共查询到20条相似文献,搜索用时 343 毫秒
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Olga Moreno-Gonzalo Irene Fernandez-Delgado Francisco Sanchez-Madrid 《Cellular and molecular life sciences : CMLS》2018,75(1):1-19
Extracellular vesicles (EVs) are released by cells to the extracellular environment to mediate inter-cellular communication. Proteins, lipids, nucleic acids and metabolites shuttled in these vesicles modulate specific functions in recipient cells. The enrichment of selected sets of proteins in EVs compared with global cellular levels suggests the existence of specific sorting mechanisms to specify EV loading. Diverse post-translational modifications (PTMs) of proteins participate in the loading of specific elements into EVs. In this review, we offer a perspective on PTMs found in EVs and discuss the specific role of some PTMs, specifically Ubiquitin and Ubiquitin-like modifiers, in exosomal sorting of protein components. The understanding of these mechanisms will provide new strategies for biomedical applications. Examples include the presence of defined PTM marks on EVs as novel biomarkers for the diagnosis and prognosis of certain diseases, or the specific import of immunogenic components into EVs for vaccine generation. 相似文献
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Chromatin assembly during S phase: contributions from histone deposition, DNA replication and the cell division cycle 总被引:7,自引:0,他引:7
During S phase of the eukaryotic cell division cycle, newly replicated DNA is rapidly assembled into chromatin. Newly synthesised
histones form complexes with chromatin assembly factors, mediating their deposition onto nascent DNA and their assembly into
nucleosomes. Chromatin assembly factor 1, CAF-1, is a specialised assembly factor that targets these histones to replicating
DNA by association with the replication fork associated protein, proliferating cell nuclear antigen, PCNA. Nucleosomes are
further organised into ordered arrays along the DNA by the activity of ATP-dependent chromatin assembly and spacing factors
such as ATP-utilising chromatin assembly and remodelling factor ACF. An additional level of controlling chromatin assembly
pathways has become apparent by the observation of functional requirements for cyclin-dependent protein kinases, casein kinase
II and protein phosphatases. In this review, we will discuss replication-associated histone deposition and nucleosome assembly
pathways, and we will focus in particular on how nucleosome assembly is linked to DNA replication and how it may be regulated
by the cell cycle control machinery. 相似文献
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T. Jenuwein G. Laible R. Dorn G. Reuter 《Cellular and molecular life sciences : CMLS》1998,54(1):80-93
The SET domain is a 130-amino acid, evolutionarily conserved sequence motif present in chromosomal proteins that function
in modulating gene activities from yeast to mammals. Initially identified as members of the Polycomb- and trithorax-group (Pc-G and trx-G) gene families, which are required to maintain expression boundaries of homeotic selector (HOM-C) genes,
SET domain proteins are also involved in position-effect-variegation (PEV), telomeric and centromeric gene silencing, and
possibly in determining chromosome architecture. These observations implicate SET domain proteins as multifunctional chromatin
regulators with activities in both eu- and heterochromatin – a role consistent with their modular structure, which combines
the SET domain with additional sequence motifs of either a cysteine-rich region/zinc-finger type or the chromo domain. Multiple
functions for chromatin regulators are not restricted to the SET protein family, since many trx-G (but only very few Pc-G)
genes are also modifiers of PEV. Together, these data establish a model in which the modulation of chromatin domains is mechanistically
linked with the regulation of key developmental loci (e.g. HOM-C). 相似文献
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Covadonga Huidobro Agustin F. Fernandez Mario F. Fraga 《Cellular and molecular life sciences : CMLS》2013,70(9):1543-1573
Epigenetic mechanisms play an important role in gene regulation during development. DNA methylation, which is probably the most important and best-studied epigenetic mechanism, can be abnormally regulated in common pathologies, but the origin of altered DNA methylation remains unknown. Recent research suggests that these epigenetic alterations could depend, at least in part, on genetic mutations or polymorphisms in DNA methyltransferases and certain genes encoding enzymes of the one-carbon metabolism pathway. Indeed, the de novo methyltransferase 3B (DNMT3B) has been recently found to be mutated in several types of cancer and in the immunodeficiency, centromeric region instability and facial anomalies syndrome (ICF), in which these mutations could be related to the loss of global DNA methylation. In addition, mutations in glycine-N-methyltransferase (GNMT) could be associated with a higher risk of hepatocellular carcinoma and liver disease due to an unbalanced S-adenosylmethionine (SAM)/S-adenosylhomocysteine (SAH) ratio, which leads to aberrant methylation reactions. Also, genetic variants of chromatin remodeling proteins and histone tail modifiers are involved in genetic disorders like α thalassemia X-linked mental retardation syndrome, CHARGE syndrome, Cockayne syndrome, Rett syndrome, systemic lupus erythematous, Rubinstein–Taybi syndrome, Coffin–Lowry syndrome, Sotos syndrome, and facioescapulohumeral syndrome, among others. Here, we review the potential genetic alterations with a possible role on epigenetic factors and discuss their contribution to human disease. 相似文献
