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Journal articles on the topic 'TET1 chromatin binding'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Li, Wenjing, Violetta Karwacki-Neisius, Chun Ma, et al. "Nono deficiency compromises TET1 chromatin association and impedes neuronal differentiation of mouse embryonic stem cells." Nucleic Acids Research 48, no. 9 (2020): 4827–38. http://dx.doi.org/10.1093/nar/gkaa213.

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Abstract NONO is a DNA/RNA-binding protein, which plays a critical regulatory role during cell stage transitions of mouse embryonic stem cells (mESCs). However, its function in neuronal lineage commitment and the molecular mechanisms of its action in such processes are largely unknown. Here we report that NONO plays a key role during neuronal differentiation of mESCs. Nono deletion impedes neuronal lineage commitment largely due to a failure of up-regulation of specific genes critical for neuronal differentiation. Many of the NONO regulated genes are also DNA demethylase TET1 targeted genes. I

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2

Weng, Hengyou, Huilin Huang, He Huang, et al. "TET1 Modulates DNA Replication in Leukemia Cells Via a Catalytic-Independent Mechanism through Cooperating with KAT8." Blood 134, Supplement_1 (2019): 1249. http://dx.doi.org/10.1182/blood-2019-127321.

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TET1 was first identified as a fusion partner of the histone H3 Lys4 (H3K4) methyltransferase MLL (mixed-lineage leukemia) in acute myeloid leukemia (AML), and then was discovered as the founding member of the Ten-Eleven-Translocation (TET) family of DNA hydroxylases which are capable of converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). Our group has previously demonstrated that TET1 plays an oncogenic role in MLL-rearranged AML (Huang H, et al. PNAS 2013; 110(29):11994-9) and also other TET1-overexpressing AMLs (e.g., t(8;21) AML and AMLs carrying FLT3-ITD and/or NPM1 mutat

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Zhu, Xingguo, Caixia Xi, Alexander Ward та ін. "NRF2 mediates γ-globin gene regulation through epigenetic modifications in a β-YAC transgenic mouse model". Experimental Biology and Medicine 245, № 15 (2020): 1308–18. http://dx.doi.org/10.1177/1535370220945305.

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NRF2 is the master regulator for the cellular oxidative stress response and regulates γ-globin gene expression in human erythroid progenitors and sickle cell disease mice. To explore NRF2 function, we established a human β-globin locus yeast artificial chromosome transgenic/NRF2 knockout (β-YAC/NRF2−/−) mouse model. NRF2 loss reduced γ-globin gene expression during erythropoiesis and abolished the ability of dimethyl fumarate, an NRF2 activator, to enhance γ-globin transcription. We observed decreased H3K4Me1 and H3K4Me3 chromatin marks and association of TATA-binding protein and RNA polymeras

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Weng, Hengyou, Huilin Huang, Xi Qin, et al. "TET1 Regulates DNA Replication through Targeting of Minichromosome Maintenance Genes." Blood 128, no. 22 (2016): 2687. http://dx.doi.org/10.1182/blood.v128.22.2687.2687.

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Abstract DNA cytosine methylation is one of the best-characterized epigenetic modifications that play important roles in diverse cellular and pathological processes. The mechanism underlying the dynamic regulation of the level and distribution of 5-methylcytosine (5mC) as well as the biological consequence of DNA methylation deregulation have been interesting research topics in recent years. TET1, first identified as a fusion partner of the histone H3 Lys4 (H3K4) methyltransferase MLL (mixed-lineage leukemia) in acute myeloid leukemia (AML), is the founding member of the Ten-Eleven-Translocati

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5

Jiang, Xi, Chao Hu, Kyle Ferchen, et al. "Targeted Inhibition of STAT/TET1 Axis As a Potent Therapeutic Strategy for Acute Myeloid Leukemia." Blood 130, Suppl_1 (2017): 857. http://dx.doi.org/10.1182/blood.v130.suppl_1.857.857.

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Abstract Acute myeloid leukemia (AML) is one of the most common and fatal forms of hematopoietic malignancies. Over 70% of patients with AML cannot survive over 5 years. Many AML subtypes, such as the MLL -rearranged AMLs, are often associated with unfavorable outcome. Current treatment frequently involves intensive chemotherapy, which impairs the quality of life of the patients. While the incidence of AML is continually rising due to aging, most elder patients cannot bear intensive chemotherapy and are associated with very poor survival. Thus, improved therapeutic strategies with less intensi

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6

Masala, L., D. Bebbere, G. P. Burrai, et al. "210 DNA METHYLATION AND HYDROXYMETHYLATION ANALYSIS IN A MODEL OF OOCYTE DIFFERENTIAL DEVELOPMENTAL COMPETENCE IN SHEEP." Reproduction, Fertility and Development 27, no. 1 (2015): 195. http://dx.doi.org/10.1071/rdv27n1ab210.

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DNA methylation is an important epigenetic mark that plays a role in gene regulation by the addition of a methyl group to CpG islands in the DNA. Despite being relatively stable in somatic cells, DNA methylation is subject to reprogramming during embryo development and gametogenesis. The aim of this work was to evaluate different aspects of DNA methylation in relation to oocyte quality in the ovine species. A model of differential developmental competence consisting in ovine oocytes and in vitro produced (IVP) blastocysts derived from adult (AD) and prepubertal (PR) donors, was used. The methy

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7

Zhu, Xingguo, Alexander H. Ward, Caixia Xi та Betty S. Pace. "NRF2 Mediates Epigenetic Changes in DNA and Chromatin Structure to Regulate γ-Globin Gene Expression in a Human βYAC Transgenic Mouse Model". Blood 132, Supplement 1 (2018): 1053. http://dx.doi.org/10.1182/blood-2018-99-116438.

