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Transcription factor

About: Transcription factor is a research topic. Over the lifetime, 82881 publications have been published within this topic receiving 5400448 citations. The topic is also known as: transcription factors.


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Journal ArticleDOI
16 Jan 2009-Immunity
TL;DR: It is found that Foxp3 controlled the elevated miR155 expression required for maintaining Treg cell proliferative activity and numbers under nonlymphopenic conditions and provides experimental support for a proposed role for miRNAs in ensuring the robustness of cellular phenotypes.

782 citations

Journal ArticleDOI
TL;DR: In this article, the lateral mesoderm-specific lncRNA Fendrr was found to be essential for proper heart and body wall development in the mouse, and the upregulation of several transcription factors was associated with a drastic reduction in PRC2 occupancy along with decreased H3K27 trimethylation.

781 citations

Journal ArticleDOI
TL;DR: YAP overexpression increases, while YAP depletion decreases, p73-mediated apoptosis following DNA damage, in an Akt inhibitable manner, and Akt phosphorylation of YAP may thus suppress the induction of the proapoptotic gene expression response following cellular damage.

781 citations

Journal ArticleDOI
10 Dec 2009-Nature
TL;DR: It is shown that addition of the FLC antisense promoter sequences to a reporter gene is sufficient to confer cold-induced silencing of the reporter, and upregulation of long non-coding antisense transcripts covering the entire FLC locus may be part of the cold-sensing mechanism.
Abstract: Transcription in eukaryotic genomes generates an extensive array of non-protein-coding RNA, the functional significance of which is mostly unknown. We are investigating the link between non-coding RNA and chromatin regulation through analysis of FLC - a regulator of flowering time in Arabidopsis and a target of several chromatin pathways. Here we use an unbiased strategy to characterize non-coding transcripts of FLC and show that sense/antisense transcript levels correlate in a range of mutants and treatments, but change independently in cold-treated plants. Prolonged cold epigenetically silences FLC in a Polycomb-mediated process called vernalization. Our data indicate that upregulation of long non-coding antisense transcripts covering the entire FLC locus may be part of the cold-sensing mechanism. Induction of these antisense transcripts occurs earlier than, and is independent of, other vernalization markers and coincides with a reduction in sense transcription. We show that addition of the FLC antisense promoter sequences to a reporter gene is sufficient to confer cold-induced silencing of the reporter. Our data indicate that cold-induced FLC antisense transcripts have an early role in the epigenetic silencing of FLC, acting to silence FLC transcription transiently. Recruitment of the Polycomb machinery then confers the epigenetic memory. Antisense transcription events originating from 3' ends of genes might be a general mechanism to regulate the corresponding sense transcription in a condition/stage-dependent manner.

781 citations

Journal ArticleDOI
TL;DR: The identification of DDX41, a member of the DEXDc family of helicases, as an intracellular DNA sensor in myeloid dendritic cells (mDCs) is reported, suggesting thatDDX41 is an additional DNA sensor that depends on STING to sense pathogenic DNA.
Abstract: The recognition of pathogenic DNA is important to the initiation of antiviral responses. Here we report the identification of DDX41, a member of the DEXDc family of helicases, as an intracellular DNA sensor in myeloid dendritic cells (mDCs). Knockdown of DDX41 expression by short hairpin RNA blocked the ability of mDCs to mount type I interferon and cytokine responses to DNA and DNA viruses. Overexpression of both DDX41 and the membrane-associated adaptor STING together had a synergistic effect in promoting Ifnb promoter activity. DDX41 bound both DNA and STING and localized together with STING in the cytosol. Knockdown of DDX41 expression blocked activation of the mitogen-activated protein kinase TBK1 and the transcription factors NF-κB and IRF3 by B-form DNA. Our results suggest that DDX41 is an additional DNA sensor that depends on STING to sense pathogenic DNA.

781 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20234,678
20226,545
20213,663
20203,530
20193,362
20183,288