Ignet

Gene Information

Gene symbol: ABL1

Gene name: c-abl oncogene 1, non-receptor tyrosine kinase

HGNC ID: 76

Synonyms: JTK7, c-ABL, p150

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	FCGR3A	1 hits
4	INPPL1	1 hits
5	NPHS1	1 hits
6	PRKAR2A	1 hits
7	SH2D5	1 hits
8	SH3YL1	1 hits
9	SRC	1 hits
10	TP53	1 hits

Related Sentences

#	PMID	Sentence
1	31891685	Here, we reported that AA induced F-actin cytoskeletal ring formation and promoted protein kinase A (PKA), nephrin and c-Abl phosphorylation.
2	31891685	Here, we reported that AA induced F-actin cytoskeletal ring formation and promoted protein kinase A (PKA), nephrin and c-Abl phosphorylation.
3	31891685	Here, we reported that AA induced F-actin cytoskeletal ring formation and promoted protein kinase A (PKA), nephrin and c-Abl phosphorylation.
4	31891685	Moreover, AA promoted c-Abl translocation from the nucleus to the cytoplasm and increased the recruitment of c-Abl to p-nephrin by the interaction between them.
5	31891685	Moreover, AA promoted c-Abl translocation from the nucleus to the cytoplasm and increased the recruitment of c-Abl to p-nephrin by the interaction between them.
6	31891685	Moreover, AA promoted c-Abl translocation from the nucleus to the cytoplasm and increased the recruitment of c-Abl to p-nephrin by the interaction between them.
7	31891685	H89 (PKA inhibitor) provided protection against AA-induced F-actin bunching remodeling, down-regulated nephrin phosphorylation, and suppressed the c-Abl translocation and activation.
8	31891685	H89 (PKA inhibitor) provided protection against AA-induced F-actin bunching remodeling, down-regulated nephrin phosphorylation, and suppressed the c-Abl translocation and activation.
9	31891685	H89 (PKA inhibitor) provided protection against AA-induced F-actin bunching remodeling, down-regulated nephrin phosphorylation, and suppressed the c-Abl translocation and activation.
10	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
11	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
12	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
13	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
14	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
15	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
16	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
17	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
18	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
19	29416010	Role of c-Abl and nephrin in podocyte cytoskeletal remodeling induced by angiotensin II.
20	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
21	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
22	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
23	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
24	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
25	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
26	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
27	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
28	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
29	29416010	Our previous study showed that angiotensin II (Ang II) exposure diminished the interaction between nephrin and c-Abl, then c-Abl mediated SHIP2-Akt pathway in the process of podocyte injury in vivo and vitro.
30	29416010	However, the relationship between nephrin and c-Abl was unknown.
31	29416010	However, the relationship between nephrin and c-Abl was unknown.
32	29416010	However, the relationship between nephrin and c-Abl was unknown.
33	29416010	However, the relationship between nephrin and c-Abl was unknown.
34	29416010	However, the relationship between nephrin and c-Abl was unknown.
35	29416010	However, the relationship between nephrin and c-Abl was unknown.
36	29416010	However, the relationship between nephrin and c-Abl was unknown.
37	29416010	However, the relationship between nephrin and c-Abl was unknown.
38	29416010	However, the relationship between nephrin and c-Abl was unknown.
39	29416010	However, the relationship between nephrin and c-Abl was unknown.
40	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
41	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
42	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
43	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
44	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
45	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
46	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
47	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
48	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
49	29416010	As a nonreceptor tyrosine kinase involved in cytoskeletal regulation, c-Abl may be a candidate of signaling proteins interacting with Src homology 2/3 (SH2/SH3) domains of nephrin.
50	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
51	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
52	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
53	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
54	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
55	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
56	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
57	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
58	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
59	29416010	Therefore, it is proposed that c-Abl contributes to nephrin-dependent cytoskeletal remodeling of podocytes.
60	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
61	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
62	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
63	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
64	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
65	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
66	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
67	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
68	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
69	29416010	Herein, we observed that nephrin-c-Abl colocalization were suppressed in glomeruli of patients with proteinuria.
70	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
71	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
72	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
73	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
74	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
75	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
76	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
77	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
78	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
79	29416010	Next, CD16/7-nephrin and c-Abl vectors were constructed to investigate the nephrin-c-Abl signaling pathway in podocyte actin-cytoskeletal remodeling.
80	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
81	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
82	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
83	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
84	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
85	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
86	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
87	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
88	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
89	29416010	The disorganized cytoskeleton stimulated by cytochalasin D in COS7 cells was dramatically restored by co-transfection with phosphorylated CD16/7-nephrin and c-Abl full-length constructs.
90	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
91	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
92	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
93	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
94	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
95	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
96	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
97	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
98	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
99	29416010	Further, co-immunoprecipitation showed that phosphorylated CD16/7-nephrin interacted with wild-type c-Abl, but not with SH2/SH3-defective c-Abl.
100	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
101	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
102	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
103	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
104	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
105	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
106	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
107	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
108	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
109	29416010	These findings suggest that phosphorylated nephrin is able to recruit c-Abl in a SH2/SH3-dependent manner and detached c-Abl from dephosphorylated nephrin contributes to cytoskeletal remodeling in podocytes.
110	26810274	c-Abl contributes to glucose-promoted apoptosis via p53 signaling pathway in podocytes.
111	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
112	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
113	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
114	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
115	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
116	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
117	26510503	Angiotensin II down-regulates nephrin-Akt signaling and induces podocyte injury: roleof c-Abl.
118	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
119	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
120	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
121	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
122	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
123	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
