Gotowe bibliografie tematyczne / Epigenetic enzymes

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Gotowa bibliografia na temat „Epigenetic enzymes”

Autor: Grafiati
Data publikacji: 7 grudnia 2024

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Artykuły w czasopismach na temat "Epigenetic enzymes"

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Zhang, Xiaolin, Zhen Dong i Hongjuan Cui. "Interplay between Epigenetics and Cellular Metabolism in Colorectal Cancer". Biomolecules 11, nr 10 (25.09.2021): 1406. http://dx.doi.org/10.3390/biom11101406.

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Cellular metabolism alterations have been recognized as one of the most predominant hallmarks of colorectal cancers (CRCs). It is precisely regulated by many oncogenic signaling pathways in all kinds of regulatory levels, including transcriptional, post-transcriptional, translational and post-translational levels. Among these regulatory factors, epigenetics play an essential role in the modulation of cellular metabolism. On the one hand, epigenetics can regulate cellular metabolism via directly controlling the transcription of genes encoding metabolic enzymes of transporters. On the other hand, epigenetics can regulate major transcriptional factors and signaling pathways that control the transcription of genes encoding metabolic enzymes or transporters, or affecting the translation, activation, stabilization, or translocation of metabolic enzymes or transporters. Interestingly, epigenetics can also be controlled by cellular metabolism. Metabolites not only directly influence epigenetic processes, but also affect the activity of epigenetic enzymes. Actually, both cellular metabolism pathways and epigenetic processes are controlled by enzymes. They are highly intertwined and are essential for oncogenesis and tumor development of CRCs. Therefore, they are potential therapeutic targets for the treatment of CRCs. In recent years, both epigenetic and metabolism inhibitors are studied for clinical use to treat CRCs. In this review, we depict the interplay between epigenetics and cellular metabolism in CRCs and summarize the underlying molecular mechanisms and their potential applications for clinical therapy.
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Kringel, Dario, Sebastian Malkusch i Jörn Lötsch. "Drugs and Epigenetic Molecular Functions. A Pharmacological Data Scientometric Analysis". International Journal of Molecular Sciences 22, nr 14 (6.07.2021): 7250. http://dx.doi.org/10.3390/ijms22147250.

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Interactions of drugs with the classical epigenetic mechanism of DNA methylation or histone modification are increasingly being elucidated mechanistically and used to develop novel classes of epigenetic therapeutics. A data science approach is used to synthesize current knowledge on the pharmacological implications of epigenetic regulation of gene expression. Computer-aided knowledge discovery for epigenetic implications of current approved or investigational drugs was performed by querying information from multiple publicly available gold-standard sources to (i) identify enzymes involved in classical epigenetic processes, (ii) screen original biomedical scientific publications including bibliometric analyses, (iii) identify drugs that interact with epigenetic enzymes, including their additional non-epigenetic targets, and (iv) analyze computational functional genomics of drugs with epigenetic interactions. PubMed database search yielded 3051 hits on epigenetics and drugs, starting in 1992 and peaking in 2016. Annual citations increased to a plateau in 2000 and show a downward trend since 2008. Approved and investigational drugs in the DrugBank database included 122 compounds that interacted with 68 unique epigenetic enzymes. Additional molecular functions modulated by these drugs included other enzyme interactions, whereas modulation of ion channels or G-protein-coupled receptors were underrepresented. Epigenetic interactions included (i) drug-induced modulation of DNA methylation, (ii) drug-induced modulation of histone conformations, and (iii) epigenetic modulation of drug effects by interference with pharmacokinetics or pharmacodynamics. Interactions of epigenetic molecular functions and drugs are mutual. Recent research activities on the discovery and development of novel epigenetic therapeutics have passed successfully, whereas epigenetic effects of non-epigenetic drugs or epigenetically induced changes in the targets of common drugs have not yet received the necessary systematic attention in the context of pharmacological plasticity.
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Ramarao-Milne, Priya, Olga Kondrashova, Sinead Barry, John D. Hooper, Jason S. Lee i Nicola Waddell. "Histone Modifying Enzymes in Gynaecological Cancers". Cancers 13, nr 4 (16.02.2021): 816. http://dx.doi.org/10.3390/cancers13040816.

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Genetic and epigenetic factors contribute to the development of cancer. Epigenetic dysregulation is common in gynaecological cancers and includes altered methylation at CpG islands in gene promoter regions, global demethylation that leads to genome instability and histone modifications. Histones are a major determinant of chromosomal conformation and stability, and unlike DNA methylation, which is generally associated with gene silencing, are amenable to post-translational modifications that induce facultative chromatin regions, or condensed transcriptionally silent regions that decondense resulting in global alteration of gene expression. In comparison, other components, crucial to the manipulation of chromatin dynamics, such as histone modifying enzymes, are not as well-studied. Inhibitors targeting DNA modifying enzymes, particularly histone modifying enzymes represent a potential cancer treatment. Due to the ability of epigenetic therapies to target multiple pathways simultaneously, tumours with complex mutational landscapes affected by multiple driver mutations may be most amenable to this type of inhibitor. Interrogation of the actionable landscape of different gynaecological cancer types has revealed that some patients have biomarkers which indicate potential sensitivity to epigenetic inhibitors. In this review we describe the role of epigenetics in gynaecological cancers and highlight how it may exploited for treatment.
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Ruoß, Marc, Georg Damm, Massoud Vosough, Lisa Ehret, Carl Grom-Baumgarten, Martin Petkov, Silvio Naddalin i in. "Epigenetic Modifications of the Liver Tumor Cell Line HepG2 Increase Their Drug Metabolic Capacity". International Journal of Molecular Sciences 20, nr 2 (16.01.2019): 347. http://dx.doi.org/10.3390/ijms20020347.

