes, and miR-30a-5p directly targets the 3'-untranslated region (3'-UTR) of the forkhead box A1 (FOXA1) and overexpression of miR-30a-5p inhibits FOXA1 expression.
5	35130620	We found that elevated Hcy downregulates miR-30a-5p expression in the mice and Hcy-treated podocytes, and miR-30a-5p directly targets the 3'-untranslated region (3'-UTR) of the forkhead box A1 (FOXA1) and overexpression of miR-30a-5p inhibits FOXA1 expression.
6	35130620	We found that elevated Hcy downregulates miR-30a-5p expression in the mice and Hcy-treated podocytes, and miR-30a-5p directly targets the 3'-untranslated region (3'-UTR) of the forkhead box A1 (FOXA1) and overexpression of miR-30a-5p inhibits FOXA1 expression.
7	35130620	Mechanistic studies indicated that DNA methyltransferase enzyme 1 (DNMT1) is the key regulator of miR-30a-5p, which in turn enhances miR-30a-5p promoter methylation level and thereby inhibits its expression.
8	35130620	Mechanistic studies indicated that DNA methyltransferase enzyme 1 (DNMT1) is the key regulator of miR-30a-5p, which in turn enhances miR-30a-5p promoter methylation level and thereby inhibits its expression.
9	35130620	Mechanistic studies indicated that DNA methyltransferase enzyme 1 (DNMT1) is the key regulator of miR-30a-5p, which in turn enhances miR-30a-5p promoter methylation level and thereby inhibits its expression.
10	34197715	Overexpression of mm9_circ_013935 alleviates renal inflammation and fibrosis in diabetic nephropathy via the miR-153-3p/NFIC axis.
11	34197715	Overexpression of mm9_circ_013935 alleviates renal inflammation and fibrosis in diabetic nephropathy via the miR-153-3p/NFIC axis.
12	34197715	Overexpression of mm9_circ_013935 alleviates renal inflammation and fibrosis in diabetic nephropathy via the miR-153-3p/NFIC axis.
13	34197715	Overexpression of mm9_circ_013935 alleviates renal inflammation and fibrosis in diabetic nephropathy via the miR-153-3p/NFIC axis.
14	34197715	The expression of proteins related to fibrosis (collagen I, collagen III, fibronectin) was detected using Western blot.
15	34197715	The expression of proteins related to fibrosis (collagen I, collagen III, fibronectin) was detected using Western blot.
16	34197715	The expression of proteins related to fibrosis (collagen I, collagen III, fibronectin) was detected using Western blot.
17	34197715	The expression of proteins related to fibrosis (collagen I, collagen III, fibronectin) was detected using Western blot.
18	34197715	The concentration of inflammation cytokines (tumor necrosis factor α, interleukin 1β (IL-1β), IL-8) in mouse podocytes was assessed by ELISA.
19	34197715	The concentration of inflammation cytokines (tumor necrosis factor α, interleukin 1β (IL-1β), IL-8) in mouse podocytes was assessed by ELISA.
20	34197715	The concentration of inflammation cytokines (tumor necrosis factor α, interleukin 1β (IL-1β), IL-8) in mouse podocytes was assessed by ELISA.
21	34197715	The concentration of inflammation cytokines (tumor necrosis factor α, interleukin 1β (IL-1β), IL-8) in mouse podocytes was assessed by ELISA.
22	34197715	The miR-153-3p was revealed to bind with circ-RBM4 and directly targeted nuclear factor I/C (NFIC) in mouse podocytes.
23	34197715	The miR-153-3p was revealed to bind with circ-RBM4 and directly targeted nuclear factor I/C (NFIC) in mouse podocytes.
24	34197715	The miR-153-3p was revealed to bind with circ-RBM4 and directly targeted nuclear factor I/C (NFIC) in mouse podocytes.
25	34197715	The miR-153-3p was revealed to bind with circ-RBM4 and directly targeted nuclear factor I/C (NFIC) in mouse podocytes.
26	34197715	Rescue assays indicated that circ-RBM4 attenuated HG-induced fibrosis and inflammation response in mouse podocytes by inhibiting miR-153-3p expression or upregulating NFIC expression.
27	34197715	Rescue assays indicated that circ-RBM4 attenuated HG-induced fibrosis and inflammation response in mouse podocytes by inhibiting miR-153-3p expression or upregulating NFIC expression.
28	34197715	Rescue assays indicated that circ-RBM4 attenuated HG-induced fibrosis and inflammation response in mouse podocytes by inhibiting miR-153-3p expression or upregulating NFIC expression.
29	34197715	Rescue assays indicated that circ-RBM4 attenuated HG-induced fibrosis and inflammation response in mouse podocytes by inhibiting miR-153-3p expression or upregulating NFIC expression.
