On the formation of a novel adenylic compound by enzymatic extracts of liver nuclei

Chambon, Pierre; Weill, J; Doly, Janine; Strosser, M.T.; Mandel, P.

doi:10.1016/0006-291x(66)90502-x

Cited by 334 publications

(105 citation statements)

References 4 publications

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“…Its localization, its association with nucelar proteins [4], its influence on DNA polymerase activity [S-7] , the stimulation of poly(ADPR) formation in vitro by exogenous DNA [ 1,8] , and the inhibition of poly(ADPR) degradation in vitro by DNA [9,10] are consistent with the postulate that the polymer might be involved in the regulation of DNA synthesis and cell proliferation [ $61. This interpretation has been questioned on the basis of similar enzymic activities per unit DNA for the formation and degradation of poly (ADPR) .…”

Section: Introductionmentioning

confidence: 62%

Nuclear poly (ADPR) and mono (ADPR) residues in tissues with different growth rates

Adamietz¹,

Bredehorst²,

Oldekop³

et al. 1974

FEBS Letters

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Section: Introductionmentioning

confidence: 62%

Nuclear poly (ADPR) and mono (ADPR) residues in tissues with different growth rates

Adamietz¹,

Bredehorst²,

Oldekop³

et al. 1974

FEBS Letters

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“…Known modifications include acetylation, methylation, biotinylation, poly(ADP-ribosylation), ubiquitination, and sumoylation (Boulikas 1988;Boulikas et al 1990;Camporeale et al 2004;Chambon et al 1966;Kouzarides and Berger 2007;Shiio and Eisenman 2003;Stanley et al 2001;Wolffe 1998). For many of these modifications, unambiguous links have been established with human disease and nutrition.…”

Section: Introductionmentioning

confidence: 99%

Nutrition, Histone Epigenetic Marks, and Disease

Zempleni

Liu

Xue

2013

Environmental Epigenomics in Health and Disease

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The dietary intake of essential nutrients and bioactive food compounds is a process that occurs on a daily basis for the entire life span. Therefore, your diet has a great potential to cause changes in the epigenome. Known histone modifications include acetylation, methylation, biotinylation, poly(ADP-ribosylation), ubiquitination, and sumoylation. Some of these modifications depend directly on dietary nutrients. For other modifications, bioactive dietary compounds may alter the activities of enzymes that establish or remove histone marks, thereby altering the epigenome. This chapter provides an overview of diet-dependent epigenomic marks in histones and their links with human health.

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“…Pellagra, the human disease of niacin deficiency, ravaged certain cornconsuming populations for several hundred years, producing the unique end points of sun-sensitivity and dementia [1]. A real understanding of sun-sensitive dermatitis was only possible after the discovery of poly(ADP-ribose) in 1966 [2]. Since that time, there has been tremendous progress in describing the many roles of poly(ADP-ribose) in DNA damage responses, which will be briefly summarized later in this article.…”

Section: Introductionmentioning

confidence: 99%

Niacin requirements for genomic stability

Kirkland

2012

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Through its involvement in over 400 NAD(P)-dependent reactions, niacin status has the potential to influence every area of metabolism. Niacin deficiency has been linked to genomic instability largely through impaired function of the poly ADP-ribose polymerase (PARP) family of enzymes. In various models, niacin deficiency has been found to cause impaired cell cycle arrest and apoptosis, delayed DNA excision repair, accumulation of single and double strand breaks, chromosomal breakage, telomere erosion and cancer development. Rat models suggest that most aspects of genomic instability are minimized by the recommended levels of niacin found in AIN-93 formulations; however, some beneficial responses do occur in the range from adequate up to pharmacological niacin intakes. Mouse models show a wide range of protection against UV-induced skin cancer well into pharmacological levels of niacin intake. It is currently a challenge to compare animal and human data to estimate the role of niacin status in the risk of genomic instability in human populations. It seems fairly certain that some portion of even affluent populations will benefit from niacin supplementation, and some subpopulations are likely well below an optimal intake of this vitamin. With exposure to stressors, like chemotherapy or excess sunlight, suraphysiological doses of niacin may be beneficial.

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On the formation of a novel adenylic compound by enzymatic extracts of liver nuclei

Cited by 334 publications

References 4 publications

Nuclear poly (ADPR) and mono (ADPR) residues in tissues with different growth rates

Nuclear poly (ADPR) and mono (ADPR) residues in tissues with different growth rates

Nutrition, Histone Epigenetic Marks, and Disease

Niacin requirements for genomic stability

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