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Relevant bibliographies by topics / MEL cells; Epigenetic marks

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Journal articles
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Academic literature on the topic 'MEL cells; Epigenetic marks'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "MEL cells; Epigenetic marks"

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Black, Kathryn, Elena Sotillo, Nicole Martinez, et al. "Regulation of CD19 Exon 2 Inclusion in B-Lymphoid Cells By Splicing Factors and Epigenetic Marks." Blood 126, no. 23 (2015): 2425. http://dx.doi.org/10.1182/blood.v126.23.2425.2425.

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Abstract CD19 is expressed broadly on the surface of B-cells during normal development and malignant growth, making it a good target for immunotherapy. While immunotherapies targeting CD19 have had great success against pediatric B-cell acute lymphoblastic leukemia (B-ALL), relapses lacking the CD19 epitope still occur (Maude et al., 2014). We have discovered that alternative splicing of CD19, in particular the skipping of exon 2, is responsible for the loss of CD19 extracellular domains, causing resistance to therapy (Sotillo et al., 2015). Here we investigate the molecular mechanism of CD19

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Karkhanis, Vrajesh, Lapo Alinari, Bethany Mundy, et al. "PRMT5 Targets Tumor Suppressor Micro RNAs to Regulate Cyclin D1 and c-MYC in Mantle Cell Lymphoma." Blood 128, no. 22 (2016): 2937. http://dx.doi.org/10.1182/blood.v128.22.2937.2937.

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Abstract Protein arginine methyltransferase-5 (PRMT5), a major type II arginine methyltransferase, is an important epigenetic modifier with oncogene-like properties due to its transcriptional repressive activity. When over-expressed, PRMT5 has been shown to target and silence the expression of multiple regulatory and tumor suppressor genes. Global symmetric dimethylation of arginine residues within the N-terminal of histones (H2A(Me2)R3, H3(Me2)R8, H4(Me2)R3) plays a critical role in B cell transformation, correlates with increased tumor cell proliferation and survival. PRMT5 expression is enh

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Arumugam, Paritha, Fabrizia Urbinati, Chinavenmeni S. Velu, H. Leighton Grimes, and Punam Malik. "The 3′ End of the Chicken Hypersensitive Site-4 Insulator Has Properties Similar to the 5′ Insulator Core and Is Necessary in Conjunction with the Core for Full Insulator Activity." Blood 112, no. 11 (2008): 817. http://dx.doi.org/10.1182/blood.v112.11.817.817.

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Abstract Genetic correction of hematologic defects is currently impeded by inefficient vector technology. We find that vectors that insulate the correcting transgene from position effects and genotoxicity compromise viral titers. Here we present an improved vector system which utilizes a modified insulator element, without sacrificing viral titers. Specifically, our genetic and epigenetic analysis of the 1.2kb chicken β-globin hypersensitive site-4 (cHS4) insulator reveal heretofore unknown activities in regions of the chicken β-globin insulator element outside the canonical and well studied 2

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Watanabe, Toshiki. "Adult T-cell leukemia: molecular basis for clonal expansion and transformation of HTLV-1–infected T cells." Blood 129, no. 9 (2017): 1071–81. http://dx.doi.org/10.1182/blood-2016-09-692574.

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Abstract Adult T-cell leukemia (ATL) is an aggressive T-cell malignancy caused by human T-cell leukemia virus type 1 (HTLV-1) that develops through a multistep carcinogenesis process involving 5 or more genetic events. We provide a comprehensive overview of recently uncovered information on the molecular basis of leukemogenesis in ATL. Broadly, the landscape of genetic abnormalities in ATL that include alterations highly enriched in genes for T-cell receptor–NF-κB signaling such as PLCG1, PRKCB, and CARD11 and gain-of function mutations in CCR4 and CCR7. Conversely, the epigenetic landscape of

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Chung, Jihyun, Vrajesh Karkhanis, Said Sif та Robert A. Baiocchi. "Protein Arginine Methyltransferase 5 Supports MYC, Survivin and Cyclin D1 Activity in Aggressive Lymphomas By Regulating the WNT/β-Catenin Pathway". Blood 124, № 21 (2014): 58. http://dx.doi.org/10.1182/blood.v124.21.58.58.

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Abstract Introduction: Aggressive histologic subtypes of lymphoma such as mantle cell (MCL) and activated B cell (ABC) are considered incurable and affected patients often have a short median survival despite multimodal therapy. It is well established that altered expression of oncogenes and epigenetic dysregulation of tumor suppressor and regulatory genes promote cellular transformation of normal B cells into malignant lymphoma. Hypermethylation of histone proteins (H3R8 and H4R3) by the protein arginine methyltransferase 5 (PRMT5) enzyme has been documented in multiple cancer types and has b

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Meng, Fanli, Kathrin Stamms, Romina Bennewitz, et al. "Targeted histone demethylation improves somatic cell reprogramming into cloned blastocysts but not postimplantation bovine concepti†." Biology of Reproduction 103, no. 1 (2020): 114–25. http://dx.doi.org/10.1093/biolre/ioaa053.

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Abstract Correct reprogramming of epigenetic marks in the donor nucleus is a prerequisite for successful cloning by somatic cell transfer (SCT). In several mammalian species, repressive histone (H) lysine (K) trimethylation (me3) marks, in particular H3K9me3, form a major barrier to somatic cell reprogramming into pluripotency and totipotency. We engineered bovine embryonic fibroblasts (BEFs) for the doxycycline-inducible expression of a biologically active, truncated form of murine Kdm4b, a demethylase that removes H3K9me3 and H3K36me3 marks. Upon inducing Kdm4b, H3K9me3 and H3K36me3 levels w

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Chung, JI Hyun, Shelby Sloan, Peggy Scherle, et al. "PRMT5 Is a Key Epigenetic Regulator That Promotes Transcriptional Activation in Mantle Cell Lymphoma By Regulating the Lysine Methyltransferase SETD7 and MLL1 Activity." Blood 134, Supplement_1 (2019): 2777. http://dx.doi.org/10.1182/blood-2019-131020.

