Ignet

Gene Information

Gene symbol: FOSL1

Gene name: FOS-like antigen 1

HGNC ID: 13718

Synonyms: fra-1

Related Genes

#	Gene Symbol	Number of hits
1	ABCA1	1 hits
2	ADIPOQ	1 hits
3	AGT	1 hits
4	EREG	1 hits
5	FOS	1 hits
6	FOSL2	1 hits
7	GTF3A	1 hits
8	INS	1 hits
9	IRF6	1 hits
10	JUN	1 hits
11	JUND	1 hits
12	PCNA	1 hits

Related Sentences

#	PMID	Sentence
1	1372897	We demonstrate here that fatty acids can regulate specific gene expression; mRNAs encoding the fatty acid binding protein adipocyte P2 (aP2) and the Fos-related transcription factor Fra1 are specifically induced at least 20-fold upon treatment of preadipocytes with oleate.
2	1372897	For aP2, the effect requires long chain fatty acids and occurs without a generalized activation of the genes linked to adipocyte differentiation.
3	1372897	Unlike aP2, Fra1 induction by fatty acids also can be detected in NIH 3T3 and 3T3-C2 fibroblasts.
4	1372897	We demonstrate here that fatty acids can regulate specific gene expression; mRNAs encoding the fatty acid binding protein adipocyte P2 (aP2) and the Fos-related transcription factor Fra1 are specifically induced at least 20-fold upon treatment of preadipocytes with oleate.
5	1372897	For aP2, the effect requires long chain fatty acids and occurs without a generalized activation of the genes linked to adipocyte differentiation.
6	1372897	Unlike aP2, Fra1 induction by fatty acids also can be detected in NIH 3T3 and 3T3-C2 fibroblasts.
7	11179452	Using mRNA differential display, we have compared 3T3-L1 cells treated to differentiate in the presence of BRL49653 with untreated 3T3-L1 cells and identified Fos-related antigen 1 (Fra-1), a member of the Fos protein family, as a novel molecular target for BRL49653 action in 3T3-L1 cells.
8	11179452	The only other member of the Fos-Jun family expressed in differentiated 3T3-L1 cells was JunD and a complex of Fra-1 and JunD was formed on a consensus AP-1 binding element in differentiated 3T3-L1 cells, suggesting that the complex of Fra-1 and JunD may play a role in the stimulation of the differentiation process of 3T3-L1 cells observed after treatment of the cells with insulin sensitizers.
9	11179452	Using mRNA differential display, we have compared 3T3-L1 cells treated to differentiate in the presence of BRL49653 with untreated 3T3-L1 cells and identified Fos-related antigen 1 (Fra-1), a member of the Fos protein family, as a novel molecular target for BRL49653 action in 3T3-L1 cells.
10	11179452	The only other member of the Fos-Jun family expressed in differentiated 3T3-L1 cells was JunD and a complex of Fra-1 and JunD was formed on a consensus AP-1 binding element in differentiated 3T3-L1 cells, suggesting that the complex of Fra-1 and JunD may play a role in the stimulation of the differentiation process of 3T3-L1 cells observed after treatment of the cells with insulin sensitizers.
11	14530283	Expression profiling identifies genes that continue to respond to insulin in adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha.
12	14530283	We have employed microarray technology using RNA from normal 3T3-L1 adipocytes and from 3T3-L1 adipocytes made insulin-resistant by treatment with tumor necrosis factor-alpha to identify a new class of insulin-responsive genes.
13	14530283	Socs-3, junB, and matrix metalloproteinase-11).
14	14530283	Glut-1 and beta3-adrenergic receptor), other novel insulin-sensitive genes were also identified (e.g.
15	14530283	Egr-1, epiregulin, Fra-1, and ABCA1).
16	14530283	Using an antisense strategy, we show that tissue factor and macrophage colony-stimulating factor, two cardiovascular risk factors, are downstream EGR-1 target genes in the adipocyte.
17	14566971	Age-related differences in MAP kinase activity in VSMC in response to glucose or TNF-alpha.
18	14566971	Activator protein-1 (AP-1) binding to DNA increased more in VSMC from old versus young rats (P < 0.02) and was related to increased expression of its components, c-Fos, Fra-1, and JunD.
19	14566971	The relationship to upstream signals, i.e., activities of mitogen-activated protein kinases (MAPK), was studied using antibodies to total and phosphorylated forms of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK) and p38.
20	14566971	High glucose and TNF-alpha increased ERK phosphorylation more in old (P < 0.05); whereas only TNF-alpha induced JNK activation in young (P < 0.04).
21	14566971	PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old.
22	14566971	Age-related differences in MAP kinase activity in VSMC in response to glucose or TNF-alpha.
