Biological functions of biotinylated histones

Kothapalli, Naga Rama; Camporeale, Gabriela; Kueh, Alice; Chew, Yap Ching; Oommen, Anna; Griffin, Jacob B.; Zempleni, Janos

doi:10.1016/j.jnutbio.2005.03.025

Cited by 95 publications

(50 citation statements)

References 29 publications

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“…Biotinylation of histones was described in several histone variants and is likely to be involved in gene silencing, cell proliferation, and cellular response to DNA damage [8,[564][565][566][567][568][569]. Amino-acid residues that undergo biotinylation have been identified in some recent studies [570,571] but the role of histone biotinylation in cancer pathologies remains largely unclear.…”

Section: Biotinylationmentioning

confidence: 99%

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Andreoli¹,

Barbosa²,

Parenti³

et al. 2012

CPD

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Abstract:Research on cancer epigenetics has flourished in the last decade. Nevertheless growing evidence point on the importance to understand the mechanisms by which epigenetic changes regulate the genesis and progression of cancer growth. Several epigenetic targets have been discovered and are currently under validation for new anticancer therapies. Drug discovery approaches aiming to target these epigenetic enzymes with small-molecules inhibitors have produced the first pre-clinical and clinical outcomes and many other compounds are now entering the pipeline as new candidate epidrugs. The most studied targets can be ascribed to histone deacetylases and DNA methyltransferases, although several other classes of enzymes are able to operate post-translational modifications to histone tails are also likely to represent new frontiers for therapeutic interventions. By acknowledging that the field of cancer epigenetics is evolving with an impressive rate of new findings, with this review we aim to provide a current overview of pre-clinical applications of smallmolecules for cancer pathologies, combining them with the current knowledge of epigenetic targets in terms of available structural data and drug design perspectives.Keywords: Epigenetics, anticancer therapy, DNA methyltransferases, protein methyltransferases, demethylases, deacetylases, acetyltransferases, histone post-translational modifications, drug design, crystallography, small-molecule inhibitors. INTRODUCTIONThe term epigenetics currently refers to the mechanisms of temporal and spatial control of gene activity that do not depend on the DNA sequence, influencing the physiological and pathological development of an organism. The molecular mechanisms by which epigenetic changes occur are complex and cover a wide range of processes including paramutation, bookmarking, imprinting, gene silencing, carcinogenesis progression, and, most importantly, regulation of heterochromatin and histone modifications [1]. At a biochemical level, epigenetic alterations in chromatin involve methylation of DNA patterns, several forms of histone modifications and microRNA (miRNA) expression. All these processes modulate the structure of chromatin leading to the activation or silencing of gene expression [2][3][4][5][6]. More specifically, the chromatin remodeling is accomplished by two main mechanisms that concern the methylation of cytosine residues in DNA and a variety of post-translational modifications (PTMs) occurring at the N-terminal tails of histone proteins. These PTMs include acetylation, methylation, phosphorylation, ubiquitylation, sumoylation, glycosylation, ADPribosylation, carbonylation, citrullination and biotinylation [7,8]. Among all PTMs for example, histone tails can have its lysine residues acetylated, methylated or ubiquitilated; arginine can be methylated; serine and threonine residues can be phosphorylated [9][10][11][12][13][14][15][16][17]. These covalent modifications are able to cause other PTMs and the ensemble of this cross-talk is known as the his...

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Section: Biotinylationmentioning

confidence: 99%

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Andreoli¹,

Barbosa²,

Parenti³

et al. 2012

CPD

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“…Modifications of histone H3: H3R2me [22,15,171], H3R2cit [37], H3T3ph [22], H3K4me [22,60], H3K4ac [60], H3K4bio [90], H3R8me [22], H3R8cit [37], H3K9ac [22,60], H3K9bio [90], H3K9me [22,60] functional information on non-enzymatic histone biotinylation [70], we excluded these marks from further calculations.…”