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Abstract NRF2 is the master regulator for the cellular anti-oxidative stress response and previously shown to activate γ-globin gene expression in human erythroid progenitor cells. The goal of this study was to expand on these findings by exploring the in vivo function of NRF2 using the human β-globin locus YAC transgenic (βYAC) mouse carrying the entire 248kb human β-globin locus (HBB). We observed that NRF2 activation by chronic dimethyl fumarate treatment of βYAC mice, induced human γ-globin gene expression, but had no effect on the adult β-globin gene. Subsequently in a novel βYAC/NRF2 kno

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8

Dolnik, Anna, Julia C. Engelmann, Maren Scharfenberger-Schmeer, et al. "Integrative Genomics Approaches Identify Novel Disease-Related Genetic Aberrations in Acute Myeloid Leukemia." Blood 118, no. 21 (2011): 402. http://dx.doi.org/10.1182/blood.v118.21.402.402.

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Abstract Abstract 402 Acute myeloid leukemia (AML) is a clonal disorder characterized by the accumulation of acquired somatic genetic alterations in hematopoietic progenitor cells that alter mechanisms of self-renewal, proliferation and differentiation. While recently numerous aberrations have been identified, many more mutations involved in the multistep pathogenesis of AML still remain to be discovered. Based on critical regions and differentially expressed genes identified by our SNP/aCGH and microarray-based gene expression profiling analysis of 320 AML cases, we designed a custom capture

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9

Lio, Chan-Wang J., Vipul Shukla, Daniela Samaniego-Castruita, et al. "TET enzymes augment activation-induced deaminase (AID) expression via 5-hydroxymethylcytosine modifications at the Aicda superenhancer." Science Immunology 4, no. 34 (2019): eaau7523. http://dx.doi.org/10.1126/sciimmunol.aau7523.

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TET enzymes are dioxygenases that promote DNA demethylation by oxidizing the methyl group of 5-methylcytosine to 5-hydroxymethylcytosine (5hmC). Here, we report a close correspondence between 5hmC-marked regions, chromatin accessibility and enhancer activity in B cells, and a strong enrichment for consensus binding motifs for basic region-leucine zipper (bZIP) transcription factors at TET-responsive genomic regions. Functionally, Tet2 and Tet3 regulate class switch recombination (CSR) in murine B cells by enhancing expression of Aicda, which encodes the activation-induced cytidine deaminase (A

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10

Cao, John Z., Hui Liu, Amittha Wickrema, and Lucy A. Godley. "HIF-1 directly induces TET3 expression to enhance 5-hmC density and induce erythroid gene expression in hypoxia." Blood Advances 4, no. 13 (2020): 3053–62. http://dx.doi.org/10.1182/bloodadvances.2020001535.

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Abstract In mammalian cells, cytosines found within cytosine guanine dinucleotides can be methylated to 5-methylcytosine (5-mC) by DNA methyltransferases and further oxidized by the Ten-eleven translocation dioxygenase (TET) enzymes to 5-hydroxymethylcytosine (5-hmC). We have previously shown that hematopoietic stem and progenitor cells (HSPCs) with TET2 mutations have aberrant 5-hmC distribution and less erythroid differentiation potential. However, these experiments were performed under standard tissue culture conditions with 21% oxygen (O2), whereas HSPCs in human bone marrow reside in ∼1%

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11

Kiel, Mark, Anagh A. Sahasrabuddhe, Thiru Velusamy, et al. "Integrated Genome Sequencing Reveals Frequent Loss of Function Alterations of ARID1A and Other Epigenetic Modifiers in Sezary Syndrome." Blood 124, no. 21 (2014): 706. http://dx.doi.org/10.1182/blood.v124.21.706.706.

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Abstract Introduction Sezary Syndrome (SS) is an aggressive mature T-cell neoplasm characterized by erythroderma, generalized lymphadenopathy and circulating T-cells. SS cells are characterized by complex karyotypes with numerous structural alterations and copy-number variants. Previous studies have implicated disruption and/or haploinsufficiency of TP53, CDKN2A, RB1 and PTEN in SS. Nevertheless, the comprehensive genetic alterations underlying the pathogenesis of SS are unknown. In this study, we used an integrated genomic sequencing approach to characterize the genetic basis of SS. Methods S

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12

Guan, Wenyue, Romain Guyot, Jacques Samarut, Frédéric Flamant, Jiemin Wong, and Karine Cécile Gauthier. "Methylcytosine dioxygenase TET3 interacts with thyroid hormone nuclear receptors and stabilizes their association to chromatin." Proceedings of the National Academy of Sciences 114, no. 31 (2017): 8229–34. http://dx.doi.org/10.1073/pnas.1702192114.

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Thyroid hormone receptors (TRs) are members of the nuclear hormone receptor superfamily that act as ligand-dependent transcription factors. Here we identified the ten-eleven translocation protein 3 (TET3) as a TR interacting protein increasing cell sensitivity to T3. The interaction between TET3 and TRs is independent of TET3 catalytic activity and specifically allows the stabilization of TRs on chromatin. We provide evidence that TET3 is required for TR stability, efficient binding of target genes, and transcriptional activation. Interestingly, the differential ability of different TRα1 mutan

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13

Lee, Minjung, Jianfang Li, Shaohai Fang, et al. "Tet2 Inactivation Enhances the Anti-Tumor Activity of Tumor-Infiltrating Lymphocytes (TILs) to Curtail Melanoma Growth." Blood 136, Supplement 1 (2020): 27. http://dx.doi.org/10.1182/blood-2020-137242.

