Ignet

Gene Information

Gene symbol: SRF

Gene name: serum response factor (c-fos serum response element-binding transcription factor)

HGNC ID: 11291

Synonyms: MCM1

Related Genes

#	Gene Symbol	Number of hits
1	ABRA	1 hits
2	CDKN2A	1 hits
3	CREB1	1 hits
4	DDHD2	1 hits
5	EGR1	1 hits
6	ELK1	1 hits
7	FOS	1 hits
8	FSD1	1 hits
9	HSPD1	1 hits
10	INS	1 hits
11	LGALS4	1 hits
12	MAP2K1	1 hits
13	MAPK1	1 hits
14	MIRN206	1 hits
15	MKL1	1 hits
16	MYOCD	1 hits
17	NFKB1	1 hits
18	NR1H2	1 hits
19	PRKAA1	1 hits
20	PRKAR2A	1 hits
21	RHOD	1 hits
22	TGFA	1 hits
23	THBS1	1 hits
24	VASP	1 hits

Related Sentences

#	PMID	Sentence
1	2358629	Hence, patients with ARF or SRF exhibited a high potential for reversible lesions.
2	2358629	We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease.
3	2358629	Hence, patients with ARF or SRF exhibited a high potential for reversible lesions.
4	2358629	We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease.
5	10829028	Activation of serum response factor in the depolarization induction of Egr-1 transcription in pancreatic islet beta-cells.
6	10829028	Pharmacological inhibition of the Egr-1 induction by H89 (48%) and calmidazolium (35%), but not by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 and 2 or phosphatidylinositol 3-kinase inhibitors, implied that protein kinase A and Ca(2+)/calmodulin pathways are involved.
7	10829028	Depolarization activation of 5XSRE-LUC and serum response factor (SRF)-GAL4 constructs, along with activation of SRF-GAL4 by co-transfection with constitutively active calmodulin kinase IV and protein kinase A, and binding of Ser(103)-phosphorylated SRF in nuclear extracts, indicated that the SRE.SRF complexes contribute to the Ca(2+)-mediated transcriptional regulation of Egr-1.
8	10829028	Activation of serum response factor in the depolarization induction of Egr-1 transcription in pancreatic islet beta-cells.
9	10829028	Pharmacological inhibition of the Egr-1 induction by H89 (48%) and calmidazolium (35%), but not by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 and 2 or phosphatidylinositol 3-kinase inhibitors, implied that protein kinase A and Ca(2+)/calmodulin pathways are involved.
10	10829028	Depolarization activation of 5XSRE-LUC and serum response factor (SRF)-GAL4 constructs, along with activation of SRF-GAL4 by co-transfection with constitutively active calmodulin kinase IV and protein kinase A, and binding of Ser(103)-phosphorylated SRF in nuclear extracts, indicated that the SRE.SRF complexes contribute to the Ca(2+)-mediated transcriptional regulation of Egr-1.
11	10835359	The structure of the MEF2S domain is entirely different from that of the equivalent SAM domain in SRF and MCM1, accounting for the absence of cross-reactivity with other proteins that interact with these transcription factors.
12	14683523	Our previous studies have found that high glucose does not induce cellular hypertrophy or expression of TGF-beta1 (transforming growth factor-beta1) in distal renal tubule cells [Yang, Guh, Yang, Lai, Tsai, Hung, Chang and Chuang (1998) J.
13	14683523	Since TSP-1 (thrombospondin-1) has been demonstrated to activate latent TGF-beta1 in a variety of systems, the following experiments were performed.
14	14683523	In addition, we observed several putative transcription factor binding sites in the TSP-1 promoter, including those for AP-1 (activator protein-1), CREB (cAMP response element binding protein), NF-kappaB (nuclear factor-kappaB), SRF (serum response factor) and HSF (heat-shock factor), by sequence mapping.
15	14683523	We showed that AP-1 and CREB were specifically induced by AGEs; furthermore, TFD (transcription factor decoy) for AP-1 could attenuate the AGE-induced increases in TSP-1 levels and cellular hypertrophy.
16	15772901	Insulin receptor structure and function as well as major pathways activated by insulin, i.e. phosphatidyl inositol-3 kinase (PI-3 K) cascade or mitogen-activated protein kinase (MAPK) cascades, were functional.
17	15772901	Abundances of the transcription factors Elk-1 and SRF being major players in coupling of MAPKs to cfos promoter activation were not altered.
18	16537394	Mimicking phosphorylation of serine-162, a target of protein kinase C-alpha, with an aspartic acid substitution (SRF-S162D) completely inhibited SRF-DNA binding and blocked alpha-actin gene transcription even in the presence of potent myogenic cofactors, while preserving c-fos promoter activity because of stabilization of the ternary complex via Elk-1.
19	16537394	Introduction of SRF-S162D into SRF null ES cells permitted transcription of the c-fos gene but was unable to rescue expression of myogenic contractile genes.
20	17082196	AMP-activated protein kinase impairs endothelial actin cytoskeleton assembly by phosphorylating vasodilator-stimulated phosphoprotein.
21	17082196	Using VASP phosphorylation status-specific antibodies, we identified AMP-activated protein kinase (AMPK), a serine-threonine kinase and fundamental sensor of energy homeostasis, in a screen for kinases that phosphorylate the Thr-278 site of VASP in endothelial cells.
