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Artykuły w czasopismach na temat „Epigentics”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 29 stycznia 2023

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Sprawdź 22 najlepszych artykułów w czasopismach naukowych na temat „Epigentics”.

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1

Ren, Jun, and Yingmei Zhang. "Emerging Therapeutic Potential Targeting Genetics and Epigentics in Heart Failure." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1863, no. 8 (August 2017): 1867–69. http://dx.doi.org/10.1016/j.bbadis.2017.05.023.

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Pisarska, M. D., G. M. Barlow, N. Xu, M. O. Goodarzi, V. Funari, and J. Williams. "Special research presentation: epigentic profiles in ART pregnancies." Fertility and Sterility 102, no. 3 (September 2014): e105-e106. http://dx.doi.org/10.1016/j.fertnstert.2014.07.362.

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Khan, Muhammad Babar, Julia R. Schneider, Kevin Kwan, and John A. Boockvar. "Epigentic Regulators of Glioma Stem Cells are Potential Therapeutic Targets." Neurosurgery 82, no. 5 (April 16, 2018): E104—E105. http://dx.doi.org/10.1093/neuros/nyy039.

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Mehboob, Riffat. "Role of Epigenetic alterations in the development of cancers." Pakistan BioMedical Journal 5, no. 2 (February 28, 2022): 01. http://dx.doi.org/10.54393/pbmj.v5i2.346.

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Many different factors are involved in the progression of cancers. Genes mutations and chromosomal abnormalities are normally considered main cause of cancers but there are some other reason for the development of cancers. Other cancer causing factors are known as epigenetic alterations [1,2]. Epigentic modification of genome is known as epigenetic alterations, lead toward cancer cells production. Epigentic modification does not cause change in sequences of nucleotide. Similar to genetic alteration epigenetic alteration can’t be ignored [3]. Basically mechanisms behind epigenetic modifications
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5

Mu, Shengyu, Tatsuo Shimosawa, Sayoko Ogura, Hong Wang, Yuzaburo Uetake, Fumiko Mori, and Toshiro Fujita. "36 SALT-SENSITIVE HYPERTENSION AND RENAL-SYMPATHETIC TONE, EPIGENTIC MODULATION OF WNK4." Journal of Hypertension 30 (September 2012): e11. http://dx.doi.org/10.1097/01.hjh.0000419862.52153.c4.

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Medley, T., R. Idrizi, J. Jowett, H. Sumer, P. Verma, and D. Kaye. "Cell of Origin Influence Transcriptional Epigentic and Functional Profiles of iPS Cell Derived Cardiomyocytes." Heart, Lung and Circulation 21 (January 2012): S75. http://dx.doi.org/10.1016/j.hlc.2012.05.189.

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Kim, K. J., Y. D. Min, T. B. Lee, and C. H. Choi. "Epigentic mechanisms involved in the differential expression of MDR1 between gastric and colon cancer cells." Journal of Clinical Oncology 23, no. 16_suppl (June 2005): 9708. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.9708.

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Takaro, Tim K., Meaghan Jones, Michael Kobor, Jeffrey Brook, Kathleen Mclean, Yayuk Joffres, Ryan Allen, Michael Brauer, and Malcolm Sears. "Epigentic Markers Of Early Life Exposures In The Canadian Healthy Infant Longitudinal Development (Child) Birth Cohort." ISEE Conference Abstracts 2015, no. 1 (August 20, 2015): 2608. http://dx.doi.org/10.1289/isee.2015.2015-2608.

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9

Lecamwasam, A., B. Novakovic, B. Meyer, E. Ekinci, K. Dwyer, and R. Saffery. "SAT-183 DNA METHYLATION PROFILING IDENTIFIES EPIGENTIC DIFFERENCES BETWEEN EARLY VERSUS LATE STAGES OF DIABETIC CHRONIC KIDNEY DISEASE." Kidney International Reports 5, no. 3 (March 2020): S78. http://dx.doi.org/10.1016/j.ekir.2020.02.195.