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Inactivation of tumor infiltrating lymphocytes (TILs) is one of the mechanisms mitigating anti-tumor immunity during tumor onset and progression. Epigenetic abnormalities are regarded as a major culprit contributing to the dysfunction of TILs within tumor microenvironments. In this study, we used a murine model of melanoma to discover that Tet2 inactivation significantly enhances the anti-tumor activity of TILs, with the efficacy comparable to immune checkpoint inhibition imposed by anti-PD-L1 treatment. Single-cell RNA-seq analysis further revealed that Tet2-deficient TILs exhibit effector-li

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14

Long, Hannah K., Neil P. Blackledge, and Robert J. Klose. "ZF-CxxC domain-containing proteins, CpG islands and the chromatin connection." Biochemical Society Transactions 41, no. 3 (2013): 727–40. http://dx.doi.org/10.1042/bst20130028.

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Vertebrate DNA can be chemically modified by methylation of the 5 position of the cytosine base in the context of CpG dinucleotides. This modification creates a binding site for MBD (methyl-CpG-binding domain) proteins which target chromatin-modifying activities that are thought to contribute to transcriptional repression and maintain heterochromatic regions of the genome. In contrast with DNA methylation, which is found broadly across vertebrate genomes, non-methylated DNA is concentrated in regions known as CGIs (CpG islands). Recently, a family of proteins which encode a ZF-CxxC (zinc finge

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15

Kim, Tae Soo, Hye Young Kim, Jin Ho Yoon, and Hyen Sam Kang. "Recruitment of the Swi/Snf Complex by Ste12-Tec1 Promotes Flo8-Mss11-Mediated Activation of STA1 Expression." Molecular and Cellular Biology 24, no. 21 (2004): 9542–56. http://dx.doi.org/10.1128/mcb.24.21.9542-9556.2004.

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ABSTRACT In the yeast Saccharomyces diastaticus, expression of the STA1 gene, which encodes an extracellular glucoamylase, is activated by the specific DNA-binding activators Flo8, Mss11, Ste12, and Tec1 and the Swi/Snf chromatin-remodeling complex. Here we show that Flo8 interacts physically and functionally with Mss11. Flo8 and Mss11 bind cooperatively to the inverted repeat sequence TTTGC-n-GCAAA (n = 97) in UAS1-2 of the STA1 promoter. In addition, Flo8 and Mss11 bind indirectly to UAS2-1 of the STA1 promoter by interacting with Ste12 and Tec1, which bind to the filamentation and invasion

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16

Nakamura, Toru M., Bettina A. Moser, and Paul Russell. "Telomere Binding of Checkpoint Sensor and DNA Repair Proteins Contributes to Maintenance of Functional Fission Yeast Telomeres." Genetics 161, no. 4 (2002): 1437–52. http://dx.doi.org/10.1093/genetics/161.4.1437.

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Abstract Telomeres, the ends of linear chromosomes, are DNA double-strand ends that do not trigger a cell cycle arrest and yet require checkpoint and DNA repair proteins for maintenance. Genetic and biochemical studies in the fission yeast Schizosaccharomyces pombe were undertaken to understand how checkpoint and DNA repair proteins contribute to telomere maintenance. On the basis of telomere lengths of mutant combinations of various checkpoint-related proteins (Rad1, Rad3, Rad9, Rad17, Rad26, Hus1, Crb2, Chk1, Cds1), Tel1, a telomere-binding protein (Taz1), and DNA repair proteins (Ku70, Rad3

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Jia, Lin, Yichen Wang, Cong Wang, et al. "Oplr16 serves as a novel chromatin factor to control stem cell fate by modulating pluripotency-specific chromosomal looping and TET2-mediated DNA demethylation." Nucleic Acids Research 48, no. 7 (2020): 3935–48. http://dx.doi.org/10.1093/nar/gkaa097.

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Abstract Formation of a pluripotency-specific chromatin network is a critical event in reprogramming somatic cells into pluripotent status. To characterize the regulatory components in this process, we used ‘chromatin RNA in situ reverse transcription sequencing’ (CRIST-seq) to profile RNA components that interact with the pluripotency master gene Oct4. Using this approach, we identified a novel nuclear lncRNA Oplr16 that was closely involved in the initiation of reprogramming. Oplr16 not only interacted with the Oct4 promoter and regulated its activity, but it was also specifically activated

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18

Li, Yuan, Ming Yue, John Anastasi, et al. "Epigenetic Modifying Drugs Inhibit MDS/AML Cell Growth through Selective Disruption of the Interactions Between Lineage-Determining Transcription Factors and DNA/Histone Modifiers." Blood 126, no. 23 (2015): 3853. http://dx.doi.org/10.1182/blood.v126.23.3853.3853.

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Abstract Normal hematopoiesis is controlled by a well-connected genetic network composed of several transcription factors (TFs) including PU.1 and GATA1. It has been postulated that both transcription factors and epigenetic modifiers work collaboratively to regulate hematopoietic stem cell differentiation and lineage specification as well as leukemogenesis. However, it is unclear about how the interplay between genetic network and epigenetic regulatory modifiers regulates locus-specific chromatin modifications and gene expression in normal hematopoiesis and hematologic malignancies such as mye

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Schaefer, Eva Johanna, Iman Fares, Clifford Meyer, et al. "Dual Effects of BCOR-PRC1.1 Dependent Gene Regulation Mediate Cooperation of BCOR and TET2 Mutations in Myeloid Transformation." Blood 132, Supplement 1 (2018): 651. http://dx.doi.org/10.1182/blood-2018-99-119519.

