Ignet

Gene Information

Gene symbol: LIMS3

Gene name: LIM and senescent cell antigen-like domains 3

HGNC ID: 30047

Related Genes

#	Gene Symbol	Number of hits
1	ILK	1 hits
2	LIMS1	1 hits
3	LIMS2	1 hits
4	PARVA	1 hits
5	TGFA	1 hits

Related Sentences

#	PMID	Sentence
1	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
2	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
3	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
4	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
5	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
6	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
7	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
8	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
9	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
10	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
11	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
12	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
13	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
14	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
15	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
16	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
17	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
18	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
19	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
20	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
21	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
22	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
23	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
24	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
25	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
26	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
27	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
28	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
29	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
30	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
31	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
32	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
33	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
34	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
35	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
36	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
37	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
38	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
39	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
40	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
41	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
42	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
43	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
44	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
45	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
46	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
47	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
48	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
49	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
50	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
51	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
52	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
53	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
54	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
55	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
56	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
57	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
58	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
59	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
60	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
61	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
62	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
63	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
64	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
65	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
66	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
67	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
68	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
69	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
70	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
71	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
72	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
73	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
74	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
75	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
76	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
77	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
78	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
79	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
80	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.
81	18480182	Roles of PINCH-2 in regulation of glomerular cell shape change and fibronectin matrix deposition.
82	18480182	The PINCH-1-integrin-linked kinase (ILK)-alpha-parvin (PIP) complex plays important roles in the regulation of glomerular cell behavior, including podocyte shape change, apoptosis, and mesangial fibronectin matrix deposition.
83	18480182	In this study, we show that PINCH-2, a protein that is structurally related to PINCH-1 but encoded by a different gene, is coexpressed with PINCH-1 in podocytes.
84	18480182	Treatment of podocytes with transforming growth factor (TGF)-beta1 elevated the level of PINCH-2, resulting in increased association of PINCH-2 with ILK and alpha-parvin and concomitant displacement of PINCH-1 from the PIP complex.
85	18480182	To gain insights into the functional consequences of elevated PINCH-2 expression, we overexpressed PINCH-2 in podocytes by infection with an adenovirus encoding PINCH-2.
86	18480182	Overexpression of PINCH-2 resulted in displacement of PINCH-1 from the PIP complex and compromised podocyte spreading.
87	18480182	The PINCH-2-mediated displacement of PINCH-1, however, did not prompt apoptosis.
88	18480182	Interestingly, the effect of PINCH-2 on podocyte spreading depends on differentiation status, as overexpression of PINCH-2 in podocytes that were not fully differentiated did not alter cell spreading.
89	18480182	Finally, we show that overexpression of PINCH-2 in mesangial cells resulted in displacement of PINCH-1 from the PIP complex but impaired neither mesangial cell spreading nor fibronectin matrix deposition.
90	18480182	These studies suggest that PINCH-2 can substitute for PINCH-1 in at least certain processes in glomerular cells (e.g., podocyte survival signaling and mesangial fibronectin matrix deposition), albeit that an aberrantly high level of PINCH-2 may contribute to TGF-beta1-induced alteration in podocyte shape modulation.