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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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Authors found that FUS (show FUS ELISA Kits), EWS and TAF15 expression is differentially regulated during brain development, both in time and in space. In particular, this study identifies a fine-tuned regulation of FUS (show FUS ELISA Kits) and EWS during neuronal differentiation.
Gnai1 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.
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.
a breakpoint in the EWSR1-ATF1 (show AFT1 ELISA Kits) fusion to be the same as that reported in HCCC. Established CCOC-T cells grew extremely slowly, but the cells showed highly invasive activity
study proposed that EWSR1 rearrangement was present in a subset of myoepithelial tumors of salivary glands, with variable morphological features
EWSR1 Gene Rearrangement is associated with Endometrial Primitive Neuroectodermal Tumor.
-cell lymphoblastic leukemia with t(11;22)(q24;q12) and EWSR1 rearrangement.
Kinetics of EWSR1 fusion sequence copy numbers in the plasma are correlated with changes of the tumor volume in patients with localized and metastatic disease.
Recent advances in biologic and genomic understanding of these two cancers has expanded the potential for therapeutic advancement and prevention. In Ewing sarcoma, directed focus on inhibition of EWSR1-FLI1 (show FLI1 ELISA Kits) and its effectors has produced promising results.
data suggest EWS/FLI (show FLII ELISA Kits) binds to "promoter-like" and "enhancer-like" microsatellites to mediate activation and repression of target genes through different regulatory mechanisms
four oncogenic ETS (show ETS1 ELISA Kits) (ERG (show ERG ELISA Kits), ETV1 (show ETV1 ELISA Kits), ETV4 (show ETV4 ELISA Kits), and ETV5), and no other ETS (show ETS1 ELISA Kits), interact with the Ewing's sarcoma breakpoint protein, EWS.
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.
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