TAF15 293T Cell Transient Overexpression Lysate

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TAF15 293T Cell Transient Overexpression Lysate

TAF15 293T Cell Transient encodes a subunit of TFIID present in a subset of TFIID Overexpression Lysate(Denatured) complexes. Translocations involving chromosome 17 and chromosome 9, where the gene for the nuclear Catalog Number: H00008148-T01 receptor CSMF is located, result in a gene fusion product that is an RNA binding protein associated with a Regulation Status: For research use only (RUO) subset of extraskeletal myxoid chondrosarcomas. Two transcripts encoding different isoforms have been Transfected Cell Line: 293T identified. [provided by RefSeq] Plasmid: pCMV-TAF15 full-length Host: Human Theoretical MW (kDa): 65.23 Applications: WB (See our web site product page for detailed applications information) Protocols: See our web site at http://www.abnova.com/support/protocols.asp or product page for detailed protocols Storage Buffer: 1X Sample Buffer (50 mM Tris-HCl, 2% SDS, 10% glycerol, 300 mM 2-mercaptoethanol, 0.01% Bromophenol blue) Storage Instruction: Store at -80°C. Aliquot to avoid repeated freezing and thawing. Entrez GeneID: 8148 Gene Symbol: TAF15 Gene Alias: Npl3, RBP56, TAF2N, TAFII68, hTAFII68 Gene Summary: Initiation of transcription by RNA polymerase II requires the activities of more than 70 polypeptides. The protein that coordinates these activities is transcription factor IID (TFIID), which binds to the core promoter to position the polymerase properly, serves as the scaffold for assembly of the remainder of the transcription complex, and acts as a channel for regulatory signals. TFIID is composed of the TATA-binding protein (TBP) and a group of evolutionarily conserved proteins known as TBP-associated factors or TAFs. TAFs may participate in basal transcription, serve as coactivators, function in promoter recognition or modify general transcription factors (GTFs) to facilitate complex assembly and transcription initiation. This gene Page 1/1 Powered by TCPDF (www.tcpdf.org).

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TAF15 Is Important for Cellular Proliferation and Regulates the Expression of a Subset of Cell Cycle Genes Through Mirnas
Oncogene (2013) 32, 4646–4655 & 2013 Macmillan Publishers Limited All rights reserved 0950-9232/13 www.nature.com/onc ORIGINAL ARTICLE TAF15 is important for cellular proliferation and regulates the expression of a subset of cell cycle genes through miRNAs M Ballarino1, L Jobert1,4, D Dembe´le´ 1, P de la Grange2, D Auboeuf3 and L Tora1 TAF15 (formerly TAFII68) is a member of the FET (FUS, EWS, TAF15) family of RNA- and DNA-binding proteins whose genes are frequently translocated in sarcomas. By performing global gene expression profiling, we found that TAF15 knockdown affects the expression of a large subset of genes, of which a significant percentage is involved in cell cycle and cell death. In agreement, TAF15 depletion had a growth-inhibitory effect and resulted in increased apoptosis. Among the TAF15-regulated genes, targets of microRNAs (miRNAs) generated from the onco-miR-17 locus were overrepresented, with CDKN1A/p21 being the top miRNAs- targeted gene. Interestingly, the levels of onco-miR-17 locus coded miRNAs (miR-17-5p and miR-20a) were decreased upon TAF15 depletion and shown to affect the post-transcriptional regulation of TAF15-dependent genes, such as CDKN1A/p21. Thus, our results demonstrate that TAF15 is required to regulate gene expression of cell cycle regulatory genes post-transcriptionally through a pathway involving miRNAs. The findings that high TAF15 levels are needed for rapid cellular proliferation and that endogenous TAF15 levels decrease during differentiation strongly suggest that TAF15 is a key regulator of maintaining a highly proliferative rate of cellular homeostasis. Oncogene (2013) 32, 4646–4655; doi:10.1038/onc.2012.490; published online 5 November 2012 Keywords: FUS/EWS/TAF15 (FET) proteins; miRNAs; transcription; proliferation; neuronal differentiation; neuroblastoma INTRODUCTION possible role of TAF15 in additional steps of RNA metabolism.
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RNA Binding Protein TAF15 Suppresses Toxicity in a Yeast Model of FUS Proteinopathy
RNA Binding Protein TAF15 Suppresses Toxicity in a Yeast Model of FUS Proteinopathy Elliott Hayden Wright State University Aicha Kebe Wright State University Shuzhen Chen Wright State University Abagail Chumley Wright State University Chenyi Xia Shanghai University of Traditional Chinese Medicine Quan Zhong Wright State University Shulin Ju ( [email protected] ) Wright State University Research Article Keywords: FUS, RNA binding protein, ALS, toxicity Posted Date: April 22nd, 2021 DOI: https://doi.org/10.21203/rs.3.rs-437201/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License RNA binding protein TAF15 suppresses toxicity in a yeast model of FUS proteinopathy Elliott Hayden1, Aicha Kebe1, Shuzhen Chen1, Abagail Chumley1, Chenyi Xia2, Quan Zhong1* and Shulin Ju1* 1Department of Biological Sciences, Wright State University, Dayton, OH 45435 2School of Basic Medicine, Shanghai University of Traditional Medicine, Shanghai, China 201203 *Corresponding authors: [email protected]; [email protected] Abstract Mutations in Fused in Sarcoma (FUS), an RNA binding protein that functions in multiple steps in gene expression regulation and RNA processing, are known to cause familial amyotrophic lateral sclerosis (ALS). Since this discovery, mutations in several other RNA binding proteins (RBPs) have also been linked to ALS. Some of these ALS-associated RBPs have been shown to colocalize with ribonucleoprotein (RNP) granules such as stress granules and processing bodies (p-bodies). Characterization of ALS-associated proteins, their mis-localization, aggregation and toxicity in cellular and animal models have provided critical insights in disease. More and more evidence has emerged supporting a hypothesis that impaired clearance, inappropriate assembly, and dysregulation of RNP granules play a role in ALS.
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FUS ALS-Causative Mutations Impact FUS Autoregulation and the Processing of RNA-Binding Proteins Through Intron Retention
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TAF15 Antibody Cat
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1 2 3 4 5 the Atypical RNA-Binding Protein TAF15 Regulates Dorsoanterior Neural Development 6 Through Diverse Mechanisms in Xeno
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The Neurodegenerative Diseases ALS and SMA Are Linked at The
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RNA-Binding Proteins with Prion-Like Domains in Health and Disease
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