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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
21 Mar 1997-Cell
TL;DR: A maternally expressed Drosophila TCF family member is cloned, dTCF, which mediates Wingless signaling as a bipartite transcription factor and binds a canonical TCF DNA motif and interacts with the beta-catenin homolog Armadillo.

1,259 citations

Journal ArticleDOI
27 Jan 1995-Cell
TL;DR: This review shall concentrate on transcriptional responses to cell surface receptor-activated signaling pathways; however, much of the discussion is also applicable to signals induced by environmental stresses or to extracellular signals that act directly on transcription factors, such as steroid hormones.

1,258 citations

Journal ArticleDOI
17 Jan 2014-Science
TL;DR: Using quantitative proteomics, it is found that lenalidomide causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKzF3, by the CRBN-CRL4 ubiquitin ligase, which are essential transcription factors in multiple myeloma.
Abstract: Lenalidomide is a drug with clinical efficacy in multiple myeloma and other B cell neoplasms, but its mechanism of action is unknown. Using quantitative proteomics, we found that lenalidomide causes selective ubiquitination and degradation of two lymphoid transcription factors, IKZF1 and IKZF3, by the CRBN-CRL4 ubiquitin ligase. IKZF1 and IKZF3 are essential transcription factors in multiple myeloma. A single amino acid substitution of IKZF3 conferred resistance to lenalidomide-induced degradation and rescued lenalidomide-induced inhibition of cell growth. Similarly, we found that lenalidomide-induced interleukin-2 production in T cells is due to depletion of IKZF1 and IKZF3. These findings reveal a previously unknown mechanism of action for a therapeutic agent: alteration of the activity of an E3 ubiquitin ligase, leading to selective degradation of specific targets.

1,254 citations

Journal Article
TL;DR: A new class of HIF-1-responsive gene is defined, the activation of which has implications for the understanding of hypoxic tumor metabolism and which may provide endogenous markers for tumor hypoxia.
Abstract: The transcriptional complex hypoxia-inducible factor-1 (HIF-1) has emerged as an important mediator of gene expression patterns in tumors, although the range of responding genes is still incompletely defined. Here we show that the tumor-associated carbonic anhydrases (CAs) are tightly regulated by this system. Both CA9 and CA12 were strongly induced by hypoxia in a range of tumor cell lines. In renal carcinoma cells that are defective for the von Hippel-Lindau (VHL) tumor suppressor, up-regulation of these CAs is associated with loss of regulation by hypoxia, consistent with the critical function of pVHL in the regulation of HIF-1. Further studies of CA9 defined a HIF-1-dependent hypoxia response element in the minimal promoter and demonstrated that tight regulation by the HIF/pVHL system was reflected in the pattern of CA IX expression within tumors. Generalized up-regulation of CA IX in VHL-associated renal cell carcinoma contrasted with focal perinecrotic expression in a variety of non-VHL-associated tumors. In comparison with vascular endothelial growth factor mRNA, expression of CA IX demonstrated a similar, although more tightly circumscribed, pattern of expression around regions of necrosis and showed substantial although incomplete overlap with activation of the hypoxia marker pimonidazole. These studies define a new class of HIF-1-responsive gene, the activation of which has implications for the understanding of hypoxic tumor metabolism and which may provide endogenous markers for tumor hypoxia.

1,253 citations

Journal ArticleDOI
TL;DR: This Review focuses on the biologic and physiologic functions of the PGC-1 coactivators, with particular emphasis on striated muscle, liver, and other organ systems relevant to common diseases such as diabetes and heart failure.
Abstract: Members of the nuclear receptor (NR) superfamily relay physiologic and nutritional cues to critical gene regulatory responses. The molecular links between external stimuli, cellular signaling events, and NR-mediated transcriptional control are currently being unraveled. New information emerging over the past decade has demonstrated that NRs receive regulatory input through multiple mechanisms including levels of endogenous ligand, availability of heterodimeric NR partners, and posttranslational modifications. Activating signals trigger the recruitment of coactivator complexes onto the NR platform, leading to enzymatic modification of chromatin, increased access of the RNA polymerase II machinery to RNA, and activation of target gene transcription (Figure ​(Figure1).1). Availability of certain coactivator proteins also serves critical regulatory functions linking physiologic stimuli to NR activity. Perhaps the best example of this latter mechanism involves the PPARγ coactivator-1 (PGC-1) family of transcriptional coactivators. PGC-1 coactivators serve as inducible NR “boosters” to equip the organism to meet the energy demands of diverse physiologic and dietary conditions. This Review will focus on the role of this interesting coactivator family in the control of organ-specific biologic responses to the physiologic and pathophysiologic milieu. Emphasis will be given to tissue-specific regulatory features relevant to heart failure and diabetes. Figure 1 The PGC-1 coactivator family: inducible boosters of gene transcription. (A) The schematic uses generic NRs as an example of how inducible PGC-1 coactivators dock to transcription factor targets and recruit protein complexes that activate transcription ...

1,253 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