Ignet

Gene Information

Gene symbol: SSR1

Gene name:

HGNC ID:

Related Genes

#	Gene Symbol	Number of hits
1	ICAM1	1 hits
2	ITGAL	1 hits
3	ITGAM	1 hits
4	ITGB2	1 hits
5	NOS3	1 hits
6	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
2	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
3	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
4	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
5	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
6	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
7	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
8	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
9	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
10	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
11	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
12	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
13	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
14	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
15	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
16	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
17	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
18	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
19	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
20	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
21	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
22	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
23	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
24	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
25	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
26	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
27	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
28	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
29	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
30	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
31	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
32	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
33	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
34	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
35	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
36	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
37	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
38	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
39	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
40	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
41	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
42	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
43	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
44	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
45	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
46	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
47	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
48	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
49	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
50	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.
51	11839570	Retinal vascular endothelial growth factor induces intercellular adhesion molecule-1 and endothelial nitric oxide synthase expression and initiates early diabetic retinal leukocyte adhesion in vivo.
52	11839570	Previous work has shown that intercellular adhesion molecule-1 (ICAM-1) and CD18 are required for these processes.
53	11839570	However the relevant in vivo stimuli for ICAM-1 and CD18 expression in diabetes remain unknown.
54	11839570	Confirmed diabetic animals were treated with a highly specific VEGF-neutralizing Flt-Fc construct (VEGF TrapA(40)).
55	11839570	Retinal ICAM-1 mRNA levels in VEGF TrapA(40)-treated diabetic animals were reduced by 83.5% compared to diabetic controls (n = 5, P < 0.0001).
56	11839570	VEGF TrapA(40) also potently suppressed diabetic leukocyte adhesion in retinal arterioles (47%, n = 11, P < 0.0001), venules (36%, n = 11, P < 0.0005), and capillaries (36%, n = 11, P < 0.001).
57	11839570	The expression of endothelial nitric oxide synthase (eNOS), a downstream mediator of VEGF activity, was increased in diabetic retina, and was potently suppressed with VEGF TrapA(40) treatment (n = 8, P < 0.005).
58	11839570	Further, VEGF TrapA(40) reduced the diabetes-related nitric oxide increases in the retinae of diabetic animals.
59	11839570	Although neutrophil CD11a, CD11b, and CD18 levels were increased in 1-week diabetic animals, VEGF TrapA(40) did not alter the expression of these integrin adhesion molecules.
60	11839570	Taken together, these data demonstrate that VEGF induces retinal ICAM-1 and eNOS expression and initiates early diabetic retinal leukocyte adhesion in vivo.