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FLI1 encodes a protein with a gelsolin-like actin binding domain and an N-terminal leucine-rich repeat-protein protein interaction domain. 再加上，我们可以发Friend Leukemia Virus Integration 1 抗体 (184) 和 Friend Leukemia Virus Integration 1 蛋白 (8)和数多这个蛋白质的别的产品。
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These results indicate that Fli1 deficiency promotes migration, proliferation and cell survival, while abating tube formation of endothelial cells, suggesting that Fli1 deficiency is potentially attributable to the development of both proliferative obliterative vasculopathy (occlusion of arterioles and small arteries) and destructive vasculopathy (loss of small vessels) characteristic of SSc (显示 CYP11A1 ELISA试剂盒) vasculopathy.
Fli1 functioned as an oncogene (显示 RAB1A ELISA试剂盒) in HCC carcinogenesis and it exerted its promoting metastatic effect primarily by modulating the matrix metalloproteinase (MMP)2 (显示 MMP2 ELISA试剂盒) signaling pathway.
Decreased serum LIF levels may be associated with vasculopathy in systemic sclerosis (SSc) and that Fli1 deficiency may contribute to the inhibition of LIF-dependent biological effects on SSc endothelial cells by suppressing the expression of LIF, LIF receptor, and gp130.
Studies demonstrate that the translocation-derived fusion protein EF (EWS (显示 EWSR1 ELISA试剂盒)-FLI1) misregulates numerous genes involved in metabolism suggesting that EF is a master regulator of metabolic reprogramming in Ewing sarcoma, diverting metabolites toward biosynthesis.
The gene that was most reproducibly up-regulated by EWS/FLI was NR0B1.
The mouse (Fli1) and human Fli1 genes are similarly regulated by Ets (显示 ETS1 ELISA试剂盒) factors in T cells.
In contrast, expression of Spi1 (显示 SPI1 ELISA试剂盒)/PU.1 in a Fli1 producing erythroleukemia cell line in which fli1 is activated, resulted in increased proliferation through activation of growth promoting proteins MAPK (显示 MAPK1 ELISA试剂盒), AKT (显示 AKT1 ELISA试剂盒), cMYC (显示 MYC ELISA试剂盒) and JAK2 (显示 JAK2 ELISA试剂盒)
CXCL6 expression is upregulated by Fli1 deficiency in fibroblasts and endothelial cells, potentially contributing to the development of fibrosis and vasculopathy in the skin, lung, and heart of systemic sclerosis.
This is the first report presenting CD13 (显示 ANPEP ELISA试剂盒) and FLI1 as important mediators of resistance to BRAF (显示 BRAF ELISA试剂盒) inhibition with potential as drug targets in BRAF (显示 BRAF ELISA试剂盒) inhibitors refractory melanoma.
This study uncovers FLI1 as an important driving factor that promotes tumor growth in SCLC through the miR-17-92 pathway. FLI1 may serve as an attractive target for therapeutic intervention of SCLC.
the Fox transcription factor binding motif was frequently observed within EWS (显示 EWSR1 ELISA试剂盒)-FLI1 peaks and Foxq1 (显示 FOXQ1 ELISA试剂盒) was identified as the cooperative partner that interacts with the EWS (显示 EWSR1 ELISA试剂盒) portion of EWS (显示 EWSR1 ELISA试剂盒)-FLI1.
Histones showed limited activation in regions of single TF binding, while enhancers that bind NF-E2 and either RUNX1 (显示 RUNX1 ELISA试剂盒), FLI1 or both TFs gave the highest signals for TF occupancy and H3K4me2; these enhancers associated best with genes activated late in MK maturation.
loss of ERG (显示 ERG ELISA试剂盒) and FLI1 might contribute to the pathogenesis of vascular lung complications through the induction of inflammation.
These results provide the first evidences that Fli-1 positively regulates LPS (显示 TLR4 ELISA试剂盒)-induced IL-27 (显示 IL27 ELISA试剂盒) production in macrophages
protective against nephritis MRL/lpr (显示 FAS ELISA试剂盒) mice
Fli1 is epigenetically suppressed and is a potential predisposing factor in the pathogenesis of systemic sclerosis. (Review)
The short nose, otitis media, and hearing impairment in Jacobsen syndrome are likely because of hemizygosity for ETS1 (显示 ETS1 ELISA试剂盒) and FLI1.
Simultaneous downregulation of KLF5 (显示 KLF5 ELISA试剂盒) and Fli1 is a key feature underlying systemic sclerosis.
bosentan...increased DNA binding of Fli1 and the suppression of type I collagen expression in systemic sclerosis fibroblasts
mesodermal Wnt3a (显示 WNT3A ELISA试剂盒)-mediated signaling via the transcription factor Lef1 (显示 LEF1 ELISA试剂盒) positively regulates EC specification (defined by kdrl expression) at the expense of primitive erythrocyte specification (defined by gata1 (显示 GATA1 ELISA试剂盒) expression) in zebrafish embryos.
Fli+ etsrp+ hemato-vascular progenitor cells proliferate at the lateral plate mesoderm during vasculogenesis in zebrafish.
These results showed that young thrombocytes have higher GATA1 (显示 GATA1 ELISA试剂盒) promoter activity, while mature thrombocytes have more fli1 gene promoter transcription.
fli1, and etsrp, demonstrated that erg and fli1 act cooperatively and are required for angiogenesis possibly via direct regulation of an endothelial cell junction molecule, VE-cadherin (显示 CDH5 ELISA试剂盒)
Interaction between EWSR1 (显示 EWSR1 ELISA试剂盒)/FLI1 and EWSR1 (显示 EWSR1 ELISA试剂盒) in Ewing sarcoma may induce mitotic defects leading to genomic instability and subsequent malignant transformation.
This gene encodes a transcription factor containing an ETS DNA-binding domain. The gene can undergo a t(11\;22)(q24\;q12) translocation with the Ewing sarcoma gene on chromosome 22, which results in a fusion gene that is present in the majority of Ewing sarcoma cases. An acute lymphoblastic leukemia-associated t(4\;11)(q21\;q23) translocation involving this gene has also been identified. Alternative splicing results in multiple transcript variants.
Ewing sarcoma breakpoint region 2
, Friend leukemia integration 1 transcription factor
, Friend leukemia virus integration 1
, proto-oncogene Fli-1
, transcription factor ERGB
, fli-1 proto-oncogene
, friend leukemia integration 1 transcription factor-like
, Friend leukemia integration 1 transcription factor-like
, retroviral integration site protein Fli-1
, retroviral integration site protein Fli-1 homolog