Gotowe bibliografie tematyczne / Epigentics

Spis treści

  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Części książek
  4. Streszczenia konferencji
  5. Raporty organizacyjne

Gotowa bibliografia na temat „Epigentics”

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

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Artykuły w czasopismach na temat "Epigentics"

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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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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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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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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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Rozprawy doktorskie na temat "Epigentics"

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Yong, Qian Yu. "A screen for modifiers of epigenetic reprogramming." Thesis, Queensland University of Technology, 2011. https://eprints.qut.edu.au/50955/1/Qian_Yu_Yong_Thesis.pdf.

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Epigenetic modifiers are the proteins involved in establishing and maintaining the epigenome of an organism. They are particularly important for development. Changes in epigenetic modifiers have been shown be lethal, or cause diseases. Our laboratory has developed an ENU mutagenesis screen to produce mouse mutants displaying altered epigenetic gene silencing. The screen relies on a GFP transgene that is expressed in red blood cells in a variegated manner. In the orginal transgenic FVB mice expression occurs in approximately 55% of red blood cells. During the course of my Masters, I ch
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Hore, Timothy Alexander, and timothy hore@anu edu au. "THE EVOLUTION OF GENOMIC IMPRINTING AND X CHROMOSOME INACTIVATION IN MAMMALS." The Australian National University. Research School of Biological Sciences, 2008. http://thesis.anu.edu.au./public/adt-ANU20081216.152553.

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Genomic imprinting is responsible for monoallelic gene expression that depends on the sex of the parent from which the alleles (one active, one silent) were inherited. X-chromosome inactivation is also a form of monoallelic gene expression. One of the two X chromosomes is transcriptionally silenced in the somatic cells of females, effectively equalising gene dosage with males who have only one X chromosome that is not complemented by a gene poor Y chromosome. X chromosome inactivation is random in eutherian mammals, but imprinted in marsupials, and in the extraembryonic membranes of some place
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Schön, Alexander [Verfasser], and Thomas [Akademischer Betreuer] Carell. "Synthese chemisch modifizierter, epigentisch relevanter Nukleoside und Oligonukleotide / Alexander Schön ; Betreuer: Thomas Carell." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2020. http://d-nb.info/1225682835/34.

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Cai, Yu. "Molecular Characterization of the mop2, a Gene Required for Epigenetic Silencing." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/195361.

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The mop2 gene is required for epigenetic silencing; it was originally defined as a mutation, Mop2-1, which when dominant prevented paramutation at b1. Paramutation is an allele communication that causes a mitotically and meiotically heritable change in gene expression. Mop2-1 was subsequently shown to be involved in maintaining the silenced paramutant state and to prevent dsRNA-mediated transcriptional gene silencing (activities revealed only when the mutation is homozygous). Understanding the product encoded by mop2 will help dissect the underlying mechanisms involved in paramutation and
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Belzeaux, Raoul. "Etudes de l'expression des ARN périphériques dans la dépression. : La régulation de l'expression génétique en question." Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX20727.

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La dépression est fréquente, sa prise en charge difficile et les connaissances de sa physiopathologie très incomplètes. Il est établi qu’il existe une composante familiale et héréditaire au trouble dépressif mais le substrat biologique de cette vulnérabilité est inconnu et souvent les études souffrent d’un manque de reproductibilité. Par ailleurs, il n’existe pas de bio-marqueur validé utilisable en pratique courante.Nous proposons dans ce travail de thèse d’explorer les ARN périphériques chez les patients souffrant de dépression de façon à explorer s’ils peuvent définir des bio-marqueurs et s
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Freyer, Jennifer Sandra Silvia. "Regulation und funktionelle Rolle des murinen Transkriptionsfaktors Foxp3 in T-Zellen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2008. http://dx.doi.org/10.18452/15841.

