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Results find that the Asp residue in TAF15 YGGDR(S/G)G repeats confers poor binding to PRMT1 indicating that YGGDR(S/G)G repeats may contribute to TAF15 specialization by enabling differential interactions with PRMT1 and reduced overall levels of TAF15 methylation compared with other FET proteins.
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weak, multivalent interactions between TAF15 fibrils and heptads throughout RNA pol II CTD collectively mediate complex formation.
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In human stem cell-derived motor neurons, the RNA profile associated with concomitant loss of both TAF15 and FUS resembles that observed in the presence of the amyotrophic lateral sclerosis (ALS)-associated mutation FUS R521G, but contrasts with late-stage sporadic ALS patients.
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In a cohort of youth at risk for bipolar disorder, pathway analysis showed an enrichment of the glucocorticoid receptor (GR) pathway with the genes MED1, HSPA1L, GTF2A1 and TAF15, which might underlie the previously reported role of stress response in the risk for bipolar disorder in vulnerable populations.
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Aggregation of FET proteins FUS, EWSR1, and TAF15 mediate a pathological change in amyotrophic lateral sclerosis. (Review)
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Studies provide evidence that FUS/TLS, EWS and TAF15 proteins play a major role in neurodegenerative disorders. (review).
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O-GlcNAc glycosylation stoichiometry of TAF15
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RNA binding by TAF-15 is dependent upon structural elements in the RNA rather than sequence.
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our data suggest that TAF15 and TLS/FUS operate within similar but not identical hnRNP M-TET protein complexes to influence the transcriptional or post-transcriptional output of a particular cell type.
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Data indicate that distinct differences in proteins becoming Poly(ADP-ribose) PARylated upon various genotoxic insults are observed, exemplified by the PARylation of RNA-processing factors THRAP3 and TAF15 under oxidative stress.
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TAF15 depletion inhibits growth & increases apoptosis. Its knockdown affects many genes involved in cell cycle & cell death. Among these, targets of microRNAs generated from the onco-miR-17 locus were overrepresented.
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Data show that FUS and TAF15 locate to cellular stress granules to a larger extend than EWS. FET-protein stress granule association most likely is a downstream response to cellular stress.
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The existence of a functionally discrete subset of U1 snRNP in association with TAF15 was suggested and provided further support for the involvement of U1 snRNP components in early steps of coordinated gene expression.
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TAF15 plays a role in RNA transport and/or local RNA translation
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Missense mutations of TAF-15, an RNA-binding protein, were found in patients with amyotrophic lateral sclerosis, and gene conferred neurodegeneration when expressend in Drosophila.
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REsults suggest the possibility that alterations of TAF15 and EWS might also be involved in the pathogenesis of FUS proteinopathies such as ALS and FTLD.
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Rare translocation t(12;17)(p13;q12), this translocation has been reported in 25 cases and its putative molecular consequence, the formation of a TAF15-ZNF384 fusion gene, in only six cases.
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These results suggest that additional studies are needed to determine whether mutations in the TAF15 gene represent a cause of familial amyotrophic lateral sclerosis.
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Elevated TAF15 mRNA levels did not translate to strongly elevated protein levels, consistent with its infrequent occurrence as translocation partner in tumors.
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Our findings define a role for a tumor-specific TAF15 antigen in malignant processes.