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Abstract Myeloid transformation occurs via stepwise acquisition of driver mutations that have distinct positions in the clonal hierarchy. BCOR mutations are common in myelodysplastic syndromes (MDS), but rarely occur as initiating events, instead typically arising in the context of other pre-existing mutations, such as TET2. BCOR encodes a subunit of the Polycomb Repressive Complex 1.1 (PRC1.1) which mediates gene repression by regulating H2AK119 via RING1 ubiquitin ligase activity. We hypothesized that BCOR mutations exert context dependent effects on chromatin regulation, thereby mediating c

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Wang, Yilin, Kathryn S. Brady, Benjamin P. Caiello, Stephanie M. Ackerson, and Jason A. Stewart. "Human CST suppresses origin licensing and promotes AND-1/Ctf4 chromatin association." Life Science Alliance 2, no. 2 (2019): e201800270. http://dx.doi.org/10.26508/lsa.201800270.

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Human CTC1-STN1-TEN1 (CST) is an RPA-like single-stranded DNA-binding protein that interacts with DNA polymerase α-primase (pol α) and functions in telomere replication. Previous studies suggest that CST also promotes replication restart after fork stalling. However, the precise role of CST in genome-wide replication remains unclear. In this study, we sought to understand whether CST alters origin licensing and activation. Replication origins are licensed by loading of the minichromosome maintenance 2–7 (MCM) complex in G1 followed by replisome assembly and origin firing in S-phase. We find th

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Mujahed, Huthayfa, Sophia Miliara, Anne Neddermeyer, et al. "AML displays increased CTCF occupancy associated with aberrant gene expression and transcription factor binding." Blood 136, no. 3 (2020): 339–52. http://dx.doi.org/10.1182/blood.2019002326.

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Abstract CCTC-binding factor (CTCF) is a key regulator of gene expression through organization of the chromatin structure. Still, it is unclear how CTCF binding is perturbed in leukemia or in cancer in general. We studied CTCF binding by chromatin immunoprecipitation sequencing in cells from patients with acute myeloid leukemia (AML) and in normal bone marrow (NBM) in the context of gene expression, DNA methylation, and azacitidine exposure. CTCF binding was increased in AML compared with NBM. Aberrant CTCF binding was enriched for motifs for key myeloid transcription factors such as CEBPA, PU

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Lebrun, Eleonore, Geneviève Fourel, Pierre-Antoine Defossez, and Eric Gilson. "A Methyltransferase Targeting Assay Reveals Silencer-Telomere Interactions in Budding Yeast." Molecular and Cellular Biology 23, no. 5 (2003): 1498–508. http://dx.doi.org/10.1128/mcb.23.5.1498-1508.2003.

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ABSTRACT We have designed a modified version of the Dam identification technique and used it to probe higher-order chromatin structure in Saccharomyces cerevisiae. We fused the bacterial DNA methyltransferase Dam to the DNA-binding domain of TetR and targeted the resulting chimera to Tet operators inserted in the yeast genome at the repressed locus HML. We then monitored the methylation status of HML and other sequences by a quantitative technique combining methylation-sensitive restriction and real-time PCR. As expected, we found that TetR-Dam efficiently methylated HML in cis. More strikingl

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Yu, Tai-Yuan, Michael T. Kimble, and Lorraine S. Symington. "Sae2 antagonizes Rad9 accumulation at DNA double-strand breaks to attenuate checkpoint signaling and facilitate end resection." Proceedings of the National Academy of Sciences 115, no. 51 (2018): E11961—E11969. http://dx.doi.org/10.1073/pnas.1816539115.

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The Mre11-Rad50-Xrs2NBS1 complex plays important roles in the DNA damage response by activating the Tel1ATM kinase and catalyzing 5′–3′ resection at DNA double-strand breaks (DSBs). To initiate resection, Mre11 endonuclease nicks the 5′ strands at DSB ends in a reaction stimulated by Sae2CtIP. Accordingly, Mre11-nuclease deficient (mre11-nd) and sae2Δ mutants are expected to exhibit similar phenotypes; however, we found several notable differences. First, sae2Δ cells exhibit greater sensitivity to genotoxins than mre11-nd cells. Second, sae2Δ is synthetic lethal with sgs1Δ, whereas the mre11-n

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Mohammad, Ghulam, and Renu A. Kowluru. "Homocysteine Disrupts Balance between MMP-9 and Its Tissue Inhibitor in Diabetic Retinopathy: The Role of DNA Methylation." International Journal of Molecular Sciences 21, no. 5 (2020): 1771. http://dx.doi.org/10.3390/ijms21051771.

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High homocysteine is routinely observed in diabetic patients, and this non-protein amino acid is considered as an independent risk factor for diabetic retinopathy. Homocysteine biosynthesis from methionine forms S-adenosyl methionine (SAM), which is a major methyl donor critical in DNA methylation. Hyperhomocysteinemia is implicated in increased oxidative stress and activation of MMP-9, and in diabetic retinopathy, the activation of MMP-9 facilitates capillary cell apoptosis. Our aim was to investigate the mechanism by which homocysteine activates MMP-9 in diabetic retinopathy. Human retinal e

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Zhang, Xiaotian, Xue Qing David Wang, Haley Gore, Pamela Himadewi, Fan Feng, and Jie Liu. "3D Genomics of Acute Meyloid Leukemia Reveals the Imbalance between DNA Methylation Canyon Interactions and Leukemic Specific Enhancer Network Interactions." Blood 136, Supplement 1 (2020): 45. http://dx.doi.org/10.1182/blood-2020-141708.