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Although human liver tumor cells have reduced metabolic functions as compared to primary human hepatocytes (PHH) they are widely used for pre-screening tests of drug metabolism and toxicity. The aim of the present study was to modify liver cancer cell lines in order to improve their drug-metabolizing activities towards PHH. It is well-known that epigenetics is strongly modified in tumor cells and that epigenetic regulators influence the expression and function of Cytochrome P450 (CYP) enzymes through altering crucial transcription factors responsible for drug-metabolizing enzymes. Therefore, we screened the epigenetic status of four different liver cancer cell lines (Huh7, HLE, HepG2 and AKN-1) which were reported to have metabolizing drug activities. Our results showed that HepG2 cells demonstrated the highest similarity compared to PHH. Thus, we modified the epigenetic status of HepG2 cells towards ‘normal’ liver cells by 5-Azacytidine (5-AZA) and Vitamin C exposure. Then, mRNA expression of Epithelial-mesenchymal transition (EMT) marker SNAIL and CYP enzymes were measured by PCR and determinate specific drug metabolites, associated with CYP enzymes by LC/MS. Our results demonstrated an epigenetic shift in HepG2 cells towards PHH after exposure to 5-AZA and Vitamin C which resulted in a higher expression and activity of specific drug metabolizing CYP enzymes. Finally, we observed that 5-AZA and Vitamin C led to an increased expression of Hepatocyte nuclear factor 4α (HNF4α) and E-Cadherin and a significant down regulation of Snail1 (SNAIL), the key transcriptional repressor of E-Cadherin. Our study shows, that certain phase I genes and their enzyme activities are increased by epigenetic modification in HepG2 cells with a concomitant reduction of EMT marker gene SNAIL. The enhancing of liver specific functions in hepatoma cells using epigenetic modifiers opens new opportunities for the usage of cell lines as a potential liver in vitro model for drug testing and development.
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Maleszewska, Marta, Bartosz Wojtas, Bartlomiej Gielniewski, Shamba Mondal, Jakub Mieczkowski, Michal Dabrowski, Janusz Siedlecki i in. "ECOA-6. Genomic and transcriptomic analyses reveal diverse mechanisms responsible for deregulation of epigenetic enzyme/modifier expression in glioblastoma". Neuro-Oncology Advances 3, Supplement_2 (1.07.2021): ii2. http://dx.doi.org/10.1093/noajnl/vdab070.006.

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Abstract Malignant gliomas represent over 70% of primary brain tumors and the most deadly is glioblastoma (GBM, WHO grade IV), due to frequent dysfunctions of tumor suppressors or/and oncogenes. Recent whole genome studies of gliomas demonstrated that besides genetic alterations, epigenetic dysfunctions contribute to tumor development and progression. Alterations in genes encoding epigenetic enzyme/protein or aberrations in epigenetic modification pattern have been found in gliomas of lower grade, yet no epigenetic driver was identified in GBM. We sought to identify different mechanisms driving aberrant expression of epigenetic genes in GBM. We analyzed gene expression and coding/non-coding regions of 96 major epigenetic enzymes and chromatin modifiers in 28 GBMs, 23 benign gliomas (juvenile pilocytic astrocytomas, JPAs, WHO grade I) and 7 normal brain samples. We found a profound and global down-regulation of expression of most tested epigenetic enzymes and modifiers in GBMs when compared to normal brains and JPAs. For some genes changes in mRNA level correlated with newly identified single nucleotide variants within non-coding regulatory regions. To find a common denominator responsible for the coordinated down-regulation of expression of epigenetic enzymes/modifiers, we employed PWMEnrich tool for DNA motif scanning and enrichment analysis. Among others, we discovered the presence of high affinity motifs for the E2F1/E2F4 transcription factors, within the promoters of the epigenetic enzyme/modifier encoding genes. Knockdown of the E2F1/E2F4 expression affected the expression of a set of epigenetic enzymes/modifiers. Altogether, our results reveal a novel epigenetic-related pathway by which E2F1/E2F4 factors contribute to glioma pathogenesis and indicate novel targets for glioma therapy. Supported by a National Science Centre grant 2013/09/B/NZ3/01402 (MM).
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Amsalem, Zohar, Tasleem Arif, Anna Shteinfer-Kuzmine, Vered Chalifa-Caspi i Varda Shoshan-Barmatz. "The Mitochondrial Protein VDAC1 at the Crossroads of Cancer Cell Metabolism: The Epigenetic Link". Cancers 12, nr 4 (22.04.2020): 1031. http://dx.doi.org/10.3390/cancers12041031.

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Carcinogenesis is a complicated process that involves the deregulation of epigenetics, resulting in cellular transformational events, such as proliferation, differentiation, and metastasis. Most chromatin-modifying enzymes utilize metabolites as co-factors or substrates and thus are directly dependent on such metabolites as acetyl-coenzyme A, S-adenosylmethionine, and NAD+. Here, we show that using specific siRNA to deplete a tumor of VDAC1 not only led to reprograming of the cancer cell metabolism but also altered several epigenetic-related enzymes and factors. VDAC1, in the outer mitochondrial membrane, controls metabolic cross-talk between the mitochondria and the rest of the cell, thus regulating the metabolic and energetic functions of mitochondria, and has been implicated in apoptotic-relevant events. We previously demonstrated that silencing VDAC1 expression in glioblastoma (GBM) U-87MG cell-derived tumors, resulted in reprogramed metabolism leading to inhibited tumor growth, angiogenesis, epithelial–mesenchymal transition and invasiveness, and elimination of cancer stem cells, while promoting the differentiation of residual tumor cells into neuronal-like cells. These VDAC1 depletion-mediated effects involved alterations in transcription factors regulating signaling pathways associated with cancer hallmarks. As the epigenome is sensitive to cellular metabolism, this study was designed to assess whether depleting VDAC1 affects the metabolism–epigenetics axis. Using DNA microarrays, q-PCR, and specific antibodies, we analyzed the effects of si-VDAC1 treatment of U-87MG-derived tumors on histone modifications and epigenetic-related enzyme expression levels, as well as the methylation and acetylation state, to uncover any alterations in epigenetic properties. Our results demonstrate that metabolic rewiring of GBM via VDAC1 depletion affects epigenetic modifications, and strongly support the presence of an interplay between metabolism and epigenetics.
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Jelinek, Mary Anne. "Biochemical Assays for Epigenetic Enzymes". Genetic Engineering & Biotechnology News 36, nr 15 (wrzesień 2016): 16–17. http://dx.doi.org/10.1089/gen.36.15.08.

