Ignet

Gene Information

Gene symbol: CASP9

Gene name: caspase 9, apoptosis-related cysteine peptidase

HGNC ID: 1511

Synonyms: MCH6, ICE-LAP6, APAF-3, PPP1R56

Related Genes

#	Gene Symbol	Number of hits
1	AKR1B1	1 hits
2	AKT1	1 hits
3	APAF1	1 hits
4	BAX	1 hits
5	BCL2	1 hits
6	BCL2L1	1 hits
7	CASP3	1 hits
8	CASP7	1 hits
9	CASP8	1 hits
10	CYCS	1 hits
11	E2F3	1 hits
12	EGFR	1 hits
13	FADD	1 hits
14	FAS	1 hits
15	HMOX1	1 hits
16	ILK	1 hits
17	INOC1	1 hits
18	MARCH8	1 hits
19	MPPED2	1 hits
20	NFE2L2	1 hits
21	NOX4	1 hits
22	PIK3CA	1 hits
23	RB1	1 hits
24	SLC47A1	1 hits
25	SMAD3	1 hits

Related Sentences

#	PMID	Sentence
1	34811512	Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
2	34811512	Furthermore, Rb1 treatment reversed high glucose-induced increases in Cyto c, Caspase 9 and mitochondrial regulatory protein NOX4, but did not affect the upregulated expression of aldose reductase (AR).
3	34811512	We compared the effects of Rb1 with eparestat, a known aldose reductase inhibitor, in high glucose-treated podocytes, and found that both alleviated high glucose-induced cell apoptosis and mitochondrial damage, and Rb1 was more effective in inhibiting apoptosis.
4	34700229	Rapamycin attenuates PLA2R activation-mediated podocyte apoptosis via the PI3K/AKT/mTOR pathway.
5	34700229	Primary MN has been associated with circulating antibodies against native podocyte antigens, including phospholipase A2 receptor (PLA2R); however, precision therapy targeting the signaling cascade of PLA2R activation is lacking.
6	34700229	We demonstrated that podocyte apoptosis was induced by Group IB secretory phospholipase A2 (sPLA2IB) in a concentration- and time-dependent manner via upregulation of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mTOR, and inhibited by rapamycin or LY294002.
7	34700229	Furthermore, aberrant activation of the PI3K/AKT/mTOR pathway triggers both extrinsic (caspase-8 and caspase-3) and intrinsic (Bcl-2-associated X protein [BAX], B-cell lymphoma 2 [BCL-2], cytochrome c, caspase-9, and caspase-3) apoptotic cascades in podocytes.
8	34700229	The therapeutic implications of our findings are that strategies to reduce PLA2R activation and PI3K/AKT/mTOR pathway inhibition in PLA2R-activated podocytes help protect podocytes from apoptosis.
9	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
10	32696822	MicroRNA-770-5p contributes to podocyte injury via targeting E2F3 in diabetic nephropathy.
11	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.
12	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.
13	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
14	32696822	Nevertheless, whether E2F3 is involved in miR-770-5p knockdown-mediated improvement of DN is still unclear.
15	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
16	32696822	The expression levels of miR-770-5p and E2F3 were detected in HG-treated podocytes by RT-qPCR.
17	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.
18	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.
19	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.
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	The interaction between miR-770-5p and E2F3 was predicted by Targetscan, and then verified by the dual-luciferase reporter assay.
23	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
24	32696822	MiR-770-5p was upregulated and E2F3 was downregulated in HG-treated podocytes.
25	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
26	32696822	MiR-770-5p inhibited proliferation and promoted apoptosis and E2F3 promoted proliferation and suppressed apoptosis in HG-treated podocytes.
27	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.
28	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.
29	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
30	32696822	MiR-770-5p deficiency blocked HG-induced APAF1/caspase9 pathway via targeting E2F3 in podocytes.
31	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
32	32696822	We firstly confirmed that E2F3 was a target of miR-770-5p in podocytes.
33	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.
34	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.
35	30734599	SS-31 prevented oxidative stress and mitochondria-dependent apoptosis signalling by HOCl-alb in vivo and in vitro, as evidenced by the release of cytochrome c (cyt c), binding of apoptosis activated factor-1 (Apaf-1) and caspase-9, and activation of caspases.
36	30116378	Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H₂O₂.
37	30116378	Reverse transcription-polymerase chain reaction and western blot results indicated that HNK significantly decreased the expression of mRNA and cleaved protein of caspase-3 and caspase-9 in podocytes pre-treated with H₂O₂.
38	30116378	Furthermore, phosphorylation of the signaling molecules protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) 1/2 appeared to increase following HNK treatment.
39	30116378	Furthermore, phosphorylation of the signaling molecules protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) 1/2 appeared to increase following HNK treatment.
40	30116378	The anti-oxidative stress mechanisms of HNK are partly due to suppressing the expression of caspase-3 and caspase-9 and upregulating phosphorylated-Akt and -Erk 1/2.
41	30116378	The anti-oxidative stress mechanisms of HNK are partly due to suppressing the expression of caspase-3 and caspase-9 and upregulating phosphorylated-Akt and -Erk 1/2.
42	29110957	The kidney expresses protease-activated receptor-1 (PAR-1).
43	29110957	PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood.
44	29110957	Pathological analysis showed that Q94 treatment significantly attenuated periodic acid-Schiff and desmin staining, indicators of podocyte injury, and also decreased glomerular levels of podocin and nephrin.
45	29110957	In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes.
46	28831032	JNK inhibitor and ILK inhibitor decreased HO-1 expression to different degrees.
47	28831032	Moreover, specific siRNAs of ILK, Nrf-2, and HO-1, and inhibitors of HO-1 and ILK significantly increased ROS generation and Caspase9/3 expression in the presence of salidroside and HG.
48	28831032	ILK/Akt, JNK, ERK1/2, p38 MAPK, and Nrf-2 are involved in salidroside-decreased podocyte apoptosis in HG condition.
49	25229402	Furthermore, an obvious translocation of p-Smad3 from the cytosol to nuclei and induction of mitochondrial Nox4 were detected following PA application.
50	25229402	Induction of Nox4 by PA administration was significantly repressed by Smad3-shRNA, while Nox4-shRNA showed no effect on PA-induced p-Smad3 activation.
51	25229402	Notably, both Smad3 and Nox4 silencing significantly prevented the reduction of the mtDNA level, restored mitochondrial function, and decreased cellular apoptosis in PA-stimulated podocytes.
52	25229402	In conclusion, our findings demonstrated that Smad3-Nox4 axis-mediated mitochondrial dysfunction is involved in PA-induced podocyte damage likely via increasing ROS generation and activating the cytochrome c-caspase9-caspase3 apoptotic signaling pathway.
53	22479191	We uncovered 6 new loci in association with estimated glomerular filtration rate (eGFR), the primary clinical measure of CKD, in or near MPPED2, DDX1, SLC47A1, CDK12, CASP9, and INO80.
54	16421179	Apoptosis induced by each TM was associated with a significant (approximately 400%) increase in caspase 8 activity, but no change in caspase 9 activity, and Western analyses revealed a marked up-regulation of Fas (approximately 500%) and FADD (approximately 300%) with no change in expression of Bax, Bcl-2, or Bcl-xL.
55	16421179	Similar to the apoptotic response, combinations of TM induced less caspase 8 activity and Fas/FADD expression than individual TM treatments.