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EWSR1 encodes a multifunctional protein that is involved in various cellular processes, including gene expression, cell signaling, and RNA processing and transport. Additionally we are shipping EWSR1 Antibodies (153) and EWSR1 Proteins (4) and many more products for this protein.
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Gnai1 (show GNAI1 ELISA Kits) function is impaired in the spinal cord of Ews/Ewsr1 KO mice
EWS is normally O-GlcNAc glycosylated in the brain.
glycosylation of EWS protein
EWSR1 is involved in the post-transcriptional regulation of Uvrag via a miRNA-dependent pathway, resulting in the deregulation of autophagy inhibition.
EWS is essential during the early steps of white adipocyte differentiation, at least in part through its regulation of BMP2 (show BMP2 ELISA Kits) and BMP4 (show BMP4 ELISA Kits) expression.
EWS has a role in mitochondrial and cellular energy homeostasis that involves controlling PGC-1alpha (show PPARGC1A ELISA Kits) protein stability
both Etv1 (show ETV1 ELISA Kits) and Ewsr1 were necessary for Fgf10 (show FGF10 ELISA Kits) expression and elongation of the limb bud.
EWS is involved in post-transcriptional regulation of Col4a1 (show COL4A1 ELISA Kits) and CTGF (show CTGF ELISA Kits) via a Drosha (show DROSHA ELISA Kits)-miRNA-dependent pathway.
These results demonstrate that EWS is essential for early brown fat lineage determination.
Forced expression of EWS/ATF1 (show AFT1 ELISA Kits) resulted in the development of EWS/ATF1 (show AFT1 ELISA Kits)-dependent sarcomas. Lineage-tracing experiments indicated that neural crest-derived cells were subject to EWS/ATF1 (show AFT1 ELISA Kits)-driven transformation.
Mutation of the EWS gene modulates Sox9 (show SOX9 ELISA Kits) gene expression essential for chondrocyte differentiation.
Ewsr1 maintains mitotic integrity and proneural cell survival in early zebrafish development
Interaction between EWSR1/FLI1 (show FLI1 ELISA Kits) and EWSR1 in Ewing sarcoma may induce mitotic defects leading to genomic instability and subsequent malignant transformation.
As spontaneous fluctuations in EWS-FLI1 (show FLI1 ELISA Kits) levels of Ewing sarcoma cells in vitro and in vivo, associated with a switch between a proliferative, non-migratory EWS-FLI1 (show FLI1 ELISA Kits)-high and a non-proliferative highly migratory EWS-FLI1 (show FLI1 ELISA Kits)-low state, were recently described, our data provide a mechanistic basis for the underlying EWS-FLI1 (show FLI1 ELISA Kits)-dependent reversible cytoskeletal reprogramming of Ewing sarcoma cells.
Fusion of short fragments of EWSR1 to FLI1 (show FLI1 ELISA Kits) is sufficient to recapitulate BAF (show BANF1 ELISA Kits) complex retargeting and EWS-FLI1 (show FLI1 ELISA Kits) activities; studies thus demonstrate that the physical properties of prion (show PRNP ELISA Kits)-like domains can retarget critical chromatin regulatory complexes to establish and maintain oncogenic gene expression programs.
Case Reports: maxillary sinus clear cell carcinomas with EWSR1-ATF1 (show AFT1 ELISA Kits) gene fusion.
Results expand the spectrum of tumor types harboring EWSR1/FUS (show FUS ELISA Kits)-ATF1 (show AFT1 ELISA Kits) gene fusions to include a subgroup of conventional epithelioid malignant mesothelioma.
papillary thyroid carcinomas with EWSR1 rearrangement disclosed a lower percentage of nuclei with EWSR1 polysomy than those without EWSR1 rearrangement
The net result of combined lurbinectedin and irinotecan treatment was a complete reversal of EWS-FLI1 (show FLI1 ELISA Kits) activity and elimination of established tumors in 30% to 70% of mice after only 11 days of therapy. Our results illustrate the preclinical safety and efficacy of a disease-specific therapy targeting the central oncogenic driver in Ewing sarcoma.
Aggregation of FET proteins FUS, EWSR1, and TAF15 mediate a pathological change in amyotrophic lateral sclerosis. (Review)
A subgroup of MAML2 fusion-negative mucoepidermoid carcinomas are actually clear cell carcinoma of the salivary gland with EWSR1 translocation.
Study found consistent DNA hypomethylation at enhancers regulated by the disease-defining EWS-FLI1 (show FLI1 ELISA Kits) fusion protein, thus establishing epigenomic enhancer reprogramming as a ubiquitous and characteristic feature of Ewing sarcoma.
Report a distinct group of myxoid mesenchymal neoplasms occurring in children or young adults with a predilection for intracranial locations with EWSR1-AFT1/CREB1 (show CREB1 ELISA Kits)/CREM (show CREM ELISA Kits) fusions.
This gene encodes a multifunctional protein that is involved in various cellular processes, including gene expression, cell signaling, and RNA processing and transport. The protein includes an N-terminal transcriptional activation domain and a C-terminal RNA-binding domain. Chromosomal translocations between this gene and various genes encoding transcription factors result in the production of chimeric proteins that are involved in tumorigenesis. These chimeric proteins usually consist of the N-terminal transcriptional activation domain of this protein fused to the C-terminal DNA-binding domain of the transcription factor protein. Mutations in this gene, specifically a t(11\;22)(q24\;q12) translocation, are known to cause Ewing sarcoma as well as neuroectodermal and various other tumors. Alternative splicing of this gene results in multiple transcript variants. Related pseudogenes have been identified on chromosomes 1 and 14.
RNA-binding protein EWS
, Ewing sarcoma RNA-binding protein
, Ewing sarcoma breakpoint region 1
, Ewing sarcoma homolog
, Ewings sarcoma EWS-Fli1 (type 1) oncogene