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Changes in 3D chromatin organization like enhancer hijacking are believed to the driver for disease development like leukemia. Here we performed high-resolution HiC assays on primary acute myeloid leukemia (AML) samples and cell lines to dissect the abnormal 3D chromatin organization in AML. Our data set covers 5 AML samples and 3 AML cell lines. This dataset includes the common genetic abnormalities in AML: MLL-rearrangement, NPM1 mutation, RUNX1 mutation, and IDH1/TET2 mutations. We have recently generated high-resolution map for normal human hematopoietic stem cells (HSC) (Zhang et al. Mole

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Bai, Jie, Sho Kubota, Takako Yokomizo, et al. "Hmga2 Functions As an Oncogene upon the Deletion of Tet2 and Promotes the Pathogenesis of Myelodysplastic Syndrome." Blood 134, Supplement_1 (2019): 3782. http://dx.doi.org/10.1182/blood-2019-127583.

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High Mobility Group AT-hook 2 (HMGA2) is a chromatin modifier and its overexpression has been found in a subset of patients with myelodysplastic syndrome (MDS). The high level of HMGA2 expression appears to predict poor prognosis in various tumors; however, it remains unclear how HMGA2 dysregulates expression of target genes to facilitate the transformation. To elucidate the mechanisms by which the overexpression of Hmga2 promotes the development of MDS, we generated an Hmga2-expressing Tet2-deficient (Hmga2-Tet2Δ/Δ) mouse model showing the progressive phenotype of MDS. We found that Hmga2-Tet

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Kirk, Karen E., Christina Christ, Jennifer M. McGuire, et al. "Abnormal Micronuclear Telomeres Lead to an Unusual Cell Cycle Checkpoint and Defects in Tetrahymena Oral Morphogenesis." Eukaryotic Cell 7, no. 10 (2008): 1712–23. http://dx.doi.org/10.1128/ec.00393-07.

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ABSTRACT Telomere mutants have been well studied with respect to telomerase and the role of telomere binding proteins, but they have not been used to explore how a downstream morphogenic event is related to the mutated telomeric DNA. We report that alterations at the telomeres can have profound consequences on organellar morphogenesis. Specifically, a telomerase RNA mutation termed ter1-43AA results in the loss of germ line micronuclear telomeres in the binucleate protozoan Tetrahymena thermophila. These cells also display a micronuclear mitotic arrest, characterized by an extreme delay in ana

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Fagnan, Alexandre, Frederik Otzen Bagger, Maria-Riera Piqué-Borràs, et al. "Human erythroleukemia genetics and transcriptomes identify master transcription factors as functional disease drivers." Blood 136, no. 6 (2020): 698–714. http://dx.doi.org/10.1182/blood.2019003062.

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Abstract Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes. To better define the underlying molecular mechanisms driving the erythroid phenotype, we studied a series of 33 AEL samples representing 3 genetic AEL subgroups including TP53-mutated, epigenetic regulator-mutated (eg, DNMT3A, TET2, or IDH2), and undefined cases with low mutational burden. We established an erythroid vs myeloid transcriptome-based s

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Chen, Li, Yuan Li, Ming Yue, et al. "Bromodomain and Extra-Terminal Motif Proteins (BETs) Mediate 5-Azacitidine Resistance in Myeloid Leukemia through Recruitment of an Active RNA Polymerase II Complex." Blood 128, no. 22 (2016): 746. http://dx.doi.org/10.1182/blood.v128.22.746.746.

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Abstract Background: BETs are evolutionarily conserved proteins that specifically bind to acetyl-lysines on histones and other proteins to recruit transcriptional machinery and influence gene expression (Shi and Vakoc. 2014 Mol Cell 54, 728-736). Small molecules that target BETs, such as JQ1 and I-BET, can effectively inhibit the growth of midline carcinoma cells that have a BRD4-NUT gene fusionas well as leukemia cells, such as AML, which have a diverse genetic background and do not have BRD4 rearrangements. DNA methyltransferase (DNMT) inhibitors, such as azacitidine (5-AZA) and decitabine,

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Kim, Taehyung, Joon Ho Moon, Jae-Sook Ahn, et al. "Residual Allelic Burden Measured By Next-Generation Sequencing (NGS) at Remission Provides Limited Prognostic Value to Predict Relapse and Long-Term Outcome in Core Binding Factor Acute Myeloid Leukemia (CBF-AML)." Blood 132, Supplement 1 (2018): 1391. http://dx.doi.org/10.1182/blood-2018-99-112906.

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Abstract Introduction NGS-based detection of minimal residual disease (MRD) has been successfully demonstrated for its correlation with relapse risk in AML. However, in a subtype of AML, CBF-AML, its clinical relevance of residual allelic burden at complete remission (CR) has not been fully explored. The standard MRD detection method in CBF-AML is quantitative PCR (qPCR). In this study, we aimed to explore applicability and feasibility of NGS-based MRD detection in CBF-AML taking various approaches, rather than simply using residual allele burden at CR. Patients and Methods Fifty-three patient

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Gebhard, Claudia, Roger Mulet-Lazaro, Lucia Schwarzfischer, et al. "Integrated Analysis of Global DNA Methylation and Transcription Reveals a Leukemia Subtype with Extreme Hypermethylation Associated with Silencing of Regulators of Differentiation." Blood 132, Supplement 1 (2018): 2608. http://dx.doi.org/10.1182/blood-2018-99-118521.

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Abstract Acute myeloid leukemia (AML) represents a highly heterogeneous myeloid stem cell disorder classified based on various genetic defects. Besides genetic alterations, epigenetic changes are recognized as an additional mechanism contributing to leukemogenesis, but insight into the latter process remains minor. Using a combination of Methyl-CpG-Immunoprecipitation (MCIp-chip) and MALDI-TOF analysis of bisulfite-treated DNA in a cohort of 196 AML patients we previously demonstrated that (cyto)genetically defined AML subtypes, including CBFB-MYH11, AML-ETO, NPM1-mut, CEBPA-mut or IDH1/2-mut

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Mazumdar, Claire, Rui Li, Jason Buenrostro, Howard Y. Chang, and Ravi Majeti. "Cohesin Complex Mutations Impair Differentiation of Human Hematopoietic Stem and Progenitor Cells." Blood 124, no. 21 (2014): 4785. http://dx.doi.org/10.1182/blood.v124.21.4785.4785.

