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Human Polyclonal FOSL2 Primary Antibody pour IP - ABIN515798
Wrann, Eguchi, Bozec, Xu, Mikkelsen, Gimble, Nave, Wagner, Ong, Rosen: FOSL2 promotes leptin gene expression in human and mouse adipocytes. dans The Journal of clinical investigation 2012
this study indicates the existence of an aberrant miR-124-3p/Fra-2 pathway that results in glioma aggressiveness
Data provide evidence that FOSL2 is the target gene of miR-143 and negatively correlated with its expression. Down-regulation of FOSL2 seems to be a critical step in regulation of OS properties and the expression of miR-143 can inhibit the proliferation, migration and invasion of OS by reducing the expression of FOSL2.
FOSL2 is a direct target of miR-597 in breast cancer cells.
The binding and expression of c-Fos/Fra-2 increased as a function of severity of tongue lesions, yet selective participation of c-Jun appears to promote poor differentiation and aggressive tumorigenesis.
FOSL2 facilitates TGF-beta1-induced migration by interaction with Smad3 in non-small cell lung cancer.FOSL2 positively regulates TGF-beta1 signalling .
FRA2 is a STAT5 target gene regulated by IL-2 in human CD4 T cells.
we show that the suppression was mediated, at least in part, by a suspension culture-driven decrease in the levels of two members of the AP1 transcription factor complex, c-Jun and Fra2
SOX4 is a direct target gene of FRA-2 and induces expression of HDAC8 in adult T-cell leukemia/lymphoma.
This study suggests that Fra-2 transgenic mice as an animal model of systemic sclerosis-associated pulmonary arterial hypertension display main characteristic features of the human disease.
results demonstrate the presence of a common oncogenic cascade initiated by FRA2/JUND in CCR4-expressing mature T-cell malignancies such as ATLL and CTCLs
FOSL2 is a critical regulator of leptin expression in adipocytes
Results suggest that Fra-2 protein may be more effective than ATF-2 protein in cyst formation originated from epithelial cells of dental follicles.
These findings reveal a novel function of Fra-2/AP-1 as a positive regulator of bone and matrix formation in mice and humans.
Fra-2 is overexpressed in SSc and acts as a novel downstream mediator of the profibrotic effects of TGFbeta and PDGF.
Fra-2 overexpression is associated with a more aggressive tumor phenotype and is probably involved in breast cancer progression in vivo.
aberrantly expressed Fra-2 in association with JunD may play a major role in CCR4 expression and oncogenesis in adult T-cell leukemia.
FRA2 and AP1 have roles in development of pulmonary fibrosis
Genes for Fra2, Id2, and CSF1-receptor are deregulated, regardless of whether the in anaplastic large cell lymphoma contains the t(2;5).
Fra-2 transgenic natural killer (NK)T cells produce unusually high amounts of interleukin (IL)-2 and IL-4, and proliferate abnormally.
Fra-2 is present in human systemic sclerosis and may contribute to the development of microvasculopathy by inducing endothelial cell apoptosis and by reducing endothelial cell migration and chemotaxis.
Fra-2 overexpression might impair myofibroblast functions crucial for secondary septation
Data show that Fos-Related Antigen-2 (Fra-2) is a key upstream regulator of forkhead box O1 (Foxo1) and interferon regulatory factor 4 (Irf4) expression and influences proliferation and differentiation of B cells at multiple stages.
Deletion of Fra-2 leads to increased PPARgamma2 expression and adipocyte differentiation as well as increased adipocyte apoptosis through upregulation of hypoxia-inducible factors.
Osteoblast-specific expression of Fra-2/AP-1 controls adiponectin and osteocalcin expression and affects metabolism.
Cytokine-mediated Fra-2 expression and stabilization is linked to regulation of myogenic progenitor cells.
AP-1 composed with JunD and Fra2 protein plays a primary role in enhancing the transcription level of the CD11c gene in dendritic cells
Identify Fra-2 as an O(2)-sensitive transcriptional regulator of inducible TGFbeta expression and position Fra-2 as an important player in reoxygenation-induced myocardial fibrosis.
Since transgenic overexpression of Fra-2 causes not only fibrosis but also vascular disease, Fra-2 might be an interesting novel candidate for molecular-targeted therapies for systemic sclerosis.
AP-1 transrepressing retinoic acid does not deplete coactivators or AP-1 monomers but may target specific Jun or Fos containing dimers
Fra2 is a novel transcription factor important for skeletogenesis by affecting chondrocyte differentiation
MEKK1 regulates Fra-2 protein stability by inducing Fra-2 ubiquitination and degradation.
NFATc1 negatively regulates osteoblst differentiation by regulating fra-2
These data identify junD proto-oncogene (JunD) and Fos-related antigen 2 (Fra-2) as the activator protein-1 (AP-1) factors responsible for the RANKL-induced upregulation of the mouse Tcirg1 gene expression.
Fos-related protein Fra-2 controls osteoclast survival and size
Fra-2 is necessary for regulation of normal invariant natural killer (iNK)T cell development and function; loss of Fra-2 causes a 2.5-fold increase in thymic iNKT cells.
Fra-2 transcripion factor induces progressive peripheral vasculopathy in mice that resembles human systemic sclerosis.
Fos-like antigen 2 (Fosl2), potentiates the rate of myocardial accretion from the zebrafish second heart field.
The Fos gene family consists of 4 members FOSL1, and FOSL2. These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family, thereby forming the transcription factor complex AP-1. As such, the FOS proteins have been implicated as regulators of cell proliferation, differentiation, and transformation.
fos-related antigen 2
, FOS-like antigen 2
, phospholipase B1