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Jasim, Dr Hiba Sabah. "The Role of Epigenetic Drugs in Cancer Therapy". South Asian Research Journal of Medical Sciences 4, nr 4 (25.08.2022): 54–62. http://dx.doi.org/10.36346/sarjms.2022.v04i04.001.

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Epigenetics refers to heritable and dynamic alterations in the whole genes which present in the sequence of nucleic acids. It consider as concurrent reaction with enzymes and several molecular ingredients. Epigenetic changes can cause the incorrect start of coding genes, allowing tumor development. Epigenetic modifiers are becoming potential targets in numerous malignant tumor therapies since they are sensitive to foreign drugs. Different epigenetic medicines that were lately refined and implicated in clinical experiences using of epigenetic medicines solitary or together with immunotherapy and chemotherapy has yielded promising outcomes, containing advanced anti-cancer impact, overcoming therapy resistant, and stimulation of the immune system defense.
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Alghamdi, Bandar Ali, Intisar Mahmoud Aljohani, Bandar Ghazi Alotaibi, Muhammad Ahmed, Kholod Abduallah Almazmomi, Salman Aloufi i Jowhra Alshamrani. "Studying Epigenetics of Cardiovascular Diseases on Chip Guide". Cardiogenetics 12, nr 3 (7.07.2022): 218–34. http://dx.doi.org/10.3390/cardiogenetics12030021.

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Epigenetics is defined as the study of inheritable changes in the gene expressions and phenotypes that occurs without altering the normal DNA sequence. These changes are mainly due to an alteration in chromatin or its packaging, which changes the DNA accessibility. DNA methylation, histone modification, and noncoding or microRNAs can best explain the mechanism of epigenetics. There are various DNA methylated enzymes, histone-modifying enzymes, and microRNAs involved in the cause of various CVDs (cardiovascular diseases) such as cardiac hypertrophy, heart failure, and hypertension. Moreover, various CVD risk factors such as diabetes mellitus, hypoxia, aging, dyslipidemia, and their epigenetics are also discussed together with CVDs such as CHD (coronary heart disease) and PAH (pulmonary arterial hypertension). Furthermore, different techniques involved in epigenetic chromatin mapping are explained. Among these techniques, the ChIP-on-chip guide is explained with regard to its role in cardiac hypertrophy, a final form of heart failure. This review focuses on different epigenetic factors that are involved in causing cardiovascular diseases.
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Bunsick, David A., Jenna Matsukubo i Myron R. Szewczuk. "Cannabinoids Transmogrify Cancer Metabolic Phenotype via Epigenetic Reprogramming and a Novel CBD Biased G Protein-Coupled Receptor Signaling Platform". Cancers 15, nr 4 (6.02.2023): 1030. http://dx.doi.org/10.3390/cancers15041030.

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The concept of epigenetic reprogramming predicts long-term functional health effects. This reprogramming can be activated by exogenous or endogenous insults, leading to altered healthy and different disease states. The exogenous or endogenous changes that involve developing a roadmap of epigenetic networking, such as drug components on epigenetic imprinting and restoring epigenome patterns laid down during embryonic development, are paramount to establishing youthful cell type and health. This epigenetic landscape is considered one of the hallmarks of cancer. The initiation and progression of cancer are considered to involve epigenetic abnormalities and genetic alterations. Cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer development, including DNA methylation, histone modifications, nucleosome positioning, non-coding RNAs, and microRNA expression. Endocannabinoids are natural lipid molecules whose levels are regulated by specific biosynthetic and degradative enzymes. They bind to and activate two primary cannabinoid receptors, type 1 (CB1) and type 2 (CB2), and together with their metabolizing enzymes, form the endocannabinoid system. This review focuses on the role of cannabinoid receptors CB1 and CB2 signaling in activating numerous receptor tyrosine kinases and Toll-like receptors in the induction of epigenetic landscape alterations in cancer cells, which might transmogrify cancer metabolism and epigenetic reprogramming to a metastatic phenotype. Strategies applied from conception could represent an innovative epigenetic target for preventing and treating human cancer. Here, we describe novel cannabinoid-biased G protein-coupled receptor signaling platforms (GPCR), highlighting putative future perspectives in this field.
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Rozprawy doktorskie na temat "Epigenetic enzymes"

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Herrlinger, Eva-Maria [Verfasser], i Manfred [Akademischer Betreuer] Jung. "Bioreductive prodrugs for the targeting of epigenetic enzymes". Freiburg : Universität, 2020. http://d-nb.info/1217193758/34.

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Saladi, SrinivasVinod. "SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival". University of Toledo Health Science Campus / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995.

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Stamatakos, Serena <1993&gt. "Effects of 3,4-methylenedioxymethamphetamine (MDMA) on BDNF pathway, HDAC epigenetic enzymes and neurofilament proteins". Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10104/1/PhD_Thesis_StamatakosSerena.pdf.