22	17082196	Quantitative fluorescence-activated cell sorter analysis and serum response factor transcriptional reporter assays, which quantify the cellular F-/G-actin equilibrium, indicated that AMPK-mediated VASP phosphorylation impaired actin stress fiber formation and altered cell morphology.
23	17082196	These findings suggest that VASP is a new AMPK substrate, that VASP Thr-278 phosphorylation translates metabolic signals into actin cytoskeleton rearrangements, and that this signaling system becomes down-regulated in diabetic vessels.
24	17626048	Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
25	17626048	The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
26	17626048	A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
27	17626048	The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
28	17626048	The Elk1 binding site also bound the serum responsive factor (SRF).
29	17626048	Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
30	17626048	Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
31	17626048	The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
32	17626048	A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
33	17626048	The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
34	17626048	The Elk1 binding site also bound the serum responsive factor (SRF).
35	17626048	Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
36	17626048	Elk1 and SRF transcription factors convey basal transcription and mediate glucose response via their binding sites in the human LXRB gene promoter.
37	17626048	The nuclear receptors LXRalpha (NR1H3) and LXRbeta (NR1H2) are attractive drug targets for the treatment of diabetes and cardiovascular disease due to their established role as regulators of cholesterol and lipid metabolism.
38	17626048	A large body of literature has recently indicated their important roles in glucose metabolism and particularly LXRbeta is important for proper insulin production in pancreas.
39	17626048	The transcription start site of the human LXRB gene was determined and we identified two highly conserved, and functional, ETS and Elk1 binding sites, respectively, in the LXRB gene promoter.
40	17626048	The Elk1 binding site also bound the serum responsive factor (SRF).
41	17626048	Furthermore, mutation of the binding sites or siRNA knockdown of SRF and Elk1 significantly reduced the promoter activity and impaired the glucose response.
42	20655308	miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes.
43	20655308	After stimulation of cardiomyocytes with high glucose in vivo and in vitro, significant up-regulation of miR-1/miR-206 and post-transcriptional modulation of Hsp 60 were observed.
44	20655308	Serum response factor (SRF) and the MEK1/2 pathway were involved in miR-1 and miR-206 expression in cardiomyocytes. miR-1 and miR-206 regulated Hsp60 expression post-transcriptionally and accelerated cardiomyocyte apoptosis through Hsp60.
45	20655308	These results revealed that miR-1 and miR-206 regulate Hsp60 expression, contributing to high glucose-mediated apoptosis in cardiomyocytes.
46	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
47	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
48	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
49	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
50	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
51	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
52	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
53	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
54	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
55	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
56	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
57	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
58	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
59	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
60	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
61	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
62	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
63	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
64	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
65	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
66	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
67	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
68	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
69	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
70	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
71	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
72	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
73	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
74	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
75	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
76	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
77	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
78	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
