Taf7

Gégonne, Anne; Devaiah, Ballachanda N.; Singer, Dinah S.

doi:10.4161/trns.22842

Cited by 18 publications

(11 citation statements)

References 28 publications

(53 reference statements)

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“…In the present study, we found that several transcription factors such as GATA1, TAF7 and EBF1 could be essential for lncRNAs expression in AF development. Pathway identification showed that GATA1, TAF7 and EBF1 played central roles in AF, which were consistent with previous reports [ 17 , 18 ]. Close physical links between lncRNAs and developmental functional genes does not necessarily indicate that there would be functional links between protein-coding genes and lncRNAs.…”

Section: Discussionsupporting

confidence: 92%

Identification of long non-coding RNAs as novel biomarker and potential therapeutic target for atrial fibrillation in old adults

Huang

et al. 2016

Oncotarget

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Atrial fibrillation (AF) is a highly prevalent cardiac arrhythmia disease, which widely leads to exacerbate heart failure and ischemic stroke in elder world. Recently, long non-coding RNAs (lncRNAs), a subclass of noncoding RNAs, have been reported to play critical roles in pathophysiology of cardiac heart. However, little is known of their role in cardiac arrhythmia. In the present study, we investigated the expression levels of lncRNAs of AF patients and healthy people with Agilent Human lncRNA array for the first time. 177 lncRNAs of 78243 and 153 mRNAs of 30215 tested were identified to be differentially expressed (≥ 2-fold change), indicating that the expression of many lncRNAs are upregulated or downregulated in AF. Among these, NONHSAT040387 and NONHSAT098586 were the most upregulated and downregulated lncRNAs. Real time quantitative PCR were employed to validate the microarray analysis findings, and the results confirmed the consistence. GO and KEGG pathway analysis were applied to explore the potential lncRNAs functions, some pathways including oxygen transporter activity and protein heterodimerization activity were speculated to be involved in AF pathogenesis. These results shed some light on lncRNAs' physiologic functions and provide useful information for exploring potential therapeutic treatments for heart rhythm disease.

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Section: Discussionsupporting

confidence: 92%

Identification of long non-coding RNAs as novel biomarker and potential therapeutic target for atrial fibrillation in old adults

Huang

et al. 2016

Oncotarget

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“…Since the same isomerization does not take place during reinitiation, it is likely that TAF1 and TAF2 do not re-form some of these promoter contacts following the first round of initiation. The release of TAF7 from TFIID following PIC assembly has been shown to be required for transcription initiation 45 , and could potentially serve as the mechanism for preventing re-engagement of the promoter DNA by TAF1 and TAF2.…”

Section: Taf-less Pic Structure and Full Pic Modelmentioning

confidence: 99%

Structure of promoter-bound TFIID and model of human pre-initiation complex assembly

Louder

López‐Blanco

et al. 2016

Nature

208

266

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The general transcription factor IID (TFIID) plays a central role in the initiation of RNA polymerase II-dependent transcription by nucleating pre-initiation complex (PIC) assembly at the core promoter. TFIID comprises the TATA-binding protein (TBP) and 13 TBP-associated factors (TAF1-13), which specifically interact with a variety of core promoter DNA sequences. Here we present the structure of human TFIID in complex with TFIIA and core promoter DNA, determined by single-particle cryo-electron microscopy (cryo-EM) at sub-nanometer resolution. All core promoter elements are contacted by subunits of TFIID, with TAF1 and TAF2 mediating major interactions with the downstream promoter. TFIIA bridges the TBP-TATA complex with lobe B of TFIID. We also present the cryo-EM reconstruction of a fully-assembled human TAF-less PIC. Superposition of common elements between the two structures provides novel insights into the general role of TFIID in promoter recognition, PIC assembly, and transcription initiation.

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“…Our data are in line with those previously published highlighting a great number of deregulated or mutated histone modifiers involved in medulloblastoma (Northcott et al, 2012) and their importance as oncogenes or as tumor suppressors (Cohen et al, 2011). Furthermore, we highlight also the deregulation of five Histone modifier Regulators, up-regulated in Set A, namely: Emd (Berk et al, 2013), Anp32a (Seo et al, 2001; Fan et al, 2006; Kular et al, 2009), Taf7 (Gegonne et al, 2001, 2013; Kloet et al, 2012), Pag2g4 (Zhang et al, 2003), Ipo7 (Jäkel et al, 1999; Mühlhäusser et al, 2001). A detailed description of Set A genes involved in epigenetic modulation is presented in Supplementary Data, at section “Epigenetic modulation.”…”

Section: Resultsmentioning

confidence: 83%

Functional Genomics Identifies Tis21-Dependent Mechanisms and Putative Cancer Drug Targets Underlying Medulloblastoma Shh-Type Development

Gentile¹,

Ceccarelli²,

Micheli³

et al. 2016

Front. Pharmacol.

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We have recently generated a novel medulloblastoma (MB) mouse model with activation of the Shh pathway and lacking the MB suppressor Tis21 (Patched1+/−/Tis21KO). Its main phenotype is a defect of migration of the cerebellar granule precursor cells (GCPs). By genomic analysis of GCPs in vivo, we identified as drug target and major responsible of this defect the down-regulation of the promigratory chemokine Cxcl3. Consequently, the GCPs remain longer in the cerebellum proliferative area, and the MB frequency is enhanced. Here, we further analyzed the genes deregulated in a Tis21-dependent manner (Patched1+/−/Tis21 wild-type vs. Ptch1+/−/Tis21 knockout), among which are a number of down-regulated tumor inhibitors and up-regulated tumor facilitators, focusing on pathways potentially involved in the tumorigenesis and on putative new drug targets. The data analysis using bioinformatic tools revealed: (i) a link between the Shh signaling and the Tis21-dependent impairment of the GCPs migration, through a Shh-dependent deregulation of the clathrin-mediated chemotaxis operating in the primary cilium through the Cxcl3-Cxcr2 axis; (ii) a possible lineage shift of Shh-type GCPs toward retinal precursor phenotype, i.e., the neural cell type involved in group 3 MB; (iii) the identification of a subset of putative drug targets for MB, involved, among the others, in the regulation of Hippo signaling and centrosome assembly. Finally, our findings define also the role of Tis21 in the regulation of gene expression, through epigenetic and RNA processing mechanisms, influencing the fate of the GCPs.

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Taf7

Cited by 18 publications

References 28 publications

Identification of long non-coding RNAs as novel biomarker and potential therapeutic target for atrial fibrillation in old adults

Identification of long non-coding RNAs as novel biomarker and potential therapeutic target for atrial fibrillation in old adults

Structure of promoter-bound TFIID and model of human pre-initiation complex assembly

Functional Genomics Identifies Tis21-Dependent Mechanisms and Putative Cancer Drug Targets Underlying Medulloblastoma Shh-Type Development

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