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3,4-methylenedioxymethamphetamine (MDMA) is a psychoactive substance used for recreational purposes. Possible clinical use of MDMA, in combination with psychotherapy, has been considered for the treatment of PTSD. However, MDMA causes neurotoxic effects and its use was associated with psychiatric symptoms, memory and cognitive deficits. To elucidate these aspects, the first aim of this study was to investigate the effects of acute and repeated MDMA treatment on BDNF/TrkB and HDACs in animal models. According to recent evidence about HDAC inhibitors, we used sodium butyrate to investigate its ability to affect MDMA-induced molecular and behavioral alterations. Moreover, considering that an alteration of BDNF has been reported in the brain of animals treated with psychoactive substances and in the blood of substance abusers, possible alterations of this neurotrophin levels were investigated in blood samples of MDMA users. Since different BDNF pools exist in plasma and serum, distinct determination of the neurotrophin were evaluated in both matrices. Furthermore, recent evidence has shown that neurofilaments can represent valid biomarkers of neural damage. Given the neurotoxic effects of ecstasy, we investigated neurofilaments in serotonergic neuronal cells. Particularly, we assessed MDMA effects on neurofilament proteins in differentiated serotonergic cells and we investigated if BDNF could protect serotonergic neurons from MDMA effects. Data showed that MDMA alters different crucial genes as well as the proteins involved in both substance use disorders and psychiatric conditions. Animal studies showed alterations both in BDNF pathways and in HDACs. Moreover, investigation in humans brought into view that peripheral BDNF could not reflect central BDNF and serum and plasma BDNF can express different types of this neurotrophin. Furthermore, data obtained in the differentiated serotonergic cell line highlight the useful role of NF-L as a biomarker of neuronal damage induced by MDMA, confirming the importance of studying NFs in the field of neuropsychiatric disorders.
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Phipps, Sharla Marion Ostein. "Genetic and epigenetic modulation of telomerase activity in development and disease". Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/phipps.pdf.

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Thesis (Ph. D.)--University of Alabama at Birmingham, 2007.
Additional advisors: Vithal K. Ghanta, J. Michael Ruppert, Theresa V. Strong, R. Douglas Watson. Description based on contents viewed Oct. 3, 2008; title from PDF t.p. Includes bibliographical references.
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Huang, Hsien-Sung. "Epigenetic Determinants of Altered Gene Expression in Schizophrenia: a Dissertation". eScholarship@UMMS, 2008. https://escholarship.umassmed.edu/gsbs_diss/365.

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Schizophrenia is a neurodevelopmental disorder affecting 1% of the general population. Dysfunction of the prefrontal cortex (PFC) is associated with the etiology of schizophrenia. Moreover, a substantial deficit of GAD1mRNA in schizophrenic PFC has been reported by different groups. However, the underlying molecular mechanisms are still unclear. Interestingly, epigenetic factors such as histone modifications and DNA methylation could be involved in the pathogenesis of schizophrenia during the maturation of the PFC. In my work, I identified potential epigenetic changes in schizophrenic PFC and developmental changes of epigenetic marks in normal human PFC. Furthermore, mouse and neuronal precursor cell models were used to confirm and investigate the molecular mechanisms of the epigenetic changes in human PFC. My initial work examined whether chromatin immunoprecipitation can be applied to human postmortem brain. I used micrococcal nuclease (MNase)-digested chromatin instead of cross-linked and sonicated chromatin for further immunoprecipitation with specific anti-methyl histone antibodies. Surprisingly, the integrity of mono-nucleosomes was still maintained at least 30 hrs after death. Moreover, differences of histone methylation at different genomic loci were detectable and were preserved within a wide range of autolysis times and tissue pH values. Interestingly, MNase-treated chromatin is more efficient for subsequent immunoprecipitation than crosslinked and sonicated chromatin. During the second part of my dissertation work, I profiled histone methylation at GABAergic gene loci during human prefrontal development. Moreover, a microarray analysis was used to screen which histone methyltransferase (HMT) could be involved in histone methylation during human prefrontal development. Mixed-lineage leukemia 1 (MLL1), an HMT for methylation at histone H3 lysine 4 (H3K4), appears to be the best candidate after interpreting microarray results. Indeed, decreased methylation of histone H3 lysine 4 at a subset of GABAergic gene loci occurred in Mll1 mutant mice. Interestingly, clozapine, but not haloperidol, increased levels of trimethyl H3K4 (H3K4me3) and Mll1 occupancy at the GAD1 promoter. I profiled histone methylation and gene expression for GAD1 in schizophrenics and their matched controls. Interestingly, there are deficits of GAD1 mRNA levels and GAD1 H3K4me3 in female schizophrenics. Furthermore, I was also interested in whether the changes of GAD1 chromatin structure could contribute to cortical pathology in schizophrenics with GAD1 SNPs. Remarkably, homozygous risk alleles for schizophrenia at the 5’ end of the GAD1 gene are associated with a deficit of GAD1 mRNA levels together with decreased GAD1 H3K4me3 and increased GAD1H3K27me3 in schizophrenics. Finally, I shifted focus on whether DNA methylation at the GAD1 promoter could contribute to a deficit of GAD1 mRNA in schizophrenia. However, no reproducible techniques are available for extracting genomic DNA specifically from GABAergic neurons in human brain. Therefore, I used an alternative approach that is based on immunoprecipitation of mononucleosomes with anti-methyl-histone antibodies differentiating between sites of active and silenced gene expression. The methylation frequencies of CpG dinucleotides at the GAD1 proximal promoter and intron 2 were determined from two chromatin fractions (H3K4me3 and H3K27me3) separately. Consistently, the proximal promoter region of GAD1 is more resistant to methylation in comparison to intron 2 of GAD1 in either open or repressive chromatin fractions. Interestingly, overall higher levels of DNA methylation were seen in repressive chromatin than in open chromatin. Surprisingly, schizophrenic subjects showed a significant decrease of DNA methylation at the GAD1proximal promoter from repressive chromatin. Taken together, my work has advanced our knowledge of epigenetic mechanisms in human prefrontal development and the potential link to the etiology of schizophrenia. It could eventually provide a new approach for the treatment of schizophrenia, especially in the regulation of methylation at histone H3 lysine 4.
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Mehta, Ninad T. "Early Epigenetic Regulation of the Adaptive Immune Response Gene CIITA". Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/biology_theses/24.