Section: Information On Dna Versus Nucleosomesmentioning

confidence: 99%

Innovation in gene regulation: The case of chromatin computation

Prohaska

Stadler

Krakauer

2010

Journal of Theoretical Biology

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Chromatin regulation is understood to be one of the fundamental modes of gene regulation in eukaryotic cells. We argue that the basic proteins that determine the chromatin architecture constitute an evolutionary ancient layer of transcriptional regulation common to all three domains of life. We explore phylogenetically, sources of innovation in chromatin regulation, focusing on protein domains related to chromatin structure and function, demonstrating a step-wise increase of complexity in chromatin regulation. Building upon the highly conserved use of variants of chromosomal architectural proteins to distinguish chromosomal states, Eukarya secondarily acquired mechanisms for "writing" chemical modifications onto chromatin that constitute persistent signals. The acquisition of reader domains enabled decoding of these complex, signal combinations and a decoupling of the signal from immediate biochemical effects. We show how the coupling of reading and writing, which is most prevalent in crown-group Eukarya, could have converted chromatin into a powerful computational device capable of storing and processing more information than pure cis-regulatory networks.Key words: Chromatin, gene regulation, evolution Summary of Findings and Evolutionary HypothesisGene regulation in extant organisms is a complex adaptive system making use of a diversity of mechanisms to ensure that proteins and complementary macromolecular components are produced and maintained at functional levels in variable environments.In this contribution we focus on one key regulatory subsystem of the cell: chromatin regulation. We argue that chromatin functioned as general regulator of transcription in the primordial nucleus, and that a series of key molecular innovations has significantly expanded the regulatory scope of the cell. In this section we summarize the key empirical results of the paper. Sections 2 through 6 provide the empirical support for these claims. In section 7, we formulate an evolutionary Email addresses: sonja@bioinf.uni-leipzig.de (Sonja J. Prohaska), studla@bioinf.uni-leipzig.de (Peter F. Stadler), krakauer@santafe.edu (David C. Krakauer) hypothesis that seeks to explain our findings in terms of the evolution of proto-genetic regulation. We then interpret this evolutionary sequence in terms of increasing computational power by locating key stages of the evolutionary sequence within a formal model of computation. Since sections 2-6 are primarily concerned with presenting evidence, those interested in the conceptual development of the argument can focus on sections 7 and 8.Two variants of Chromosomal Architectural Proteins (ChAPs) are sufficient to define binary genomic, and potentially phenotypic, states. We show how extensions to this binary system lead to potential distinctions among an increasing number of genomic states, culminating in forms of control localized to specific sites in the genome, as illustrated for example by extant mammalian histone variants capable of differential expression and/or localization to r...

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“…These immortal cells highly biosynthesize biotin (Keränen, 1972), and biotinylation onto the lysine residues of histone H3.1 may occur (Kothapalli et al, 2005). Although, cancer-tissue cells do not actively synthesize the histone H3.1, high content of biotin in cancer tissues (Hayakawa & Nagamine, 2009) may biotinylate histone H3.1, this may cause the enhancement of the synthesis of the membrane-protein receptors to occur.…”

Section: Tissue Membrane-protein Receptors Synthesis and Liver Diseasesmentioning

confidence: 99%

The Fascio Effect: Biotin and Sleep

Hayakawa¹,

Nagamine²

2016

IJB

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An Italian maxim says "I bambini che dormono tanto crescono bene", and the English maxim also says that "All children need to sleep in order to grow and develop". In this review, we would like to demonstrate the truth of this proverb about sleep together with biotin (vitamin H) and lipoic acid (thioctic acid). Recently, we have found that D-biotin regulates the membrane biosynthesis in the cells. Previously, we have found that purified biotin-recycling enzyme biotinidase is also able to hydrolyze enkephalin and neuro-peptides. Thus, biotin state and sleep should be strongly linked to each other. In this report, we have investigated the expression of hormone receptors in some diseases using the new proteomics of protein-direct-microsequencing-deciphering (PDMD) method, and have indicated that having adequate sleep and nutrition is important to for healthy immunological and mental conditions in humans. It is also summarized that human breast milk is superior to bovine milk for human healthy babies to sleep and grow well.

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Biological functions of biotinylated histones

Cited by 95 publications

References 29 publications

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Modulation of Epigenetic Targets for Anticancer Therapy: Clinicopathological Relevance, Structural Data and Drug Discovery Perspectives

Innovation in gene regulation: The case of chromatin computation

The Fascio Effect: Biotin and Sleep

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