30	34197715	Circ-RBM4 alleviated the renal inflammation and renal fibrosis in DN by targeting the miR-153-3p/NFIC axis.
31	34197715	Circ-RBM4 alleviated the renal inflammation and renal fibrosis in DN by targeting the miR-153-3p/NFIC axis.
32	34197715	Circ-RBM4 alleviated the renal inflammation and renal fibrosis in DN by targeting the miR-153-3p/NFIC axis.
33	34197715	Circ-RBM4 alleviated the renal inflammation and renal fibrosis in DN by targeting the miR-153-3p/NFIC axis.
34	33296289	Long noncoding RNA Kcnq1ot1 promotes sC5b-9-induced podocyte pyroptosis by inhibiting miR-486a-3p and upregulating NLRP3.
35	33296289	Long noncoding RNA Kcnq1ot1 promotes sC5b-9-induced podocyte pyroptosis by inhibiting miR-486a-3p and upregulating NLRP3.
36	33296289	Long noncoding RNA Kcnq1ot1 promotes sC5b-9-induced podocyte pyroptosis by inhibiting miR-486a-3p and upregulating NLRP3.
37	33296289	We also identified the interaction between Kcnq1ot1 and miR-486a-3p, through which Kcnq1ot1 mediated miR-486a-3p inhibition by sC5b-9.
38	33296289	We also identified the interaction between Kcnq1ot1 and miR-486a-3p, through which Kcnq1ot1 mediated miR-486a-3p inhibition by sC5b-9.
39	33296289	We also identified the interaction between Kcnq1ot1 and miR-486a-3p, through which Kcnq1ot1 mediated miR-486a-3p inhibition by sC5b-9.
40	33296289	Furthermore, miR-486a-3p reduced the transcriptional activity of NLRP3, while the overexpression of NLRP3 enhanced sC5b-9's effect on podocyte pyroptosis through activating NLRP3 inflammasome. sC5b-9 induces pyroptosis in podocytes through modulating the Kcnq1ot1/miR-486a-3p/NLRP3 regulatory axis, and these uncovered key molecules might facilitate podocyte-targeted treatment for renal inflammatory diseases.
41	33296289	Furthermore, miR-486a-3p reduced the transcriptional activity of NLRP3, while the overexpression of NLRP3 enhanced sC5b-9's effect on podocyte pyroptosis through activating NLRP3 inflammasome. sC5b-9 induces pyroptosis in podocytes through modulating the Kcnq1ot1/miR-486a-3p/NLRP3 regulatory axis, and these uncovered key molecules might facilitate podocyte-targeted treatment for renal inflammatory diseases.
42	33296289	Furthermore, miR-486a-3p reduced the transcriptional activity of NLRP3, while the overexpression of NLRP3 enhanced sC5b-9's effect on podocyte pyroptosis through activating NLRP3 inflammasome. sC5b-9 induces pyroptosis in podocytes through modulating the Kcnq1ot1/miR-486a-3p/NLRP3 regulatory axis, and these uncovered key molecules might facilitate podocyte-targeted treatment for renal inflammatory diseases.
43	32972755	Ablation of lncRNA MIAT mitigates high glucose-stimulated inflammation and apoptosis of podocyte via miR-130a-3p/TLR4 signaling axis.
44	32972755	Ablation of lncRNA MIAT mitigates high glucose-stimulated inflammation and apoptosis of podocyte via miR-130a-3p/TLR4 signaling axis.
45	32972755	Ablation of lncRNA MIAT mitigates high glucose-stimulated inflammation and apoptosis of podocyte via miR-130a-3p/TLR4 signaling axis.
46	32972755	Ablation of lncRNA MIAT mitigates high glucose-stimulated inflammation and apoptosis of podocyte via miR-130a-3p/TLR4 signaling axis.
47	32972755	Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β.
48	32972755	Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β.
49	32972755	Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β.
50	32972755	Additionally, lack of MIAT mitigated HG-evoked inflammatory reaction in podocytes as evidenced by the diminished the release of inflammatory mediators TNF-α, IL-6 and IL-1β.
51	32972755	Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes.
52	32972755	Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes.
53	32972755	Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes.
54	32972755	Moreover, depletion of MIAT evidently amplified cell viability and alleviated HG-triggered apoptosis, reflected as the downregulation of Bax expression concomitant with the enhancement of Bcl-2 expression in HG-exposed podocytes.
55	32972755	Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p.
56	32972755	Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p.
57	32972755	Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p.
58	32972755	Mechanistically, MIAT effectively modulated TLR4 expression through acting as a competing endogenous sponge of miR-130a-3p, and TLR4 was confirmed as a specific target gene of miR-130a-3p.
59	32972755	More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage.
60	32972755	More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage.
61	32972755	More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage.