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Abstract The cohesin complex is a multiprotein complex involved in a number of cellular processes including sister chromatid cohesion in mitosis, replication fork organization, and regulation of chromatin accessibility for gene expression. Mutations in genes encoding the members of the cohesin complex (SMC1A, SMC3, STAG2, and RAD21) occur in about 10-15% of de novo acute myeloid leukemia (AML) patients. Apart from AML, cohesin mutations have been found in many human cancers indicating a central role for this complex in oncogenesis. In AML, our prior studies have demonstrated that cohesin mutat

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Eisfeld, Ann-Kathrin, Krzysztof Mrózek, Jessica Kohlschmidt, et al. "The Mutational Patterns Associated with Cytogenetic Subsets of De Novo Acute Myeloid Leukemia (AML): A Study of 1603 Adult Patients (Pts)." Blood 128, no. 22 (2016): 287. http://dx.doi.org/10.1182/blood.v128.22.287.287.

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Abstract The classification of AML is based on the morphology of leukemic blasts, their immunophenotypes, and the presence of specific chromosomal abnormalities and selected gene mutations. It is widely acknowledged that some gene mutations are enriched in certain cytogenetic subsets, in which they may serve as therapeutic targets. We created a comprehensive oncoprint of mutations associated with centrally reviewed cytogenetic findings in 1603 adults (1080 aged <60 years, and 523 aged ≥60 years) with de novo AML (excluding acute promyelocytic leukemia) who were treated on CALGB/ALLIANCE pro

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Fiskus, Warren, Christopher Peter Mill, Raffaella Soldi, et al. "Synergistic Pre-Clinical Activity of Targeted Inhibition of KDM1A and BET Proteins Against Human AML Blast Progenitor Cells." Blood 132, Supplement 1 (2018): 3930. http://dx.doi.org/10.1182/blood-2018-99-114198.

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Abstract There is a clear need to develop novel therapies that would overcome differentiation block and eliminate AML stem/progenitor cells. Genetic and epigenetic dysregulation of enhancers regulates expressions of myeloid lineage transcriptional regulators and their target genes in AML stem/progenitor cells. LSD1 (KDM1A) is an FAD-dependent amine-oxidase that demethylates mono and dimethyl histone H3 lysine 4 (H3K4Me1 and H3K4Me2), which regulates enhancer maintenance and transcription in AML stem/progenitor cells (LSCs). LSD1 is part of the repressor complexes involving HDACs, CoREST or GFI

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Khandanpour, Cyrus, Joseph Krongold, Judith Schütte, et al. "The Growth Factor Independence 1 variant form GFI136N Predisposes to Acute Myeloid Leukemia by Inducing Epigenetic Changes in Oncogenes Such As Hoxa9." Blood 118, no. 21 (2011): 223. http://dx.doi.org/10.1182/blood.v118.21.223.223.

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Abstract Abstract 223 A coding variant form of GFI1 (GFI136N) increases the risk to develop AML by 60% and is present in about 10–15 % of all Caucasian AML patients. To determine the underlying molecular mechanism and potentially develop new therapeutic approaches, we generated “knockin” mouse strains wherein the endogenous murine Gfi1 gene was replaced either by the human GFI1 variant (GFI136N, the form predisposing to AML) or by the more common form of GFI1 (GFI136S). In most hematopoietic compartments no difference was observable between GFI136N and GFI136S expressing mice; however, there w

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Karjalainen, Riikka, Minxia Liu, Ashwini Kumar, et al. "Combined Targeting of BET Family Proteins and BCL2 Is Synergistic in Acute Myeloid Leukemia Cells Overexpressing S100A8 and S100A9." Blood 132, Supplement 1 (2018): 2634. http://dx.doi.org/10.1182/blood-2018-99-118890.

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Abstract Background The 5-year survival rate for acute myeloid leukemia (AML) remains poor with most patients succumbing to relapse or refractory disease. Recently, the BCL2 specific inhibitor venetoclax has shown promising anti-leukemia activity in high-risk AML patients. Most patients, however, ultimately develop resistance to monotherapy and novel combination treatments with venetoclax are needed for patients with no other therapy options available. In this study we identified high expression of calcium binding protein S100A8/S100A9 to be associated with venetoclax resistance and looked for

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Jeong, Mira, Deqiang Sun, Min Luo, et al. "Large Conserved Domains Of Low DNA Methylation Maintained By 5-Hydroxymethycytosine and Dnmt3a." Blood 122, no. 21 (2013): 2406. http://dx.doi.org/10.1182/blood.v122.21.2406.2406.

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Abstract Identification of recurrent leukemia-associated mutations in genes encoding regulators of DNA methylation such as DNMT3A and TET2 have underscored the critical importance of DNA methylation in maintenance of normal physiology. To gain insight into how DNA methylation exerts the central role, we sought to determine the genome-wide pattern of DNA methylation in the normal precursors of leukemia cells: the hematopoietic stem cell (HSC), and investigate the factors that affect alterations in DNA methylation and gene expression. We performed whole genome bisulfite sequencing (WGBS) on puri

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Awada, Hassan, Carmelo Gurnari, Arda Durmaz, et al. "Comparative Genomic Analysis of Adolescents and Young Adults Versus Elderly with Acute Myeloid Leukemia." Blood 136, Supplement 1 (2020): 18. http://dx.doi.org/10.1182/blood-2020-141577.