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In dieser Arbeit wurde die funktionelle Rolle und Regulation des murinen Transkriptionsfaktor Foxp3 untersucht. Der erste wesentliche Teil zur Analyse der funktionellen Rolle war dabei die Erzeugung einer BAC- transgenen Maus. Hierfür wurde ein Zielgenvektor mit der kodierenden Region des eYFPs und einer dualen Selektionskassette sowie die Methode des ET- Klonierens verwendet. Leider war die homologe Rekombination des Zielgenvektors in den BAC nicht erfolgreich. Es kam zu einer ungeklärten Rekombination mit Fremd- DNS. Die Erzeugung der transgenen Maus wurde nach diesem Ergebnis eingestellt, u
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Dyer, Ethan. "The Effects of Topical Dose Delivery of Corticosterone on the Development and Hatching Success of the Zebra Finch." 2013. http://scholarworks.gsu.edu/biology_hontheses/5.

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The Australian Zebra Finch (Taeniopygia guttata) is an important animal model for vertebrate development and behavior. New research initiatives in the fields of epigenetics rely heavily on injecting hormones and environmental toxins directly into the eggs of different bird species such as zebra finches and other passerine songbirds to replicate the effects maternal condition on offspring. However, the widely used method of egg-injections does not accurately replicate physiological conditions, as the injected substances remain concentrated at the injection site for extended periods and do not d
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Hore, Tim. "The Evolution of Genomic Imprinting and X Chromosome Inactivation in Mammals." Phd thesis, 2008. http://hdl.handle.net/1885/49309.

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Genomic imprinting is responsible for monoallelic gene expression that depends on the sex of the parent from which the alleles (one active, one silent) were inherited. X-chromosome inactivation is also a form of monoallelic gene expression. One of the two X chromosomes is transcriptionally silenced in the somatic cells of females, effectively equalising gene dosage with males who have only one X chromosome that is not complemented by a gene poor Y chromosome. X chromosome inactivation is random in eutherian mammals, but imprinted in marsupials, and in the extraembryonic membranes of some place
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Khromov, Tatjana. "Pluripotency of multipotent adult germ-line stem cells: analysis of apoptotic and epigenetic features." Doctoral thesis, 2011. http://hdl.handle.net/11858/00-1735-0000-000D-EF56-E.

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Houston, Kerryn. "Epigentic silencing of the glucocorticoid receptor in small cell lung cancer cells." Thesis, 2013. http://hdl.handle.net/10413/9855.

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Small cell lung cancer (SCLC) is an aggressive neuroendocrine tumour which secretes ACTH and other related peptides. Contrary to normal production by the pituitary, ACTH production is not inhibited by glucocorticoids (Gcs) in SCLC. This insensitivity to Gc action can be attributed to impaired Gc receptor (GR) expression in these cells. Over-expression of the GR induces apoptosis both in vitro and in vivo. Evasion of GR signalling thus confers a significant survival advantage to SCLC cells. Re-expression of endogenous GR in SCLC cells may provoke the same effect. Many tumours silence the expres
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Części książek na temat "Epigentics"

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Zawia, Nasser H., and Riyaz Basha. "Developmental Lead Exposure, Epigentics and Late Onset Alzheimer's Disease." In Developmental Neurotoxicology Research, 143–62. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470917060.ch9.

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Streszczenia konferencji na temat "Epigentics"

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Li, Yingqin, Na Liu, and Jun Ma. "Abstract 485: Epigentic silencing of miR-142-3p promotes metastasis by targeting ZEB2 in NPC." In 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.am2017-485.

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Raporty organizacyjne na temat "Epigentics"

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Gur, Amit, Edward Buckler, Joseph Burger, Yaakov Tadmor, and Iftach Klapp. Characterization of genetic variation and yield heterosis in Cucumis melo. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7600047.bard.

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Project objectives: 1) Characterization of variation for yield heterosis in melon using Half-Diallele (HDA) design. 2) Development and implementation of image-based yield phenotyping in melon. 3) Characterization of genetic, epigenetic and transcriptional variation across 25 founder lines and selected hybrids. The epigentic part of this objective was modified during the course of the project: instead of characterization of chromatin structure in a single melon line through genome-wide mapping of nucleosomes using MNase-seq approach, we took advantage of rapid advancements in single-molecule se
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