23	14566971	Activator protein-1 (AP-1) binding to DNA increased more in VSMC from old versus young rats (P < 0.02) and was related to increased expression of its components, c-Fos, Fra-1, and JunD.
24	14566971	The relationship to upstream signals, i.e., activities of mitogen-activated protein kinases (MAPK), was studied using antibodies to total and phosphorylated forms of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK) and p38.
25	14566971	High glucose and TNF-alpha increased ERK phosphorylation more in old (P < 0.05); whereas only TNF-alpha induced JNK activation in young (P < 0.04).
26	14566971	PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old.
27	15145956	Glucose regulates interleukin-8 production in aortic endothelial cells through activation of the p38 mitogen-activated protein kinase pathway in diabetes.
28	15145956	This increased adhesion is mediated primarily through induction of interleukin (IL)-8 via activation of the transcription factor AP-1 (Srinivasan, S., Yeh, M., Danziger, E.
29	15145956	In the current study, we identified the elements in the AP-1 transcriptional complex that are activated by glucose.
30	15145956	These elements include c-Jun, c-Fos, and Fra-1.
31	15145956	AP-1 is activated by cellular oxidative stress, and we have reported significant production of ROS by high glucose-cultured cells.
32	15145956	We examined signaling pathways upstream of AP-1 in EC that lead to AP-1 activation by HG.
33	15145956	Inhibition of the p38 pathway using 5 microm SB203580 significantly reduced glucose-mediated IL-8 mRNA production by 60%.
34	15145956	Thus, glucose-stimulated monocyte adhesion is primarily regulated through phosphorylation of p38 with subsequent activation of AP-1, leading to IL-8 production.
35	15145956	Taken together, these data indicate that chronic elevated glucose in diabetes activates the p38 MAP kinase pathway to increase inflammatory IL-8 gene induction and monocyte/endothelial adhesion.
36	16224068	Transcriptional repression of ATP-binding cassette transporter A1 gene in macrophages: a novel atherosclerotic effect of angiotensin II.
37	16224068	Herein, we describe a novel transcription mechanism through which Ang II inhibits macrophage expression of the ATP-binding cassette transporter A1 (ABCA1), a key regulator of reverse cholesterol transport.
38	16224068	We demonstrate that chronic Ang II infusion substantially promotes macrophage infiltration, foam cell formation, and atherosclerosis in low-density lipoprotein receptor-deficient mice and significantly reduces ABCA1 expression in peripheral macrophages.
39	16224068	Administration of the Ang II type 1 receptor blocker valsartan inhibited Ang II-induced ABCA1 mRNA repression, macrophage cholesterol accumulation, and atherosclerosis.
40	16224068	Ang II treatment reduced ABCA1 promoter activity of in vitro cultured mouse peritoneal macrophages, inducing fos-related antigen 2 (Fra2) protein binding to an ABCA1 promoter E-box motif, a site known to negatively regulate macrophage ABCA1 transcription.
41	16224068	Valsartan pretreatment blocked Fra2 binding to the ABCA1 promoter, and Fra2 small interfering RNA pretreatment attenuated Ang II-mediated ABCA1 transcriptional inhibition, confirming the role of Fra2 in this process.
42	16224068	This new evidence suggests that Ang II, a well-known proinflammatory and pro-oxidative factor, alters macrophage cholesterol homeostasis by repressing ABCA1 to promote foam cell formation and atherosclerosis.
43	22386866	Different signaling mechanisms regulating IL-6 expression by LPS between gingival fibroblasts and mononuclear cells: seeking the common target.
44	22386866	To reduce connective tissue IL-6 level stimulated by LPS, it is essential to control IL-6 expression in both mononuclear cells and fibroblasts.
45	22386866	In this study, we found that signaling pathways mediating LPS-stimulated IL-6 in mononuclear U937 cells and fibroblasts were different.
46	22386866	Furthermore, our studies showed that while LPS activated AP-1 and NFκB in U937 cells, it only activated NFκB in fibroblasts.
47	22386866	Analysis of nuclear AP-1 subunits showed that LPS stimulated c-Fos, Fra-1 and Jun D activities in U937 cells, but not fibroblasts.
48	22386866	The lack of ERK involvement in LPS-stimulated IL-6 in fibroblasts was further supported by the observations that simvastatin, which is known to target ERK-AP-1, failed to inhibit LPS-stimulated IL-6 by fibroblasts.
49	22386866	Finally, we showed that targeting NFκB pathway was highly effective in inhibition of LPS-stimulated IL-6 in coculture of U937 cells and fibroblasts.