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Prognosis and survival outcomes of acute myeloid leukemia (AML) strongly depend on age at diagnosis. In fact, long-term survival rates range from 60% in children and adolescent/young adults (AYA-AML: aged 15-39 years) to 10-15% in elderly patients (E-AML: aged &gt;70 years). The currently available classification and prognostication models incorporate genomic features that include cytogenetics and molecular mutations based on adult AML clinical trials that mainly enroll patients outlying these two age categories. Consequently, prognostication models might still not account for the invarian

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Hansen, Marcus Celik, Charlotte Guldborg Nyvold, Anne Stidsholt Roug, Line Nederby, and Peter Hokland. "A New Approach to Identify Pathogenic Mutations and Inherited Variants By Exome Sequencing – Using a Pair of Identical Twins with Monoclonal Lymphosis As Case Model." Blood 124, no. 21 (2014): 1979. http://dx.doi.org/10.1182/blood.v124.21.1979.1979.

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Abstract Genome-wide association studies (GWAS) have identified common susceptibility loci in developing chronic lymphocytic leukemia (CLL). As the price on whole exome and genome sequencing continues to drop, large sequencing studies become more feasible and will change our understanding of the biological fundament of malignancy - and of the premalignant state of monoclonal lymphocytosis toward leukemic status. However, CLL is heterogeneous and, while co-inheritance of multiple low-risk variants govern predisposition, GWAS cannot yet be expected to contribute sufficiently in delineating indiv

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Saenz, Dyana T., Warren Fiskus, Kanak Raina, et al. "Superior Lethal Activity of Novel BET Protein Proteolysis Targeting Chimera (BETP-PROTACs) Versus Betp Bromodomain Inhibitor (BETi) Against Post-Myeloproliferative Neoplasm (MPN) Secondary (s) AML Cells." Blood 128, no. 22 (2016): 747. http://dx.doi.org/10.1182/blood.v128.22.747.747.

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Abstract Hematopoietic stem/progenitor cells (HPCs) of BCR-ABL1-negative myeloproliferative neoplasms with myelofibrosis (MPN-MF) exhibit mutations in JAK2, c-MPL, or calreticulin (CALR) gene and display constitutive activation of JAK-STAT signaling. In MPN-MF, transformation to AML (sAML) occurs in up to 20% of patients. Ruxolitinib (R) is a type I, ATP-competitive, JAK1 & 2 inhibitor (JAKi), which is currently used in the therapy of MPN-MF. Treatment with R confers notable clinical benefit in MPN-MF, but exhibits only modest activity and does not significantly impact the clinical outcome

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Shiba, Norio, Kenichi Yoshida, Yasunobu Nagata, et al. "Whole-Exome Resequencing Identifies Somatic Mutations Of BCOR and BCORL1 Transcriptional Corepressor Genes and Major Cohesin Complex Component Genes In Pediatric Acute Myeloid Leukemia." Blood 122, no. 21 (2013): 834. http://dx.doi.org/10.1182/blood.v122.21.834.834.

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Abstract Background Acute myeloid leukemia (AML) is a molecularly and clinically heterogeneous disease. Currently, targeted sequencing efforts have identified several mutations that carry diagnostic and prognostic information such as RAS, KIT, and FLT3 in both adult and pediatric AML, and NPM1 and TET2 in adult AML. Meanwhile, the recent development of massively parallel sequencing technologies has provided a new opportunity to discover genetic changes across the entire genomes or protein-coding sequences in human cancers at a single-nucleotide level, which could be enabled the discovery of re

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Giacopelli, Brian, Min Wang, Ada C. Cleary, et al. "DNA Methylation-Based Classification Highlights the Role of the JAK-STAT Pathway in Acute Myeloid Leukemia." Blood 134, Supplement_1 (2019): 1413. http://dx.doi.org/10.1182/blood-2019-126212.

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Background Acute myeloid leukemia (AML) is a clinically and molecularly heterogeneous disease with poor survival. Recurrent genetic aberrations, such as chromosomal rearrangements and gene mutations, are currently used for patient classification and prognosis, and form the basis of our current understanding of pathogenic mechanisms. However, these markers incompletely predict disease behavior and outcomes. Alterations in DNA methylation patterns are a major hallmark of cancer and recent studies have demonstrated differential global DNA methylation patterns among AML patients. Here we sought to

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Wang, Hongye, Yile Huang, Ming Yu, et al. "Muscle regeneration controlled by a designated DNA dioxygenase." Cell Death & Disease 12, no. 6 (2021). http://dx.doi.org/10.1038/s41419-021-03817-2.

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AbstractTet dioxygenases are responsible for the active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2, but not Tet1 and Tet3, is specifically required for muscle regeneration in vivo. Loss of Tet2 leads to severe muscle regeneration defects. Further analysis indicates that Tet2 regulates myoblast differentiation and fusion. Tet2 activates transcription of the key differentiation modulator Myogenin (MyoG) by actively demethylating its enhancer region. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differe

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Du, Zhonghua, Xue Wen, Yichen Wang, et al. "Chromatin lncRNA Platr10 controls stem cell pluripotency by coordinating an intrachromosomal regulatory network." Genome Biology 22, no. 1 (2021). http://dx.doi.org/10.1186/s13059-021-02444-6.