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The precise regulation of Major Histocompatibility class II (MHC-II) genes plays an important role in the control of the adaptive immune response. MHC-II genes are expressed constitutively in only a few cell types, but their expression can be induced by the inflammatory response cytokine interferon gamma (INF-γ). The regulation of MHC-II is controlled by a Master Regulator, the class II transactivator (CIITA). Multiple studies have shown that CIITA regulated expression of MHC-II is controlled and induced by INF-γ. It has been also shown that a functional CIITA gene is necessary for the expression of MHC-II genes. CIITA is thus a general regulator of both constitutive and inducible MHC-II expression. Although much is known about the transcription factors necessary for CIITA expression, there is little information as to the epigenetic modifications and the requisite enzymes needed to provide these transcription factors access to DNA. Previous studies in the Greer lab have shown that increased levels of acetylation of histones H3 upon INF-γ stimulation, as does tri-methylation of H3K4 upon prolonged cytokine stimulation. Similar observations were made at early time points post IFN-γ stimulation, where there is an instantaneous increase in the levels of H3K18ac and H3K4me3. In contrast to this, the levels of silencing modifications begin to drop with in the first 20 minutes of IFN-γ stimulation. The binding of STAT1 reaches its peak at about 60 minutes and the first transcripts for the protein start to appear as early as 40 minutes post the cytokines stimulation. Our study is the first to link the rapidly occurring epigenetic changes at the CIITA promoter pIV to EZH2
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Truax, Agnieszka D. "The 26S Proteasome and Histone Modifying Enzymes Regulate". Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/biology_diss/91.

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Major Histocompatibility Complex Class-II (MHC-II) molecules are critical regulators of adaptive immunity that present extracellular antigens required to activate CD4+ T cells. MHC-II are regulated at the level of transcription by master regulator, the Class II Transactivator (CIITA), whose association with the MHC-II promoter is necessary to initiate transcription. Recently, much research focused on novel mechanisms of transcriptional regulation of critical genes like MHC-II and CIITA; findings that the macromolecular complex of the 26S-proteasome is involved in transcription have been perhaps the most exciting as they impart novel functions to a well studied system. Proteasome is a multi-subunit complex composed of a 20S-core particle capped by a 19S-regulatory particle. The 19S contains six ATPases which are required for transcription initiation and elongation. We demonstrate that 19S ATPase-S6a inducibly associates with CIITA promoters. Decreased expression of S6a negatively impacts recruitment of the transcription factors STAT-1 and IRF-1 to the CIITA due to significant loss in histone H3 and H4 acetylation. S6a is robustly recruited to CIITA coding regions, where S6a binding coordinates with that of RNA polymerase II. RNAi mediated S6a knockdown significantly diminishes recruitment of Pol II and P-TEF-b components to CIITA coding regions, indicating S6a plays important roles in transcriptional elongation. Our research is focused on the ways in which accessibility to and transcription of DNA is regulated. While cancers are frequently linked to dysregulated gene expression, contribution of epigenetics to cancers remains unknown. To achieve metastatic ability, tumors alter gene expression to escape host immunosurveilance. MHC-II and CIITA expression are significantly downregulated in highly metastatic MDA-MB-435 breast cancer cells. This suppression correlates with elevated levels of the silencing modification H3K27me3 at CIITA and a significant reduction in Pol II recruitment. We observe elevated binding of the histone methyltransferase to CIITApIV and demonstrate this enzyme is a master regulator of CIITA gene expression. EZH2 knockdown results in significant increases in CIITA and MHC-II transcript levels in metastatic cells. In sum, transcriptional regulation by the 19S-proteasome and histone modifying enzymes represents novel mechanisms of control of mammalian gene expression and present novel therapeutic targets for manipulating MHC expression in disease.
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Islam, Abul 1978. "Delineating epigenetic regulatory mechanisms of cell profileration and differentiation". Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/85721.

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Recent advances in high throughput technology have opened the door to systematic studies of epigenetic mechanisms. One of the key components in the regulation of the cell cycle and differentiation is the retinoblastoma protein (pRB), a component of the RB/E2F tumor suppressor pathway that is frequently deregulated in cancer. The RBP2/KDM5A histone demethylase was shown to interact with pRB and regulate pRB function during differentiation. However, how precisely differentiation is coupled with halted cell cycle progression and whether an epigenetic mechanism is involved remain unknown. In the present study, I analyzed gene expression levels of human histone methyltransferases (HMT) and demethylases (HDM), as well as their targets in human cancers; and focused on RB/KDM5A connection in control of cell cycle and differentiation. In particular, I used Drosophila as a model to describe a novel mechanism where the RB/E2F pathway interacts with the Hippo tumor suppressor pathway to synergistically control cell cycle exit upon differentiation. Studying the role of miR-11, I found that the inhibition of dE2F1-induced cell death is its highly specialized function. Furthermore, I studied the induction of differentiation and apoptosis as the consequences of KDM5A deletion in cells derived from Rb knockout mice. I concluded that during differentiation, KDM5A plays a critical role at the enhancers of cell type-specific genes and at the promoters of E2F targets; in cooperation with other repressor complexes, it silences cell cycle genes. I found that KDM5A binds to transcription start sites of the majority of genes with H3K4 methylation. These are highly expressed genes, involved in certain biological processes, and occupied by KDM5A in an isoform-specific manner. KDM5A plays a unique and non-redundant role in histone demethylation and its promoter binding pattern highly overlaps with the opposing enzyme, MLL1. Finally, I found that HMT and HDM enzymes exhibit a distinct co-expression pattern in different cancer types, and this determines the level of expression of their target genes.
Los avances recientes en las tecnologías de alto flujo han abierto el camino a los estudios sistemáticos de los mecanismos epigenéticos. La proteína retinoblastoma (pRB), uno de los elementos de la ruta de supresión de tumores RB/E2F que se encuentra desregulado con frecuencia en el cáncer, es uno de los componentes esenciales de la regulación del ciclo celular y la diferenciación. Sin embargo, aún no se conoce de qué manera precisa la diferenciación se acopla a la detención del avance del ciclo celular y si hay algún mecanismo epigenético vinculado a este proceso. En este estudio, he analizado los niveles de expresión de histona metiltransferasas (HMT) y desmetilasas humanas (HDM), así como sus dianas en cánceres humanos, y me he centrado en la conexión de RB/KDM5A en el control del ciclo celular y la diferenciación. Específicamente, utilicé Drosophila como modelo para describir un mecanismo nuevo mediante el cual RB/E2F interactúa con la ruta Hippo de supresión de tumores para controlar de manera sinérgica la detención del ciclo celular relacionada con la diferenciación. Mediante la investigación del papel de miR-11, determiné que su función altamente especializada es la inhibición de la muerte celular inducida por dE2F1. Además, estudié la inducción de la diferenciación y la apoptosis como consecuencia de la pérdida de KDMA5 en células obtenidas a partir de ratones sin Rb. Extraje como conclusión que, durante la diferenciación, KDMA5 desempeña un papel esencial sobre los estimuladores de los genes específicos de los tipos celulares, así como en los promotores de las dianas de E2F; en cooperación con otros complejos represores silencia a los genes del ciclo celular. Investigué el mecanismo de reclutamiento de KDM5A y encontré que se une al sitio de inicio de la transcripción de la mayoría de los genes que poseen metilación en H3K4. Estos genes tienen elevados niveles de expresión, están involucrados en determinados procesos biológicos y están ocupados por diferentes isoformas de KDM5A. KDM5A desempeña un papel único y no redundante en la desmetilación de las histonas y que en gran medida se solapa con la enzima con la función opuesta, MLL1. Para terminar, encontré que las enzimas HMT y HDM muestran patrones de co-expresión distintos en diferentes tipos de cáncer, y que este hecho determina los niveles de expresión de sus genes diana.
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Koues, Olivia I. "The Epigenetic Regulation of Cytokine Inducible Mammalian Transcription by the 26S Proteasome". Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/59.