79	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
80	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
81	21393865	Increased SRF transcriptional activity in human and mouse skeletal muscle is a signature of insulin resistance.
82	21393865	Actin cytoskeleton genes regulated by serum response factor (SRF) and its coactivator megakaryoblastic leukemia 1 (MKL1) had increased expression in T2D and FH(+) groups.
83	21393865	Furthermore, striated muscle activator of Rho signaling (STARS), an activator of SRF, was upregulated in T2D and FH(+) and was inversely correlated with insulin sensitivity.
84	21393865	Skeletal muscle from insulin-resistant mice recapitulated this gene expression pattern and showed reduced G-actin and increased nuclear localization of MKL1, each of which regulates SRF activity.
85	21393865	Overexpression of MKL1 or reduction in G-actin decreased insulin-stimulated Akt phosphorylation, whereas reduction of STARS expression increased insulin signaling and glucose uptake.
86	21393865	Pharmacological SRF inhibition by CCG-1423 reduced nuclear MKL1 and improved glucose uptake and tolerance in insulin-resistant mice in vivo.
87	21393865	Thus, SRF pathway alterations are linked to insulin resistance, may contribute to T2D pathogenesis, and could represent therapeutic targets.
88	21950552	Reduced expression of myocardin and serum response factor in the cavernous tissue of diabetic rats.
89	21950552	This study aimed to investigate the expression of myocardin and serum response factor (SRF) in the cavernous tissue of diabetic rats.
90	21950552	Western blot and qRT-PCR were used to determine the protein and mRNA expression levels of myocardin and SRF.
91	21950552	The mRNA and protein expression levels of myocardin and SRF were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.001).
92	21950552	It is concluded that diabetes inhibits the mRNA and protein expression of both myocardin and SRF in the cavernous tissue.
93	21950552	Reduced expression of myocardin and serum response factor in the cavernous tissue of diabetic rats.
94	21950552	This study aimed to investigate the expression of myocardin and serum response factor (SRF) in the cavernous tissue of diabetic rats.
95	21950552	Western blot and qRT-PCR were used to determine the protein and mRNA expression levels of myocardin and SRF.
96	21950552	The mRNA and protein expression levels of myocardin and SRF were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.001).
97	21950552	It is concluded that diabetes inhibits the mRNA and protein expression of both myocardin and SRF in the cavernous tissue.
98	21950552	Reduced expression of myocardin and serum response factor in the cavernous tissue of diabetic rats.
99	21950552	This study aimed to investigate the expression of myocardin and serum response factor (SRF) in the cavernous tissue of diabetic rats.
100	21950552	Western blot and qRT-PCR were used to determine the protein and mRNA expression levels of myocardin and SRF.
101	21950552	The mRNA and protein expression levels of myocardin and SRF were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.001).
102	21950552	It is concluded that diabetes inhibits the mRNA and protein expression of both myocardin and SRF in the cavernous tissue.
103	21950552	Reduced expression of myocardin and serum response factor in the cavernous tissue of diabetic rats.
104	21950552	This study aimed to investigate the expression of myocardin and serum response factor (SRF) in the cavernous tissue of diabetic rats.
105	21950552	Western blot and qRT-PCR were used to determine the protein and mRNA expression levels of myocardin and SRF.
106	21950552	The mRNA and protein expression levels of myocardin and SRF were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.001).
107	21950552	It is concluded that diabetes inhibits the mRNA and protein expression of both myocardin and SRF in the cavernous tissue.
108	21950552	Reduced expression of myocardin and serum response factor in the cavernous tissue of diabetic rats.
109	21950552	This study aimed to investigate the expression of myocardin and serum response factor (SRF) in the cavernous tissue of diabetic rats.
110	21950552	Western blot and qRT-PCR were used to determine the protein and mRNA expression levels of myocardin and SRF.
111	21950552	The mRNA and protein expression levels of myocardin and SRF were reduced in the cavernous tissue of diabetic rats compared with the control group (P < 0.001).
112	21950552	It is concluded that diabetes inhibits the mRNA and protein expression of both myocardin and SRF in the cavernous tissue.
113	23178076	SMA expression is regulated by transforming growth factor (TGF)-β1 and cell contact disruption, through signaling events targeting the serum response factor-myocardin-related transcription factor (MRTF) complex.
114	23178076	When co-expressed, it inhibited the stimulatory effects of MRTF-A, MRTF-B or the constitutive active forms of RhoA, Rac1, or Cdc42 on the SMA promoter.