124	26510503	Recent studies have shown that nephrin plays a vital role in angiotensin II (Ang II)-induced podocyte injury and thus contributes to the onset of proteinuria and the progression of renal diseases, but its specific mechanism remains unclear. c-Abl is an SH2/SH3 domain-containing nonreceptor tyrosine kinase that is involved in cell survival and regulation of the cytoskeleton.
125	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
126	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
127	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
128	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
129	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
130	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
131	26510503	Phosphorylated nephrin is able to interact with molecules containing SH2/SH3 domains, suggesting that c-Abl may be a downstream molecule of nephrin signaling.
132	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
133	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
134	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
135	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
136	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
137	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
138	26510503	Here we report that Ang II-infused rats developed proteinuria and podocyte damage accompanied by nephrin dephosphorylation and minimal interaction between nephrin and c-Abl.
139	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
140	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
141	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
142	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
143	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
144	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
145	26510503	In vitro, Ang II induced podocyte injury and nephrin and Akt dephosphorylation, which occurred in tandem with minimal interaction between nephrin and c-Abl.
146	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
147	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
148	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
149	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
150	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
151	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
152	26510503	Moreover, Ang II promoted c-Abl phosphorylation and interaction between c-Abl and SH2 domain-containing 5'-inositol phosphatase 2 (SHIP2). c-Abl small interfering RNA (siRNA) and STI571 (c-Abl inhibitor) provided protection against Ang II-induced podocyte injury, suppressed the Ang II-induced c-Abl-SHIP2 interaction and SHIP2 phosphorylation, and maintained a stable level of nephrin phosphorylation.
153	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
154	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
155	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
156	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
157	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
158	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
159	26510503	These results indicate that c-Abl is a molecular chaperone of nephrin signaling and the SHIP2-Akt pathway and that the released c-Abl contributes to Ang II-induced podocyte injury.
160	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
161	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
162	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
163	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
164	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
165	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
166	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
167	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
168	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
169	23515840	c-Abl mediates angiotensin II-induced apoptosis in podocytes.
170	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
171	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
172	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
173	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
174	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
175	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
176	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
177	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
178	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
179	23515840	In the present study, we investigated the role of the nonreceptor tyrosine kinase c-Abl in Ang II-induced podocyte apoptosis.
180	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
181	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
182	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
183	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
184	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
185	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
186	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
187	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
188	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
189	23515840	In vitro studies, conditionally immortalized mouse podocytes were treated with Ang II (10(-9)-10(-6) M) in the presence or absence of either c-Abl inhibitor, Src-I1, specific c-Abl siRNA, or c-Abl plasmid alone.
190	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
191	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
192	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
193	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
194	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
195	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
196	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
197	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
198	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
199	23515840	The nuclear c-Abl and p53 were quantified by co-immunoprecipitation and Western blotting studies.
200	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
201	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
202	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
203	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
204	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
205	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
206	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
207	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
208	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
209	23515840	Ang II-receiving rats displayed enhanced podocyte c-Abl expression.
210	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
211	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
212	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
213	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
214	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
215	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
216	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
217	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
218	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
219	23515840	And Ang II significantly stimulated c-Abl expression in cultured podocytes.
220	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
221	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
222	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
223	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
224	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
225	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
226	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
227	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
228	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
229	23515840	Furthermore Ang II upregulated podocyte c-Abl phosphorylation at Y245 and Y412.
230	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
231	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
232	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
233	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
234	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
235	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
236	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
237	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
238	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
239	23515840	Ang II also induced an increase of nuclear p53 protein and nuclear c-Abl-p53 complexes in podocytes and podocyte apoptosis.
240	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
241	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
242	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
243	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
244	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
245	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
246	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
247	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
248	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
249	23515840	Down-regulation of c-Abl expression by c-Abl inhibitor (Src-I1) as well as specific siRNA inhibited Ang II-induced podocyte apoptosis; conversely, podoctyes transfected with c-Abl plasmid displayed enhanced apoptosis.
250	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
251	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
252	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
253	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
254	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
255	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
256	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
257	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
258	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.
259	23515840	These findings indicate that c-Abl may mediates Ang II-induced podocyte apoptosis, and inhibition of c-Abl expression can protect podocytes from Ang II-induced injury.