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It is evident that components of the 26S proteasome function beyond protein degradation in the regulation of transcription. Studies in yeast implicate the 26S proteasome, specifically the 19S cap, in the epigenetic regulation of transcription. Saccharomyces cerevisiae 19S ATPases remodel chromatin by facilitating histone acetylation and methylation. However, it is unclear if the 19S ATPases play similar roles in mammalian cells. We previously found that the 19S ATPase Sug1 positively regulates transcription of the critical inflammatory gene MHC-II and that the MHC-II promoter fails to efficiently bind transcription factors upon Sug1 knockdown. MHC-II transcription is regulated by the critical coactivator CIITA. We now find that Sug1 is crucial for regulating histone H3 acetylation at the cytokine inducible MHC-II and CIITA promoters. Histone H3 acetylation is dramatically decreased upon Sug1 knockdown with a preferential loss occurring at lysine 18. Research in yeast indicates that the ortholog of Sug1, Rpt6, acts as a mediator between the activating modifications of histone H2B ubiquitination and H3 methylation. Therefore, we characterized the role the 19S proteasome plays in regulating additional activating modifications. As with acetylation, Sug1 is necessary for proper histone H3K4 and H3R17 methylation at cytokine inducible promoters. In the absence of Sug1, histone H3K4me3 and H3R17me2 are substantially inhibited. Our observation that the loss of Sug1 has no significant effect on H3K36me3 implies that Sug1’s regulation of histone modifications is localized to promoter regions as H3K4me3 but not H3K36me3 is clustered around gene promoters. Here we show that multiple H3K4 histone methyltransferase subunits bind constitutively to the inducible MHC-II and CIITA promoters and that over-expressing one subunit significantly enhances promoter activity. Furthermore, we identified a critical subunit of the H3K4 methyltransferase complex that binds multiple histone modifying enzymes, but fails to bind the CIITA promoter in the absence of Sug1, implicating Sug1 in recruiting multi-enzyme complexes responsible for initiating transcription. Finally, Sug1 knockdown maintains gene silencing as elevated levels of H3K27 trimethylation are observed upon Sug1 knockdown. Together these studies strongly implicate the 19S proteasome in mediating the initial reorganization events to relax the repressive chromatin structure surrounding inducible genes.
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Jiang, Zhongliang. "Epigenetic Instability Induced by DNA Base Lesion via DNA Base Excision Repair". FIU Digital Commons, 2017. https://digitalcommons.fiu.edu/etd/3566.

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DNA damage can cause genome instability, which may lead to human cancer. The most common form of DNA damage is DNA base damage, which is efficiently repaired by DNA base excision repair (BER). Thus BER is the major DNA repair pathway that maintains the stability of the genome. On the other hand, BER mediates DNA demethylation that can occur on the promoter region of important tumor suppressor genes such as Breast Cancer 1 (BRCA1) gene that is also involved in prevention and development of cancer. In this study, employing cell-based and in vitro biochemical approaches along with bisulfite DNA sequencing, we initially discovered that an oxidized nucleotide, 5’,2-cyclo-2-deoxyadenosine in DNA duplex can either cause misinsertion by DNA polymerase β (pol β) during pol β-mediated BER or inhibit lesion bypass of pol β resulting in DNA strand breaks. We then explored how a T/G mismatch resulting from active DNA demethylation can affect genome integrity during BER and found that pol β can extend the mismatched T to cause mutation. We found that AP endonuclease 1 (APE1) can use its 3'-5' exonuclease to remove the mismatched T before pol β can extend the nucleotide preventing a C to T mutation. The results demonstrate that the 3'-5' exonuclease activity of APE1 can serve as a proofreader for pol β to prevent mutation. We further explored the effects of exposure of environmental toxicants, bromate and chromate on the DNA methylation pattern on the promoter region of BRCA1 gene with bisulfite DNA sequencing. We found that bromate and chromate induced demethylation of 5-methylcytosines (5mC) at the CpG sites as well as created additional methylation at several unmethylated CpG sites at BRCA1 gene in human embryonic kidney (HEK) 293 cells. We further demonstrated that the demethylation was mediated by pol β nucleotide misinsertion and an interaction between pol β and DNA methyltransferase 1 (DNMT1) suggesting a cross-talk between BER and DNA methyltransferases. We suggest that DNA base damage and BER govern the interactions among the environment, the genome and epigenome, modulating the stability of the genome and epigenome and disease development.
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Książki na temat "Epigenetic enzymes"

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Marmorstein, Ronen. Enzymes of Epigenetics. Elsevier Science & Technology, 2016.

