Ignet

Gene Information

Gene symbol: E2F3

Gene name: E2F transcription factor 3

HGNC ID: 3115

Related Genes

#	Gene Symbol	Number of hits
1	APAF1	1 hits
2	BAX	1 hits
3	BCL2	1 hits
4	CASP3	1 hits
5	CASP7	1 hits
6	CASP9	1 hits
7	MARCH8	1 hits
8	MIRN503	1 hits
9	MIRN770	1 hits

Related Sentences

#	PMID	Sentence
1	30834596	MicroRNA-503 contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
2	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
3	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
4	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
5	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
6	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
7	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
8	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
9	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
10	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
11	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
12	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
13	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
14	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
15	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
16	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
17	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
18	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
19	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
20	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
21	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
22	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
23	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
24	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
25	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
26	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
27	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
28	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
29	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
30	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
31	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
32	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
33	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
34	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
35	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
36	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
37	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
38	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
39	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
40	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
41	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
42	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
43	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
44	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
45	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
46	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
47	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
48	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
49	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
50	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
51	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
52	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
53	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
54	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
55	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
56	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
57	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
58	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
59	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
60	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
61	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
62	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
63	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
64	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
65	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
66	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
67	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
68	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
69	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
70	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
71	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
72	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
73	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
74	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
75	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
76	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
77	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
78	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
79	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
80	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
81	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
82	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
83	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
84	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
85	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
86	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
87	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
88	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
89	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
90	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
91	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
92	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
93	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
94	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
95	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
96	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
97	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
98	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
99	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
100	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
101	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
102	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
103	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
104	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
105	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
106	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
107	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
108	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
109	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
110	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
111	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
112	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
113	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
114	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
115	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
116	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
117	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
118	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
119	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
120	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
121	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
122	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
123	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
124	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
125	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
126	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
127	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
128	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
129	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
130	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
131	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
132	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
133	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
134	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
135	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
136	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
137	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
138	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
139	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
140	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
141	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
142	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
143	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
144	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
145	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
146	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
147	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
148	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
149	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
150	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
151	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
152	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
153	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
154	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
155	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
156	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
157	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.
158	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
159	32696822	MicroRNA-770-5p depletion could repress high glucose (HG)-triggered apoptosis in podocytes, and downregulation of E2F transcription factor 3 (E2F3) could facilitate podocyte injury.
160	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
161	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
162	32696822	The expression levels of E2F3, apoptosis-related proteins Bcl-2 related X protein (Bax), B-cell lymphoma-2 (Bcl-2), Bad, apoptotic peptidase activating factor 1 (APAF1), C-caspase3, C-caspase7, and C-caspase9 were detected by western blot assay.
163	32696822	The effects of miR-770-5p and E2F3 on HG-treated podocytes proliferation and apoptosis were detected by CCK-8 and flow cytometry assays.
164	32696822	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
165	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
166	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
167	32696822	E2F3 is a target gene of miR-770-5p and it partially abolished the effect of miR-770-5p in HG-triggered proliferation and apoptosis of podocytes.
168	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
169	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
170	32696822	These findings suggested that miR-770-5p expedited podocyte injury by targeting E2F3, and the miR-770-5p/E2F3 axis might represent a pathological mechanism of DN progression.