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      HMGB1 binds to the KRAS promoter G-quadruplex: a new player in oncogene transcriptional regulation?

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          Abstract

          Biophysical and biological data reveal that HMGB1 binds to the KRAS G-quadruplex and suggest that it is involved in oncogene transcriptional regulation.

          Abstract

          This communication reports on a possible distinct role of HMGB1 protein. Biophysical studies revealed that HMGB1 binds and stabilizes the G-quadruplex of the KRAS promoter element that is responsible for most of the transcriptional activity. Biological data showed that inhibition of HMGB1 increases KRAS expression. These results suggest that HMGB1 could play a role in the gene transcriptional regulation via the functional recognition of the G-quadruplex.

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          HMG proteins: dynamic players in gene regulation and differentiation.

          Marco Bianchi, Alessandra Agresti (2005)
          Core histones package the genome into nucleosomes and control its accessibility to transcription factors. High mobility group proteins (HMGs) are, after histones, the second most abundant chromatin proteins and exert global genomic functions in establishing active or inactive chromatin domains. It is becoming increasingly clear that they also specifically control the expression of a limited number of genes. Moreover, they contribute to the fine tuning of transcription in response to rapid environmental changes. They do so by interacting with nucleosomes, transcription factors, nucleosome-remodelling machines, and with histone H1.
          Article 0 comments Cited 157 times – based on 0 reviews     Review now
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            Non-B DNA structure-induced genetic instability and evolution.

            Guliang Wang, Albino Bacolla, Gissella M Vásquez … (2009)
            Repetitive DNA motifs are abundant in the genomes of various species and have the capacity to adopt non-canonical (i.e., non-B) DNA structures. Several non-B DNA structures, including cruciforms, slipped structures, triplexes, G-quadruplexes, and Z-DNA, have been shown to cause mutations, such as deletions, expansions, and translocations in both prokaryotes and eukaryotes. Their distributions in genomes are not random and often co-localize with sites of chromosomal breakage associated with genetic diseases. Current genome-wide sequence analyses suggest that the genomic instabilities induced by non-B DNA structure-forming sequences not only result in predisposition to disease, but also contribute to rapid evolutionary changes, particularly in genes associated with development and regulatory functions. In this review, we describe the occurrence of non-B DNA-forming sequences in various species, the classes of genes enriched in non-B DNA-forming sequences, and recent mechanistic studies on DNA structure-induced genomic instability to highlight their importance in genomes.
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              G4-associated human diseases.

              Nancy Maizels (2015)
              Recent research has established clear connections between G-quadruplexes and human disease. Features of quadruplex structures that promote genomic instability have been determined. Quadruplexes have been identified as transcriptional, translational and epigenetic regulatory targets of factors associated with human genetic disease. An expandable GGGGCC motif that can adopt a G4 structure, located in the previously obscure C9ORF72 locus, has been shown to contribute to two well-recognized neurodegenerative diseases, amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). This review focuses on these advances, which further dispel the view that genomic biology is limited to the confines of the canonical B-form DNA duplex, and show how quadruplexes contribute spatial and temporal dimensionalities to linear sequence information. This recent progress also has clear practical ramifications, as prevention, diagnosis, and treatment of disease depend on understanding the underlying mechanisms.
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                Author and article information

                Journal
                Journal ID (publisher-id): CHCOFS
                Title: Chemical Communications
                Abbreviated Title: Chem. Commun.
                Publisher: Royal Society of Chemistry (RSC)
                ISSN (Print): 1359-7345
                ISSN (Electronic): 1364-548X
                Publication date Created: 2018
                Publication date (Electronic): 2018
                Volume: 54
                Issue: 68
                Pages: 9442-9445
                Affiliations
                [1 ]Department of Pharmacy, University of Naples “Federico II”
                [2 ]80131 Naples
                [3 ]Italy
                [4 ]College of Pharmacy
                [5 ]University of Arizona
                [6 ]Tucson
                [7 ]USA
                Article
                DOI: 10.1039/C8CC03614D
                PubMed ID: 30079419
                SO-VID: 7df23653-34b1-443e-aeec-aa15e252a7db
                Copyright © © 2018
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                http://rsc.li/journals-terms-of-use

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