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Abstract Background A specific 3-dimensional intrachromosomal architecture of core stem cell factor genes is required to reprogram a somatic cell into pluripotency. As little is known about the epigenetic readers that orchestrate this architectural remodeling, we used a novel chromatin RNA in situ reverse transcription sequencing (CRIST-seq) approach to profile long noncoding RNAs (lncRNAs) in the Oct4 promoter. Results We identify Platr10 as an Oct4 - Sox2 binding lncRNA that is activated in somatic cell reprogramming. Platr10 is essential for the maintenance of pluripotency, and lack of this

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Zheng, Zhaoqing, Ganesh Ambigapathy, and Joyce Keifer. "MeCP2 regulates Tet1-catalyzed demethylation, CTCF binding, and learning-dependent alternative splicing of the BDNF gene in Turtle." eLife 6 (June 8, 2017). http://dx.doi.org/10.7554/elife.25384.

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MECP2 mutations underlying Rett syndrome cause widespread misregulation of gene expression. Functions for MeCP2 other than transcriptional are not well understood. In an ex vivo brain preparation from the pond turtle Trachemys scripta elegans, an intraexonic splicing event in the brain-derived neurotrophic factor (BDNF) gene generates a truncated mRNA transcript in naïve brain that is suppressed upon classical conditioning. MeCP2 and its partners, splicing factor Y-box binding protein 1 (YB-1) and methylcytosine dioxygenase 1 (Tet1), bind to BDNF chromatin in naïve but dissociate during condit

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Fang, Shaohai, Jia Li, Yang Xiao, et al. "Tet inactivation disrupts YY1 binding and long-range chromatin interactions during embryonic heart development." Nature Communications 10, no. 1 (2019). http://dx.doi.org/10.1038/s41467-019-12325-z.

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Abstract Tet-mediated DNA demethylation plays an important role in shaping the epigenetic landscape and chromatin accessibility to control gene expression. While several studies demonstrated pivotal roles of Tet in regulating embryonic development, little is known about their functions in heart development. Here we analyze DNA methylation and hydroxymethylation dynamics during early cardiac development in both human and mice. We find that cardiac-specific deletion of Tet2 and Tet3 in mice (Tet2/3-DKO) leads to ventricular non-compaction cardiomyopathy (NCC) with embryonic lethality. Single-cel

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Tsujimura, Taro, Osamu Takase, Masahiro Yoshikawa, et al. "Controlling gene activation by enhancers through a drug-inducible topological insulator." eLife 9 (May 5, 2020). http://dx.doi.org/10.7554/elife.47980.

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While regulation of gene-enhancer interaction is intensively studied, its application remains limited. Here, we reconstituted arrays of CTCF-binding sites and devised a synthetic topological insulator with tetO for chromatin-engineering (STITCH). By coupling STITCH with tetR linked to the KRAB domain to induce heterochromatin and disable the insulation, we developed a drug-inducible system to control gene activation by enhancers. In human induced pluripotent stem cells, STITCH inserted between MYC and the enhancer down-regulated MYC. Progressive mutagenesis of STITCH led to a preferential esca

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Raj, Samhitha, Yasuhiro Kyono, Christopher J. Sifuentes, Elvira del Carmen Arellanes-Licea, Arasakumar Subramani, and Robert J. Denver. "Thyroid Hormone Induces DNA Demethylation in Xenopus Tadpole Brain." Endocrinology 161, no. 11 (2020). http://dx.doi.org/10.1210/endocr/bqaa155.

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Abstract Thyroid hormone (T3) plays pivotal roles in vertebrate development, acting via nuclear T3 receptors (TRs) that regulate gene transcription by promoting post-translational modifications to histones. Methylation of cytosine residues in deoxyribonucleic acid (DNA) also modulates gene transcription, and our recent finding of predominant DNA demethylation in the brain of Xenopus tadpoles at metamorphosis, a T3-dependent developmental process, caused us to hypothesize that T3 induces these changes in vivo. Treatment of premetamorphic tadpoles with T3 for 24 or 48 hours increased immunoreact

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van Kessel, Julia C., Luke E. Ulrich, Igor B. Zhulin, and Bonnie L. Bassler. "Analysis of Activator and Repressor Functions Reveals the Requirements for Transcriptional Control by LuxR, the Master Regulator of Quorum Sensing in Vibrio harveyi." mBio 4, no. 4 (2013). http://dx.doi.org/10.1128/mbio.00378-13.

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ABSTRACT LuxR-type transcription factors are the master regulators of quorum sensing in vibrios. LuxR proteins are unique members of the TetR superfamily of transcription factors because they activate and repress large regulons of genes. Here, we used chromatin immunoprecipitation and nucleotide sequencing (ChIP-seq) to identify LuxR binding sites in the Vibrio harveyi genome. Bioinformatics analyses showed that the LuxR consensus binding site at repressed promoters is a symmetric palindrome, whereas at activated promoters it is asymmetric and contains only half of the palindrome. Using a gene

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Lu, Fang, Andreas Wiedmer, Kayla A. Martin, Priyankara J. M. S. Wickramasinghe, Andrew V. Kossenkov, and Paul M. Lieberman. "Coordinate Regulation of TET2 and EBNA2 Controls the DNA Methylation State of Latent Epstein-Barr Virus." Journal of Virology 91, no. 20 (2017). http://dx.doi.org/10.1128/jvi.00804-17.

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ABSTRACT Epstein-Barr virus (EBV) latency and its associated carcinogenesis are regulated by dynamic changes in DNA methylation of both virus and host genomes. We show here that the ten-eleven translocation 2 (TET2) gene, implicated in hydroxymethylation and active DNA demethylation, is a key regulator of EBV latency type DNA methylation patterning. EBV latency types are defined by DNA methylation patterns that restrict expression of viral latency genes. We show that TET2 mRNA and protein expression correlate with the highly demethylated EBV type III latency program permissive for expression o

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