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Marmorstein, Ronen. Enzymes of Epigenetics. Elsevier Science & Technology Books, 2016.

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Enzymes of Epigenetics, Part A. Elsevier, 2016. http://dx.doi.org/10.1016/s0076-6879(16)x0005-5.

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Enzymes of Epigenetics, Part B. Elsevier, 2016. http://dx.doi.org/10.1016/s0076-6879(16)x0006-7.

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Marmorstein, Ronen. Enzymes of Epigenetics Part B. Elsevier Science & Technology Books, 2016.

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Marmorstein, Ronen. Enzymes of Epigenetics Part B. Elsevier Science & Technology Books, 2016.

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Pharmaceutical Biocatalysis: Drugs, Genetic Diseases, and Epigenetics. Jenny Stanford Publishing, 2020.

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Grunwald, Peter. Pharmaceutical Biocatalysis: Drugs, Genetic Diseases, and Epigenetics. Jenny Stanford Publishing, 2020.

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Grunwald, Peter. Pharmaceutical Biocatalysis: Drugs, Genetic Diseases, and Epigenetics. Jenny Stanford Publishing, 2020.

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Grunwald, Peter. Pharmaceutical Biocatalysis: Drugs, Genetic Diseases, and Epigenetics. Jenny Stanford Publishing, 2020.

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Części książek na temat "Epigenetic enzymes"

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Dalmizrak, Aysegul, i Ozlem Dalmizrak. "Epigenetic Enzymes and Their Mutations in Cancer". W Epigenetics and Human Health, 31–76. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-42365-9_2.

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Ganai, Shabir Ahmad. "Overview of Epigenetic Signatures and Their Regulation by Epigenetic Modification Enzymes". W Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 1–33. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_1.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro i Anton Wutz. "Epigenetics and Metabolism". W Introduction to Epigenetics, 179–201. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_9.

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AbstractMost chromatin-modifying enzymes use metabolites as cofactors. Consequently, the cellular metabolism can influence the capacity of the cell to write or erase chromatin marks. This points to an intimate relationship between metabolic and epigenetic regulation. In this chapter, we describe the biosynthetic pathways of cofactors that are implicated in epigenetic and chromatin regulation and provide examples of how metabolic pathways can influence chromatin and epigenetic processes as well as their interplay in developmental and cancer biology.
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Ganesan, A. "The Discovery of Anticancer Drugs Targeting Epigenetic Enzymes". W Analogue-Based Drug Discovery III, 111–39. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527651085.ch5.

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Ganai, Shabir Ahmad. "Epigenetic Enzymes and Drawbacks of Conventional Therapeutic Regimens". W Histone Deacetylase Inhibitors — Epidrugs for Neurological Disorders, 11–19. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8019-8_2.

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Ganai, Shabir Ahmad. "Epigenetic Regulator Enzymes and Their Implications in Distinct Malignancies". W Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 35–65. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_2.

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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro i Anton Wutz. "Chromatin Dynamics". W Introduction to Epigenetics, 29–47. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_2.

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AbstractThe nucleus of a eukaryotic cell is a very busy place. Not only during replication of the DNA, but at any time in the cell cycle specific enzymes need access to genetic information to process reactions such as transcription and DNA repair. Yet, the nucleosomal structure of chromatin is primarily inhibitory to these processes and needs to be resolved in a highly orchestrated manner to allow developmental, organismal, and cell type-specific nuclear activities. This chapter explains how nucleosomes organize and structure the genome by interacting with specific DNA sequences. Variants of canonical histones can change the stability of the nucleosomal structure and also provide additional epigenetic layers of information. Chromatin remodeling complexes work locally to alter the regular beads-on-a-string organization and provide access to transcription and other DNA processing factors. Conversely, factors like histone chaperones and highly precise templating and copying mechanisms are required for the reassembly of nucleosomes and reestablishment of the epigenetic landscape after passage of activities processing DNA sequence information. A very intricate molecular machinery ensures a highly dynamic yet heritable chromatin template.
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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro i Anton Wutz. "Biology of Chromatin". W Introduction to Epigenetics, 1–28. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_1.

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AbstractThis chapter provides an introduction to chromatin. We will examine the organization of the genome into a nucleosomal structure. DNA is wrapped around a globular complex of 8 core histone proteins, two of each histone H2A, H2B, H3, and H4. This nucleosomal arrangement is the context in which information can be established along the sequence of the DNA for regulating different aspects of the chromosome, including transcription, DNA replication and repair processes, recombination, kinetochore function, and telomere function. Posttranslational modifications of histone proteins and modifications of DNA bases underlie chromatin-based epigenetic regulation. Enzymes that catalyze histone modifications are considered writers. Conceptually, erasers remove these modifications, and readers are proteins binding these modifications and can target specific functions. On a larger scale, the 3-dimensional (3D) organization of chromatin in the nucleus also contributes to gene regulation. Whereas chromosomes are condensed during mitosis and segregated during cell division, they occupy discrete volumes called chromosome territories during interphase. Looping or folding of DNA can bring regulatory elements including enhancers close to gene promoters. Recent techniques facilitate understanding of 3D contacts at high resolution. Lastly, chromatin is dynamic and changes in histone occupancy, histone modifications, and accessibility of DNA contribute to epigenetic regulation.
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Ganai, Shabir Ahmad. "Modulating Epigenetic Modification Enzymes Through Relevant Epidrugs as a Timely Strategy in Anticancer Therapy". W Histone Deacetylase Inhibitors in Combinatorial Anticancer Therapy, 137–57. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-8179-3_7.

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Zeng, Hao, i Wei Xu. "Enzymatic Assays of Histone Methyltransferase Enzymes". W Epigenetic Technological Applications, 333–61. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-801080-8.00016-8.

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Streszczenia konferencji na temat "Epigenetic enzymes"

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Venkatesan, Thiagarajan, Umamaheswari Natarajan i Appu Rathinavelu. "Abstract 4681: Effect of SAHA on epigenetic chromatin modification enzymes in LNCaP and MCF-7 cells". W Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4681.

