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Artykuły w czasopismach na temat „Dot1x”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 15 lutego 2022

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1

Zhang, Wenzheng, Zhiyuan Yu, Hongyu Wu, Lihe Chen, Qun Kong та Bruce C. Kone. "An Af9 cis-element directly targets Dot1a to mediate transcriptional repression of the αENaC gene". American Journal of Physiology-Renal Physiology 304, № 4 (2013): F367—F375. http://dx.doi.org/10.1152/ajprenal.00537.2011.

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The epithelial Na+ channel subunit-α ( αENaC) of the distal nephron is essential for salt balance. We previously demonstrated that the histone methyltransferase Dot1a and its protein partner Af9 basally repress αENaC transcription in mouse inner medullary collecting duct type 3 (mIMCD3) cells and link aldosterone-elicited chromatin modifications to αENaC transcriptional activation. Af9 DNA-binding activity has never been demonstrated, and whether and where Af9 binds to the αENaC promoter to target Dot1a are unknown. The present study sought to identify functional Af9 cis-element(s) in the −57/

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2

Zhang, Long, Lihe Chen, Chao Gao, et al. "Loss of Histone H3 K79 Methyltransferase Dot1l Facilitates Kidney Fibrosis by Upregulating Endothelin 1 through Histone Deacetylase 2." Journal of the American Society of Nephrology 31, no. 2 (2019): 337–49. http://dx.doi.org/10.1681/asn.2019070739.

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BackgroundThe progression rate of CKD varies substantially among patients. The genetic and epigenetic contributions that modify how individual patients respond to kidney injury are largely unknown. Emerging evidence has suggested that histone H3 K79 methyltransferase Dot1l has an antifibrotic effect by repressing Edn1, which encodes endothelin 1 in the connecting tubule/collecting duct.MethodsTo determine if deletion of the Dot1l gene is a genetic and epigenetic risk factor through regulating Edn1, we studied four groups of mice: wild-type mice, connecting tubule/collecting duct–specific Dot1l

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3

Wysocki, Robert, Ali Javaheri, Stéphane Allard, Fei Sha, Jacques Côté, and Stephen J. Kron. "Role of Dot1-Dependent Histone H3 Methylation in G1 and S Phase DNA Damage Checkpoint Functions of Rad9." Molecular and Cellular Biology 25, no. 19 (2005): 8430–43. http://dx.doi.org/10.1128/mcb.25.19.8430-8443.2005.

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ABSTRACT We screened radiation-sensitive yeast mutants for DNA damage checkpoint defects and identified Dot1, the conserved histone H3 Lys 79 methyltransferase. DOT1 deletion mutants (dot1Δ) are G1 and intra-S phase checkpoint defective after ionizing radiation but remain competent for G2/M arrest. Mutations that affect Dot1 function such as Rad6-Bre1/Paf1 pathway gene deletions or mutation of H2B Lys 123 or H3 Lys 79 share dot1Δ checkpoint defects. Whereas dot1Δ alone confers minimal DNA damage sensitivity, combining dot1Δ with histone methyltransferase mutations set1Δ and set2Δ markedly enha

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4

Wu, Aiwei, Junhong Zhi, Tian Tian, et al. "DOT1L complex regulates transcriptional initiation in human erythroleukemic cells." Proceedings of the National Academy of Sciences 118, no. 27 (2021): e2106148118. http://dx.doi.org/10.1073/pnas.2106148118.

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DOT1L, the only H3K79 methyltransferase in human cells and a homolog of the yeast Dot1, normally forms a complex with AF10, AF17, and ENL or AF9, is dysregulated in most cases of mixed-lineage leukemia (MLLr), and has been believed to regulate transcriptional elongation on the basis of its colocalization with RNA polymerase II (Pol II), the sharing of subunits (AF9 and ENL) between the DOT1L and super elongation complexes, and the distribution of H3K79 methylation on both promoters and transcribed regions of active genes. Here we show that DOT1L depletion in erythroleukemic cells reduces its g

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5

Singer, Miriam S., Alon Kahana, Alexander J. Wolf, et al. "Identification of High-Copy Disruptors of Telomeric Silencing in Saccharomyces cerevisiae." Genetics 150, no. 2 (1998): 613–32. http://dx.doi.org/10.1093/genetics/150.2.613.

