Topic
Transcription (biology)
About: Transcription (biology) is a research topic. Over the lifetime, 56532 publications have been published within this topic receiving 2952782 citations. The topic is also known as: genetic transcription & transcription, genetic.
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TL;DR: This work has shown that transcriptional regulators may be modified in an allosteric manner by response elements themselves to generate the pattern of regulation that is appropriate to an individual gene.
Abstract: Selective gene transcription is mediated in part by regulatory proteins that bind to DNA response elements These regulatory proteins receive global information from signal-transduction events But transcriptional regulators may also be modified in an allosteric manner by response elements themselves to generate the pattern of regulation that is appropriate to an individual gene
490 citations
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TL;DR: BRCA1 increases p53-dependent transcription from the p21WAF1/CIP1 and bax promoters and interacts with p53 proteins both in vitro and in vivo, indicating that BRCA 1 and p53 may coordinately regulate gene expression in their role as tumor suppressors.
Abstract: Mutations of the BRCA1 tumor suppressor gene are the most commonly detected alterations in familial breast and ovarian cancer. Although BRCA1 is required for normal mouse development, the molecular basis for its tumor suppressive function remains poorly understood. We show here that BRCA1 increases p53-dependent transcription from the p21WAF1/CIP1 and bax promoters. We also show that BRCA1 and p53 proteins interact both in vitro and in vivo. The interacting regions map, in vitro, to aa 224-500 of BRCA1 and the C-terminal domain of p53. Tumor-derived transactivation-deficient BRCA1 mutants are defective in co-activation of p53-dependent transcription and a truncation mutant of BRCA1 that retains the p53-interacting region acts as a dominant inhibitor of p53-dependent transcription. BRCA1 and p53 cooperatively induce apoptosis of cancer cells. The results indicate that BRCA1 and p53 may coordinately regulate gene expression in their role as tumor suppressors.
490 citations
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TL;DR: Using fibroblast lineages in different stages of transformation, it is found that c-Myc and Sp1 were induced to a dramatic extent when cells overcame replicative senescence and obtained immortal characteristics, in association with telomerase activation.
Abstract: Telomerase activation is thought to be a critical step in cellular immortalization and carcinogenesis. The human telomerase catalytic subunit (hTERT) is a rate limiting determinant of the enzymatic activity of human telomerase. In the previous study, we identified the proximal 181 bp core promoter responsible for transcriptional activity of the hTERT gene. To identify the regulatory factors of transcription, transient expression assays were performed using hTERT promoter reporter plasmids. Serial deletion assays of the core promoter revealed that the 5′-region containing the E-box, which binds Myc/Max, as well as the 3′-region containing the GC-box, which binds Sp1, are essential for transactivation. The mutations introduced in the E-box or GC-box significantly decreased transcriptional activity of the promoter. Overexpression of Myc/Max or Sp1 led to significant activation of transcription in a cell type-specific manner, while Mad/Max introduction repressed it. However, the effects of Myc/Max on transactivation were marginal when Sp1 sites were mutated. Western blot analysis using various cell lines revealed a positive correlation between c-Myc and Sp1 expression and transcriptional activity of hTERT. Using fibroblast lineages in different stages of transformation, we found that c-Myc and Sp1 were induced to a dramatic extent when cells overcame replicative senescence and obtained immortal characteristics, in association with telomerase activation. These findings suggest that c-Myc and Sp1 cooperatively function as the major determinants of hTERT expression, and that the switching functions of Myc/Max and Mad/Max might also play roles in telomerase regulation.
490 citations
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TL;DR: A detailed review of the structural investigations of various Pt-DNA adducts and the effects of these lesions on global DNA geometry and a mechanistic analysis of how DNA structural distortions induced by platinum damage may inhibit RNA synthesis in vivo are presented.
Abstract: Cisplatin, carboplatin, and oxaliplatin are three FDA-approved members of the platinum anticancer drug family. These compounds induce apoptosis in tumor cells by binding to nuclear DNA, forming a variety of structural adducts and triggering cellular responses, one of which is the inhibition of transcription. In this report we present (i) a detailed review of the structural investigations of various Pt–DNA adducts and the effects of these lesions on global DNA geometry; (ii) research detailing inhibition of cellular transcription by Pt–DNA adducts; and (iii) a mechanistic analysis of how DNA structural distortions induced by platinum damage may inhibit RNA synthesis in vivo. A thorough understanding of the molecular mechanism of action of platinum antitumor agents will aid in the development of new compounds in the family.
489 citations
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TL;DR: From the large, complex arrays of composite RNA structures, numerous insights into the RNA splicing mechanisms were inferred.
488 citations