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Cabang, April B., Yuan Fang, Jay Morris i Michael J. Wargovich. "Abstract 410: Epigallocatechin gallate inhibits colon cancer cell proliferation by modulating epigenetic enzymes (DNMTs, HDACs, and HATs)". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-410.

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Mateen, Samiha, Komal Raina, Chapla Agarwal i Rajesh Agarwal. "Abstract 3796: Inhibition of epigenetic chromatin-modification enzymes: histone deacetylases and DNA methyltransferases by silibinin in human NSCLC H1299 cells". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3796.

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Pappa, Aglaia, Ioannis Anestopoulos, Alexandros Kontopoulos, Ariel Klavaris i Mihalis Panayiotidis. "The anticancer potential of silibinin is associated with alterations in gene expression levels of major epigenetic enzymes in prostate carcinoma". W The 1st International E-Conference on Antioxidants in Health and Disease. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cahd2020-08862.

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Sengupta, Surojeet, Shuait Nair, Lu Jin, Catherine M. Sevigny, Brandon Jones i Robert Clarke. "Abstract PS17-50: Nuclear expression of acetyl-CoA producing enzymes and their roles in epigenetic reprogramming in breast cancer cells". W Abstracts: 2020 San Antonio Breast Cancer Virtual Symposium; December 8-11, 2020; San Antonio, Texas. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.sabcs20-ps17-50.

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Dent, Sharon Y. R., Boyko Atanassov, Calley Hirsch, Evangelia Koutelou i John Latham. "Abstract IA07: New functions for histone modifying enzymes". W Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia07.

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Schreiber, Stuart L. "Abstract IA25: Linking genetic features of human cancers and histone-modifying enzymes for future cancer therapies". W Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia25.

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Keung, Emily Z., Kunal Rai, Kadir C. Akdemir, Liren Li, Sneha Sharma, Bryce Axelrad i Lynda Chin. "Abstract LB-134: The identification and characterization of MLL2, an epigenetic enzyme, as a novel tumor suppressor in melanoma". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-lb-134.

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Verrijzer, Peter. "Abstract IA09: Nucleotide biosynthetic enzyme GMP Synthase is a relay of p53 stabilization in response to genomic stress". W Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-ia09.

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Lee, Jin-Hee, Melissa Boersma, Bing Yang, Nathan Damaschke, Eva Corey, John Denu i David F. Jarrard. "Abstract 5389: A personalized medicine approach to identifying dysregulated epigenetic enzyme activity in the development of castrate-resistant prostate cancer". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5389.

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Raporty organizacyjne na temat "Epigenetic enzymes"

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Meiri, Noam, Michael D. Denbow i Cynthia J. Denbow. Epigenetic Adaptation: The Regulatory Mechanisms of Hypothalamic Plasticity that Determine Stress-Response Set Point. United States Department of Agriculture, listopad 2013. http://dx.doi.org/10.32747/2013.7593396.bard.

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Our hypothesis was that postnatal stress exposure or sensory input alters brain activity, which induces acetylation and/or methylation on lysine residues of histone 3 and alters methylation levels in the promoter regions of stress-related genes, ultimately resulting in long-lasting changes in the stress-response set point. Therefore, the objectives of the proposal were: 1. To identify the levels of total histone 3 acetylation and different levels of methylation on lysine 9 and/or 14 during both heat and feed stress and challenge. 2. To evaluate the methylation and acetylation levels of histone 3 lysine 9 and/or 14 at the Bdnfpromoter during both heat and feed stress and challenge. 3. To evaluate the levels of the relevant methyltransferases and transmethylases during infliction of stress. 4. To identify the specific localization of the cells which respond to both specific histone modification and the enzyme involved by applying each of the stressors in the hypothalamus. 5. To evaluate the physiological effects of antisense knockdown of Ezh2 on the stress responses. 6. To measure the level of CpG methylation in the promoter region of BDNF in thermal treatments and free-fed, 12-hour fasted, and re-fed chicks during post-natal day 3, which is the critical period for feed-control establishment, and 10 days later to evaluate longterm effects. 7. The phenotypic effect of antisense “knock down” of the transmethylaseDNMT 3a. Background: The growing demand for improvements in poultry production requires an understanding of the mechanisms governing stress responses. Two of the major stressors affecting animal welfare and hence, the poultry industry in both the U.S. and Israel, are feed intake and thermal responses. Recently, it has been shown that the regulation of energy intake and expenditure, including feed intake and thermal regulation, resides in the hypothalamus and develops during a critical post-hatch period. However, little is known about the regulatory steps involved. The hypothesis to be tested in this proposal is that epigenetic changes in the hypothalamus during post-hatch early development determine the stress-response set point for both feed and thermal stressors. The ambitious goals that were set for this proposal were met. It was established that both stressors i.e. feed and thermal stress, can be manipulated during the critical period of development at day 3 to induce resilience to stress later in life. Specifically it was established that unfavorable nutritional conditions during early developmental periods or heat exposure influences subsequent adaptability to those same stressful conditions. Furthermore it was demonstrated that epigenetic marks on the promoter of genes involved in stress memory are altered both during stress, and as a result, later in life. Specifically it was demonstrated that fasting and heat had an effect on methylation and acetylation of histone 3 at various lysine residues in the hypothalamus during exposure to stress on day 3 and during stress challenge on day 10. Furthermore, the enzymes that perform these modifications are altered both during stress conditioning and challenge. Finally, these modifications are both necessary and sufficient, since antisense "knockdown" of these enzymes affects histone modifications, and as a consequence stress resilience. DNA methylation was also demonstrated at the promoters of genes involved in heat stress regulation and long-term resilience. It should be noted that the only goal that we did not meet because of technical reasons was No. 7. In conclusion: The outcome of this research may provide information for the improvement of stress responses in high yield poultry breeds using epigenetic adaptation approaches during critical periods in the course of early development in order to improve animal welfare even under suboptimum environmental conditions.
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