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Abstract The ends of chromosomes in Saccharomyces cerevisiae initiate a repressive chromatin structure that spreads internally and inhibits the transcription of nearby genes, a phenomenon termed telomeric silencing. To investigate the molecular basis of this process, we carried out a genetic screen to identify genes whose overexpression disrupts telomeric silencing. We thus isolated 10 DOT genes (disruptor of telomeric silencing). Among these were genes encoding chromatin component Sir4p, DNA helicase Dna2p, ribosomal protein L32, and two proteins of unknown function, Asf1p and Ifh1p. The coll

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6

Kim, Wootae, Ranah Kim, Geunyeong Park, Jong-Wan Park, and Ja-Eun Kim. "Deficiency of H3K79 Histone Methyltransferase Dot1-like Protein (DOT1L) Inhibits Cell Proliferation." Journal of Biological Chemistry 287, no. 8 (2011): 5588–99. http://dx.doi.org/10.1074/jbc.m111.328138.

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7

Kim, Wootae, Minji Choi, and Ja-Eun Kim. "The histone methyltransferase Dot1/DOT1L as a critical regulator of the cell cycle." Cell Cycle 13, no. 5 (2014): 726–38. http://dx.doi.org/10.4161/cc.28104.

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8

Puddu, Fabio, Magda Granata, Lisa Di Nola, et al. "Phosphorylation of the Budding Yeast 9-1-1 Complex Is Required for Dpb11 Function in the Full Activation of the UV-Induced DNA Damage Checkpoint." Molecular and Cellular Biology 28, no. 15 (2008): 4782–93. http://dx.doi.org/10.1128/mcb.00330-08.

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ABSTRACT Following genotoxic insults, eukaryotic cells trigger a signal transduction cascade known as the DNA damage checkpoint response, which involves the loading onto DNA of an apical kinase and several downstream factors. Chromatin modifications play an important role in recruiting checkpoint proteins. In budding yeast, methylated H3-K79 is bound by the checkpoint factor Rad9. Loss of Dot1 prevents H3-K79 methylation, leading to a checkpoint defect in the G1 phase of the cell cycle and to a reduction of checkpoint activation in mitosis, suggesting that another pathway contributes to Rad9 r

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9

Wood, Adam, Jessica Schneider, and Ali Shilatifard. "Cross-talking histones: implications for the regulation of gene expression and DNA repair." Biochemistry and Cell Biology 83, no. 4 (2005): 460–67. http://dx.doi.org/10.1139/o05-116.

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The regulation of chromatin structure is essential to life. In eukaryotic organisms, several classes of protein exist that can modify chromatin structure either through ATP-dependent remodeling or through the post-translational modification of histone proteins. A vast array of processes ranging from transcriptional regulation to DNA repair rely on these histone-modifying enzymes. In the last few years, enzymes involved in the post-translational modification of histone proteins have become a topic of intense interest. Our work and the work of several other laboratories has focused largely on un

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10

Jo, Stephanie Y., Eric M. Granowicz, Ivan Maillard, Dafydd Thomas, and Jay L. Hess. "Requirement for Dot1l in murine postnatal hematopoiesis and leukemogenesis by MLL translocation." Blood 117, no. 18 (2011): 4759–68. http://dx.doi.org/10.1182/blood-2010-12-327668.

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Abstract Disruptor of telomeric silencing 1-like (Dot1l) is a histone 3 lysine 79 methyltransferase. Studies of constitutive Dot1l knockout mice show that Dot1l is essential for embryonic development and prenatal hematopoiesis. DOT1L also interacts with translocation partners of Mixed Lineage Leukemia (MLL) gene, which is commonly translocated in human leukemia. However, the requirement of Dot1l in postnatal hematopoiesis and leukemogenesis of MLL translocation proteins has not been conclusively shown. With a conditional Dot1l knockout mouse model, we examined the consequences of Dot1l loss in

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11

Morello, Giulia, Patrizia Porazzi, Enrico Moro, et al. "Zebrafish Ortholog of Human DOT1L Regulates Primitive and Transient Definitive Hematopoiesis and Controls hoxa9 and meis1 Expression." Blood 120, no. 21 (2012): 849. http://dx.doi.org/10.1182/blood.v120.21.849.849.