62	32972755	More importantly, the miR-130a-3p/TLR4 crosstalk contributed to the protective effect of MIAT knockdown on HG-provoked podocyte damage.
63	32972755	Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.
64	32972755	Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.
65	32972755	Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.
66	32972755	Collectively, these findings highlighted that blocking MIAT/miR-130a-3p/TLR4 network play vital regulatory roles in mitigating HG-induced inflammation damage and apoptosis, thereby protecting podocyte from HG-stimulated injury, implying that MIAT might be a promising therapeutic strategy for developing effective treatments against DN progression.
67	32580945	We exposed mouse glomerular podocytes and MP5 cells to high glucose (HG), ADSC-derived EVs, miR-26a-5p inhibitor/antagomir, Toll-like receptor 4 (TLR4) plasmids, or the NF-κB pathway activator (phorbol-12-myristate-13-acetate, or PMA).
68	32580945	We exposed mouse glomerular podocytes and MP5 cells to high glucose (HG), ADSC-derived EVs, miR-26a-5p inhibitor/antagomir, Toll-like receptor 4 (TLR4) plasmids, or the NF-κB pathway activator (phorbol-12-myristate-13-acetate, or PMA).
69	32580945	We exposed mouse glomerular podocytes and MP5 cells to high glucose (HG), ADSC-derived EVs, miR-26a-5p inhibitor/antagomir, Toll-like receptor 4 (TLR4) plasmids, or the NF-κB pathway activator (phorbol-12-myristate-13-acetate, or PMA).
70	32580945	We found that in DN, miR-26a-5p is expressed at very low levels, whereas TLR4 is highly expressed.
71	32580945	We found that in DN, miR-26a-5p is expressed at very low levels, whereas TLR4 is highly expressed.
72	32580945	We found that in DN, miR-26a-5p is expressed at very low levels, whereas TLR4 is highly expressed.
73	32580945	We also found that miR-26a-5p protects HG-induced MP5 cells from injury by targeting TLR4, inactivating the NF-κB pathway, and downregulating vascular endothelial growth factor A (VEGFA).
74	32580945	We also found that miR-26a-5p protects HG-induced MP5 cells from injury by targeting TLR4, inactivating the NF-κB pathway, and downregulating vascular endothelial growth factor A (VEGFA).
75	32580945	We also found that miR-26a-5p protects HG-induced MP5 cells from injury by targeting TLR4, inactivating the NF-κB pathway, and downregulating vascular endothelial growth factor A (VEGFA).
76	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
77	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
78	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
79	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
80	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
81	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
82	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
83	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
84	32104249	Expression levels of miR-145-5p and its target, Notch1, and other key factors involved in the apoptosis signaling pathway were detected and measured by reverse transcription-quantitative PCR and western blotting.
85	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
86	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
87	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
88	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
89	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
90	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
91	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
92	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
93	32104249	The functions of miR-145-5p in apoptosis were detected using flow cytometry and TUNEL staining.
94	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
95	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
96	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
97	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
98	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
99	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
100	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
101	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
102	32104249	The present study demonstrated that in HG conditions, miR-145-5p overexpression inhibited Notch1, Notch intracellular domain, Hes1 and Hey1 expression at the mRNA and protein levels.
103	32104249	Notch1 was identified as a direct target of miR-145-5p.
104	32104249	Notch1 was identified as a direct target of miR-145-5p.
105	32104249	Notch1 was identified as a direct target of miR-145-5p.
106	32104249	Notch1 was identified as a direct target of miR-145-5p.
107	32104249	Notch1 was identified as a direct target of miR-145-5p.
108	32104249	Notch1 was identified as a direct target of miR-145-5p.
109	32104249	Notch1 was identified as a direct target of miR-145-5p.
110	32104249	Notch1 was identified as a direct target of miR-145-5p.
111	32104249	Notch1 was identified as a direct target of miR-145-5p.
112	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
113	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
114	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
115	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
116	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
117	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
118	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
119	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
120	32104249	Furthermore, cleaved caspase-3, Bcl-2 and Bax levels were reduced significantly by miR-145-5p overexpression.
121	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
122	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
123	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
124	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
125	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
126	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
127	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
128	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
129	32104249	These results indicate that miR-145-5p overexpression inhibited the Notch signaling pathway and podocyte lesions induced by HG.
130	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
131	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
132	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
133	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
134	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
135	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
136	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
137	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
138	32104249	In conclusion, the results of the present study suggested that miR-145-5p may be a regulator of DN.
139	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
140	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
141	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
142	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
143	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
144	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
145	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
146	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
147	32104249	Additionally, miR-145-5p inhibited HG-induced apoptosis by directly targeting Notch1 and dysregulating apoptotic factors, including cleaved caspase-3, Bcl-2 and Bax.
