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TAF15 encodes a member of the TET family of RNA-binding proteins. Additionally we are shipping TAF15 Antibodies (84) and and many more products for this protein.
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FUS and TAF15 exhibit similar global RNA interaction profiles in vivo, but affect a strikingly small subset of common genes. Unexpectedly, TAF15 influences a small fraction of amyotrophic lateral sclerosis events compared with TDP-43 and FUS in the mouse CNS.
TAF15 is required for a critical alternative splicing event of the zeta-1 subunit of the glutamate N-methyl-D-aspartate receptor (show GRIN3A Proteins) (Grin1 (show GRIN1 Proteins)) that controls the activity and trafficking of NR1 (show GRIN1 Proteins).
weak, multivalent interactions between TAF15 fibrils and heptads throughout RNA pol II CTD collectively mediate complex formation.
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.
In a cohort of youth at risk for bipolar disorder, pathway analysis showed an enrichment of the glucocorticoid receptor (GR (show NR3C1 Proteins)) pathway with the genes MED1 (show MED1 Proteins), HSPA1L (show HSPA1L Proteins), GTF2A1 (show GTF2A1 Proteins) and TAF15, which might underlie the previously reported role of stress response in the risk for bipolar disorder in vulnerable populations.
Aggregation of FET proteins FUS (show FUS Proteins), EWSR1 (show EWSR1 Proteins), and TAF15 mediate a pathological change in amyotrophic lateral sclerosis. (Review)
Studies provide evidence that FUS/TLS (show FUS Proteins), EWS (show EWSR1 Proteins) and TAF15 proteins play a major role in neurodegenerative disorders. (review).
O-GlcNAc (show OGT Proteins) glycosylation stoichiometry of TAF15
RNA binding by TAF-15 is dependent upon structural elements in the RNA rather than sequence.
our data suggest that TAF15 and TLS/FUS (show FUS Proteins) operate within similar but not identical hnRNP M (show HNRNPM Proteins)-TET protein complexes to influence the transcriptional or post-transcriptional output of a particular cell type.
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.
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.
This gene encodes a member of the TET family of RNA-binding proteins. The encoded protein plays a role in RNA polymerase II gene transcription as a component of a distinct subset of multi-subunit transcription initiation factor TFIID complexes. Translocations involving this gene play a role in acute leukemia and extraskeletal myxoid chondrosarcoma, and mutations in this gene may play a role in amyotrophic lateral sclerosis. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
TAF15 RNA polymerase II, TATA box binding protein (TBP)-associated factor, 68 kDa
, TATA box binding protein (TBP)-associated factor, RNA polymerase II, N, 68kD (RNA binding protein 56)
, TATA-binding protein-associated factor 2N
, RBP56/CSMF fusion
, TATA box binding protein (TBP)-associated factor, RNA polymerase II, N, 68kD (RNA-binding protein 56)
, TATA box-binding protein-associated factor 2N (RNA-binding protein 56)
, TBP-associated factor 15