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Introduction: Post-translational histone modifications directly modify chromatin structure to influence a wide variety of cellular events including gene expression, DNA replication and repair, and cell cycle control. While histone lysine methylation can confer either transcriptionally active or repressive states, the symmetric dimethylation of arginine residues on histone tails is generally associated with transcriptional repression. Overexpression and dysregulation of PRMT5, the major type II protein arginine methyltransferase, has been shown to drive cellular proliferation and survival of mu

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Lichtenberg, Jens, Elisabeth F. Heuston, Cheryl A. Keller, Ross C. Hardison, and David M. Bodine. "Comparison of Expression and Epigenetic Profiles in Human and Mouse Erythropoiesis and Megakaryopoiesis Using a Systems Biology Model." Blood 126, no. 23 (2015): 2383. http://dx.doi.org/10.1182/blood.v126.23.2383.2383.

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Abstract To date numerous datasets of gene expression and epigenetic profiles for mouse and human hematopoietic cells have been generated. While individual data sets for a particular cell type have been correlated, no approach exists to harness all expression and epigenetic profiles for the different types of hematopoietic cells. Our goal is to develop a systems biology platform to compare epigenetic profiles of hematopoietic cells towards a better understanding of epigenetic mechanisms governing hematopoiesis. To provide the necessary foundation to support systematic studies of hematopoiesis,

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Fiskus, Warren, Rekha Rao, Ramesh Balusu, et al. "Efficacy of Combined Epigenetic Targeting of Histone Methyltransferase EZH2 and Histone deacetylases Against Human Mantle Cell Lymphoma Cells." Blood 116, no. 21 (2010): 2488. http://dx.doi.org/10.1182/blood.v116.21.2488.2488.

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Abstract Abstract 2488 Lysine specific histone methylation and deacetylation are chromatin modifications that, along with DNA methylation, are involved in the epigenetic silencing of tumor suppressor genes (TSGs). This silencing is mediated by multi-protein complexes PRC (polycomb repressive complexes) 1 and 2. Of the three core protein components of PRC2, i.e., EZH2, SUZ12 and EED, EZH2 has the SET domain with its intrinsic histone methyltransferase activity, which induces the trimethylation (Me3) of lysine (K) 27 on histone (H) 3-a repressive histone modification mediating gene repression. T

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Gambacorta, Valentina, Daniela Gnani, Laura Zito, et al. "Integrated Epigenetic Profiling Identifies EZH2 As a Therapeutic Target to Re-Establish Immune Recognition of Leukemia Relapses with Loss of HLA Class II Expression." Blood 134, Supplement_1 (2019): 514. http://dx.doi.org/10.1182/blood-2019-127395.

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Background It is becoming increasingly recognized that evasion from immune control represents one of the main drivers of acute myeloid leukemia (AML) relapse after allogeneic hematopoietic cell transplantation (allo-HCT). In particular, alterations in the antigen processing and presentation machinery represent one of the most effective strategies enacted by tumor cells to avoid recognition from T cells. Whereas it is now well recognized that genomic loss of HLA is frequently at the basis of post-transplantation relapse, it was only recently reported that up to 40% of AML relapses display trans

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Dissertations / Theses on the topic "MEL cells; Epigenetic marks"

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Clements, Andrew R. N. "The regulation of globin gene expression." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365687.

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Cao, Kaixiang. "Genome-wide profiling of H1 linker histone variants in mouse embryonic stem cells." Diss., Georgia Institute of Technology, 2014. http://hdl.handle.net/1853/51777.

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H1 linker histone facilitates the formation of higher order chromatin structure and is essential for mammalian development. Mice have 11 H1 variants which are differentially regulated and conserved in human. Previous research indicates that H1 regulates the expression of specific genes in mouse embryonic stem cells (ESCs). However, whether individual variants have distinct functions and how H1 participates in gene regulation remain elusive. An investigation of the precise localization of individual H1 variants in vivo would facilitate the elucidation of mechanisms underlying chromatin compacti

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Miranda, Juliana Xavier de. "Efeitos do tratamento com selênio no crescimento e marcas epigenéticas de células de adenocarcinoma mamário humano MCF-7." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9132/tde-11032013-090654/.

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O câncer de mama representa problema mundial de saúde pública e a causa mais frequente de morte por câncer entre as mulheres. A identificação de agentes moduladores de marcas epigenéticas, tais como metilação global do DNA e modificações pós-tradução em histonas, compreende alternativa promissora para estabelecimento de estratégias de controle da carcinogênese mamária. Dentre os nutrientes, o elemento traço essencial selênio (Se) pode ser destacado como agente dietético com potencial anti-câncer de mama e que poderia atuar modulando processos epigenéticos. Entretanto seus mecanismos de ação sã

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Komashko, Vitalina M. "Global analysis of repressive epigenetic marks on promoter regions in mammalian cells using chromatin immunoprecipitation coupled with DNA microarrays." Diss., 2009. http://proquest.umi.com/pqdweb?did=1987390581&sid=1&Fmt=2&clientId=48051&RQT=309&VName=PQD.

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Conference papers on the topic "MEL cells; Epigenetic marks"

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Simpson, Natalie E., Igor P. Pogribny, and Frederick A. Beland. "Abstract 4096: Correction of metabolically sensitive histone epigenetic marks mediates the drug sensitivity of MDA-MB-231 human breast cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4096.

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