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Zijun Wang Hai Long Christopher Chang Ming Zhao Qianjin Lu 《Cellular and molecular life sciences : CMLS》2018,75(18):3353-3369
Little information is available regarding mechanistic links between epigenetic modifications and autoimmune diseases. It seems plausible to surmise that aberrant gene expression and energy metabolism would disrupt immune tolerance, which could ultimately result in autoimmune responses. Metaboloepigenetics is an emerging paradigm that defines the interrelationships between metabolism and epigenetics. Epigenetic modifications, such as the methylation/demethylation of DNA and histone proteins and histone acetylation/deacetylation can be dynamically produced and eliminated by a group of enzymes that consume several metabolites derived from various physiological pathways. Recent insights into cellular metabolism have demonstrated that environmental stimuli such as dietary exposure and nutritional status act through the variation in concentration of metabolites to affect epigenetic regulation and breakdown biochemical homeostasis. Metabolites, including S-adenosylmethionine, acetyl-CoA, nicotinamide adenine dinucleotide, α-ketoglutarate, and ATP serve as cofactors for chromatin-modifying enzymes, such as methyltransferases, deacetylases and kinases, which are responsible for chromatin remodelling. The concentration of crucial nutrients, such as glucose, glutamine, and oxygen, spatially and temporally modulate epigenetic modifications to regulate gene expression and the reaction to stressful microenvironments in disease pathology. In this review, we focus on the interaction between metabolic intermediates and epigenetic modifications, integrating environmental signals with programmes through modification of the epigenome–metabolome to speculate as to how this may influence autoimmune diseases. 相似文献
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DNA damage repair and transcription 总被引:2,自引:0,他引:2
Berardi P Russell M El-Osta A Riabowol K 《Cellular and molecular life sciences : CMLS》2004,61(17):2173-2180
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The effect of intraperitonal cycloheximide administration on acid-soluble rat liver chromatin proteins has been investigated by electrophoresis in acetic acid-urea polyacrylamide gels. A nonhistone protein, which migrates between oxidized histone H3 and histone H1 has been found to be increased in amount following cycloheximide treatment. This protein seems to be identical with semihistone protein H24 (uH2A). A possible relationship of uH2A to the inhibition of rRNA synthesis is discussed. 相似文献
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Dewei Chen Wenxiang Gao Shouxian Wang Bing Ni Yuqi Gao 《Cellular and molecular life sciences : CMLS》2017,74(20):3789-3808
Pulmonary arterial hypertension (PAH) is characterized by persistent pulmonary vasoconstriction and pulmonary vascular remodeling. The pathogenic mechanisms of PAH remain to be fully clarified and measures of effective prevention are lacking. Recent studies; however, have indicated that epigenetic processes may exert pivotal influences on PAH pathogenesis. In this review, we summarize the latest research findings regarding epigenetic regulation in PAH, focusing on the roles of non-coding RNAs, histone modifications, ATP-dependent chromatin remodeling and DNA methylation, and discuss the potential of epigenetic-based therapies for PAH. 相似文献
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Emerging connections between DNA methylation and histone acetylation 总被引:18,自引:0,他引:18
Modifications of both DNA and chromatin can affect gene expression and lead to gene silencing. Evidence of links between
DNA methylation and histone hypoacetylation is accumulating. Several proteins that specifically bind to methylated DNA are
associated with complexes that include histone deacetylases (HDACs). In addition, DNA methyltransferases of mammals appear
to interact with HDACs. Experiments with animal cells have shown that HDACs are responsible for part of the repressive effect
of DNA methylation. Evidence was found in Neurospora that protein acetylation can in some cases affect DNA methylation. The available data suggest that the roles of DNA methylation
and histone hypoacetylation, and their relationship with each other, can vary, even within an organism. Some open questions
in this emerging field that should be answered in the near future are discussed. 相似文献
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A. Shukla P. Chaurasia S. R. Bhaumik 《Cellular and molecular life sciences : CMLS》2009,66(8):1419-1433
Methylation of lysine residues of histones is associated with functionally distinct regions of chromatin, and, therefore,
is an important epigenetic mark. Over the past few years, several enzymes that catalyze this covalent modification on different
lysine residues of histones have been discovered. Intriguingly, histone lysine methylation has also been shown to be cross-regulated
by histone ubiquitination or the enzymes that catalyze this modification. These covalent modifications and their cross-talks
play important roles in regulation of gene expression, heterochromatin formation, genome stability, and cancer. Thus, there
has been a very rapid progress within past several years towards elucidating the molecular basis of histone lysine methylation
and ubiquitination, and their aberrations in human diseases. Here, we discuss these covalent modifications with their cross-regulation
and roles in controlling gene expression and stability.
Received 24 September 2008; received after revision 21 November 2008; accepted 28 November 2008 相似文献