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10

Thakur, Vikram, Brian R. Davis, Irene Sarosiek, Richard W. McCallum, and Munmun Chattopadhyay. "Tu1310 ALTERATIONS IN EPIGENTIC MODIFIERS IN GASTRIC ANTRAL SMOOTH MUSCLE OF PATIENTS WITH DIABETIC GASTROPARESIS COMPARED TO IDIOPATHIC ETIOLOGY." Gastroenterology 158, no. 6 (May 2020): S—1052. http://dx.doi.org/10.1016/s0016-5085(20)33317-5.

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11

Mullur, Rashmi, Yan-Yun Liu, and Gregory A. Brent. "Thyroid Hormone Regulation of Metabolism." Physiological Reviews 94, no. 2 (April 2014): 355–82. http://dx.doi.org/10.1152/physrev.00030.2013.

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Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5′-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone
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12

Levine, Arnold J. "The p53 protein plays a central role in the mechanism of action of epigentic drugs that alter the methylation of cytosine residues in DNA." Oncotarget 8, no. 5 (January 24, 2017): 7228–30. http://dx.doi.org/10.18632/oncotarget.14805.

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13

Bellmunt, Joaquim, Guangwu Guo, Stephanie A. Mullane, Anna Orsola, Lillian Werner, Paul Van Hummelen, Aaron Thorner, et al. "Genomic landscape of high-grade T1 micropapillary bladder tumors." Journal of Clinical Oncology 33, no. 7_suppl (March 1, 2015): 299. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.299.

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299 Background: The genomic landscape of high-grade T1 micropapillary bladder tumors (HGT1micropap) is unknown. Clinically, micropapillary bladder cancer is an aggressive and possibly lethal disease. Our main objective was to assess the genomic landscape of HGT1micropap through identifying mutations, insertions/deletions (indels), translocations, and copy number variations (CNVs). Methods: We prospectively identified nine HGT1micropap with 45.4 months of median follow up. Patients were treated in a uniform manner using TUR, BCG, and appropriate follow up. We performed whole exome sequencing us
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14

Orlacchio, Arturo, Daniel Weissinger, Catherine Do, Benjamin Tycko, Diane M. Simeone, and Tamas Gonda. "Abstract C041: Hypomethylating therapy induces a potential immuno-suppressive myeloid phenotype by altering cancer cell cytokine secretion in PDAC." Cancer Research 82, no. 22_Supplement (November 15, 2022): C041. http://dx.doi.org/10.1158/1538-7445.panca22-c041.

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Abstract Introduction: We have previously shown using the KPC (KrasLSL G12D/+; p53 r172H/+; Pdx1-Cre) mouse model of PDAC that sequential treatment with the DNA hypomethylating agents (HMA) followed by anti-PD-1 led to increased tumor necrosis, slowed tumor growth, increased tumor-infiltrating CD8+ cells, and significantly increased mean survival. However, acquired treatment resistance occurred, with emergence of a specific subtype of M2-polarized putatively immunosuppressive Chi3l3+ macrophages. In this study, we characterize the mechanism of polarization of these cells, define their function
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15

Daw, Jennifer, Devin Saunders, Adria Vasquez, and Celina Valencia. "Abstract B013: Epigenetic clocks and breast cancer outcomes: A scoping review. [R]." Cancer Research 83, no. 2_Supplement_1 (January 15, 2023): B013. http://dx.doi.org/10.1158/1538-7445.agca22-b013.

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Abstract Introduction: Age is a strong predictor for breast cancer (BCa) risk. The median age at diagnosis varies by race/ethnicity. In the United States (U.S.), non-White women are more likely to be diagnosed at a younger age than non-Hispanic White (NHW) women. Epigenetic age, measured as changes to DNA via methylation (DNAm) using epigentic clocks, is highly accurate at estimating cellular age using several tissues and cell types may differ from chronological age. Epigenetic age is more robust than other molecular markers of aging, such as telomere length. Differences between epigenetic age
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16

Hemmerich, Peter, Stefanie Weidtkamp-Peters, Christian Hoischen, Lars Schmiedeberg, Indri Erliandri, and Stephan Diekmann. "CENP-I as a new epigentic mark at centromere chromatin." GBM Annual Spring meeting Mosbach 2008 2008, Spring (March 2008). http://dx.doi.org/10.1240/sav_gbm_2008_m_002212.