148	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
149	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
150	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
151	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
152	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
153	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
154	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
155	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
156	32104249	The results of the present study provided evidence that miR-145-5p may offer a novel approach for the treatment of DN.
157	31658856	We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway.
158	31658856	We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway.
159	31658856	We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway.
160	31658856	We found the targets of miR-15a-5p, miR-15b-5p, and miR-16-5p were involved in mTOR signaling pathway, and those of miR-29b-3p and miR-16-5p were enriched in PI3K-Akt signaling pathway.
161	31658856	RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network.
162	31658856	RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network.
163	31658856	RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network.
164	31658856	RNAs including miR-15b-5p, miR-15a-5p, miR-107, XIST, miR-16-5p, and cullin 3 gene (CUL3) were included in the ceRNA regulatory network.
165	31658856	The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR.
166	31658856	The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR.
167	31658856	The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR.
168	31658856	The downregulation of miR-15a-5p and miR-15b-5p and the upregulation of lncRNA XIST and CUL3 gene were validated using qPCR.
169	31658856	We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3.
170	31658856	We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3.
171	31658856	We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3.
172	31658856	We confirmed that LPS inhibited the growth of mouse podocytes and seven of the ten miRNAs, but upregulated XIST and CUL3.
173	31658856	Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.
174	31658856	Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.
175	31658856	Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.
176	31658856	Transfection analysis showed XIST siRNA enhanced LPS-induced MPC5 cell apoptosis and miR-15a-5p inhibitor reserved it, so did as CUL3 overexpression for miR-15a-5p mimics.
177	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
178	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
179	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
180	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
181	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
182	31531679	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes.
183	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
184	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
185	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
186	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
187	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
188	31531679	FOXC2 is a transcription factor essential for inducing podocyte differentiation, development and maturation, and is considered to be the earliest podocyte marker. miRNA prediction analysis revealed a full-length target site for the primate-specific miR-548c-5p at a genomic region > 8 kb upstream of FOXC2.
189	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
190	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
191	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
192	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
193	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
194	31531679	We hypothesised that the transcription rates of FOXC2 during podocyte differentiation might be tuned by miR-548c-5p through this target site.
195	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
196	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
197	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
198	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
199	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
200	31531679	In cultured podocytes, FOXC2 mRNA and protein levels responded to miR-548c-5p abundance in a coordinated manner before and after induction of differentiation, with high statistical significance.
201	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
202	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
203	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
204	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
205	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
206	31531679	Moreover, the expression pattern of FOXC2 during podocyte differentiation seems to be affected by miR-548c-5p, as removal of either endogenous or mimic miR-548c-5p results in increased FOXC2 protein levels and cells resembling those undergoing differentiation.
207	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
208	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
209	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
210	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
211	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
212	31531679	Collectively, results indicate a well-orchestrated regulatory model of FOXC2 expression by a remote upstream target site for miR-548c-5p.
213	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
214	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
215	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
216	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
217	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
218	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
219	31131477	Excessive apoptosis of podocytes caused by dysregulation of microRNA-182-5p and CD2AP confers to an increased risk of diabetic nephropathy.
220	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
221	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
222	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
223	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
224	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
225	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
226	31131477	Here, we studied the roles and relationship between miR-182-5p and CD2AP in the development of DN.
227	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
228	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
229	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
230	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
231	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
232	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
233	31131477	We used real-time polymerase chain reaction (PCR) to compare miR-182-5p expression between DN and control groups, while computational analysis and luciferase assays were used to confirm CD2AP as a miR-182-5p target.
234	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
235	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
236	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
237	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
238	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
239	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
240	31131477	Western blot and real-time PCR were then used to measure the messenger RNA (mRNA) and protein expression of CD2AP in the presence of miR-182-5p.
241	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
242	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
243	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
244	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
245	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
246	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
247	31131477	In addition, the luciferase activity of cells transfected with wild-type/mutant CD2AP confirmed CD2AP as a direct target of miR-182-5p.
248	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
249	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
250	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
251	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
252	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
253	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
254	31131477	In addition, the expression levels of CD2AP mRNA and protein were evidently increased by a miR-182-5p inhibitor, but notably downregulated by miR-182-5p mimics or CD2AP small interfering RNA (siRNA).
255	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
256	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
257	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
258	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
259	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
260	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
261	31131477	Furthermore, miR-182-5p and CD2Ap siRNA significantly reduced the survival rate and viability of transfected cells, while the miR-182-5p inhibitor exhibited an opposite effect.
262	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
263	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
264	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
265	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
266	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
267	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.
268	31131477	These findings indicated the presence of a negative regulatory relationship between miR-182-5p and CD2AP in podocytes cells and suggested that the overexpression of miR-182-5p contributes to the pathogenesis of DN.