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FOSL2 is a direct target of miR (show MLXIP Proteins)-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 (show TGFB1 Proteins)-induced migration by interaction with Smad3 (show SMAD3 Proteins) in non-small cell lung cancer.FOSL2 positively regulates TGF-beta1 (show TGFB1 Proteins) signalling .
FRA2 is a STAT5 (show STAT5A Proteins) target gene regulated by IL-2 (show IL2 Proteins) in human CD4 (show CD4 Proteins) 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 (show FOSB Proteins) transcription factor complex, c-Jun (show JUN Proteins) and Fra2
SOX4 is a direct target gene of FRA-2 and induces expression of HDAC8 (show HDAC8 Proteins) 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 (show JUND Proteins) in CCR4 (show CCR4 Proteins)-expressing mature T-cell malignancies such as ATLL and CTCLs
FOSL2 is a critical regulator of leptin (show LEP Proteins) expression in adipocytes
Results suggest that Fra-2 protein may be more effective than ATF-2 (show ATF2 Proteins) protein in cyst formation originated from epithelial cells of dental follicles.
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 (show FOXO1 Proteins)) and interferon regulatory factor 4 (Irf4 (show IRF4 Proteins)) expression and influences proliferation and differentiation of B cells at multiple stages.
Deletion of Fra-2 leads to increased PPARgamma2 (show PPARG Proteins) expression and adipocyte differentiation as well as increased adipocyte apoptosis through upregulation of hypoxia-inducible factors.
Osteoblast-specific expression of Fra-2/AP-1 (show JUN Proteins) controls adiponectin and osteocalcin (show BGLAP Proteins) expression and affects metabolism.
Cytokine-mediated Fra-2 expression and stabilization is linked to regulation of myogenic progenitor cells.
AP-1 (show JUN Proteins) composed with JunD (show JUND Proteins) and Fra2 protein plays a primary role in enhancing the transcription level of the CD11c (show ITGAX Proteins) gene in dendritic cells
Identify Fra-2 as an O(2)-sensitive transcriptional regulator of inducible TGFbeta (show TGFB1 Proteins) expression and position Fra-2 as an important player in reoxygenation-induced myocardial fibrosis.
These findings reveal a novel function of Fra-2/AP-1 (show JUN Proteins) as a positive regulator of bone and matrix formation in mice and humans.
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.
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