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17

Lemche, Erwin, Oleg S. Chaban, and Alexandra V. Lemche. "Neuroendorine and Epigentic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome." Frontiers in Neuroscience 10 (April 14, 2016). http://dx.doi.org/10.3389/fnins.2016.00142.

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18

Knestrick, M., D. Demers, R. Fleeman, B. Vesely, A. Azhari, DE Kyle, LN Shaw, and BJ Baker. "An epigentic-based fungal metabolite screening protocol for discovery of potential lead compounds for drug treatments." Planta Medica 80, no. 10 (July 14, 2014). http://dx.doi.org/10.1055/s-0034-1382618.

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Beaver, Mariah, Akanksha Bhatnagar, Priyalakshmi Panikker, Haolin Zhang, Renee Snook, Visha Parmar, Gayathri Vijayakumar, Niteesha Betini, Sunya Akhter, and Felice Elefant. "Disruption of Tip60 HAT mediated neural histone acetylation homeostasis is an early common event in neurodegenerative diseases." Scientific Reports 10, no. 1 (October 26, 2020). http://dx.doi.org/10.1038/s41598-020-75035-3.

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AbstractEpigenetic dysregulation is a common mechanism shared by molecularly and clinically heterogenous neurodegenerative diseases (NDs). Histone acetylation homeostasis, maintained by the antagonistic activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs), is necessary for appropriate gene expression and neuronal function. Disruption of neural acetylation homeostasis has been implicated in multiple types of NDs including Alzheimer’s disease (AD), yet mechanisms underlying alterations remain unclear. We show that like AD, disruption of Tip60 HAT/HDAC2 balance with conc
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20

Pangeni, Rajendra P., Ivonne Olivaries, David Huen, Vannessa C. Buzatto, Timothy P. Dawson, Katherine M. Ashton, Charles Davis, et al. "Genome-wide methylation analyses identifies Non-coding RNA genes dysregulated in breast tumours that metastasise to the brain." Scientific Reports 12, no. 1 (January 20, 2022). http://dx.doi.org/10.1038/s41598-022-05050-z.

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AbstractBrain metastases comprise 40% of all metastatic tumours and breast tumours are among the tumours that most commonly metastasise to the brain, the role that epigenetic gene dysregulation plays in this process is not well understood. We carried out 450 K methylation array analysis to investigate epigenetically dysregulated genes in breast to brain metastases (BBM) compared to normal breast tissues (BN) and primary breast tumours (BP). For this, we referenced 450 K methylation data for BBM tumours prepared in our laboratory with BN and BP from The Cancer Genome Atlas. Experimental validat
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21

Liu, Zhi-ping, and Qing-Jun Zhang. "Abstract 118: Role Of Histone Trimethyl Demethylase Jmjd2A In Cardiac Hypertrophy And Heart Development." Circulation Research 113, suppl_1 (August 2013). http://dx.doi.org/10.1161/res.113.suppl_1.a118.

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Epigentic regulation via histone memethylation has been shown to play important role in embryonic development and pathogenesis of adult diseases. Methylation of histone H3 lysine 9 (H3K9) mediates heterochromatin formation and also participates in inhibition of gene transcription at euchromatic sites. Methylation of H3K9 is required for proper embryonic development as shown by various genetic studies of H3K9 methyltransferases in mice. Histone demethylases for methylated H3K9 have been shown to play important role in tumorigenesis. However, their roles in development and in adult cardiovascula
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22

Malherbe, Delphine C., and Ilhem Messaoudi. "Transcriptional and Epigenetic Regulation of Monocyte and Macrophage Dysfunction by Chronic Alcohol Consumption." Frontiers in Immunology 13 (June 29, 2022). http://dx.doi.org/10.3389/fimmu.2022.911951.

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Drinking alcohol, even in moderation, can affect the immune system. Studies have shown disproportionate effects of alcohol on circulating and tissue-resident myeloid cells (granulocytes, monocytes, macrophages, dendritic cells). These cells orchestrate the body’s first line of defense against microbial challenges as well as maintain tissue homeostasis and repair. Alcohol’s effects on these cells are dependent on exposure pattern, with acute drinking dampening but chronic drinking enhancing production of inflammatory mediators. Although chronic drinking is associated with heightened systemic in
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