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Abstract Abstract 849 Objective: DOT1L is a H3K79 methyltransferase implicated in multiple biological processes including embryonic development, cell proliferation, DNA damage repair and hematopoiesis. Recently, it was reported that DOT1L interacts with various transcription factor MLL partner proteins, and that aberrant DOT1L methyltransferase activity is essential for the form of leukemogenesis mediated by MLL fusion oncoproteins. These findings led to current efforts in therapeutic targeting of DOT1L for MLL-rearranged leukemias. However, the role of DOT1L in hematopoiesis is incompletely u

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12

Grigsby, Sierrah M., Ann Friedman, Jennifer Chase, et al. "Elucidating the Importance of DOT1L Recruitment in MLL-AF9 Leukemia and Hematopoiesis." Cancers 13, no. 4 (2021): 642. http://dx.doi.org/10.3390/cancers13040642.

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MLL1 (KMT2a) gene rearrangements underlie the pathogenesis of aggressive MLL-driven acute leukemia. AF9, one of the most common MLL-fusion partners, recruits the histone H3K79 methyltransferase DOT1L to MLL target genes, constitutively activating transcription of pro-leukemic targets. DOT1L has emerged as a therapeutic target in patients with MLL-driven leukemia. However, global DOT1L enzymatic inhibition may lead to off-target toxicities in non-leukemic cells that could decrease the therapeutic index of DOT1L inhibitors. To bypass this problem, we developed a novel approach targeting specific

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13

Cao, Kaixiang, Michal Ugarenko, Patrick A. Ozark, et al. "DOT1L-controlled cell-fate determination and transcription elongation are independent of H3K79 methylation." Proceedings of the National Academy of Sciences 117, no. 44 (2020): 27365–73. http://dx.doi.org/10.1073/pnas.2001075117.

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Actively transcribed genes in mammals are decorated by H3K79 methylation, which is correlated with transcription levels and is catalyzed by the histone methyltransferase DOT1L. DOT1L is required for mammalian development, and the inhibition of its catalytic activity has been extensively studied for cancer therapy; however, the mechanisms underlying DOT1L’s functions in normal development and cancer pathogenesis remain elusive. To dissect the relationship between H3K79 methylation, cellular differentiation, and transcription regulation, we systematically examined the role of DOT1L and its catal

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14

Marcos-Villar, Laura, Estanislao Nistal-Villan, Noelia Zamarreño, Urtzi Garaigorta, Pablo Gastaminza та Amelia Nieto. "Interferon-β Stimulation Elicited by the Influenza Virus Is Regulated by the Histone Methylase Dot1L through the RIG-I-TRIM25 Signaling Axis". Cells 9, № 3 (2020): 732. http://dx.doi.org/10.3390/cells9030732.

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Influenza virus infection increases the methylation of lysine 79 of histone 3 catalyzed by the Dot1L enzyme. The role of Dot1L against infections was highlighted by an increase of influenza A and vesicular stomatitis virus replication in Dot1L-inhibited cells mediated by a decreased antiviral response. Interferon-beta (IFN-β) reporter assays indicate that Dot1L is involved in the control of retinoic acid-inducible gene-I protein (RIG-I) signaling. Accordingly, Dot1L inhibition decreases the IFN-β promoter stimulation and RIG-I- mitochondria-associated viral sensor (RIG-I-MAVS) association upon

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15

Jo, Stephanie Y., Eric M. Granowicz, and Jay L. Hess. "Assessment of DOT1L as a Therapeutic Target In Acute Leukemia." Blood 116, no. 21 (2010): 3291. http://dx.doi.org/10.1182/blood.v116.21.3291.3291.

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Abstract Abstract 3291 Histone modifying enzymes are crucial regulators of hematopoiesis that are commonly disrupted in acute leukemia. DOT1L has emerged as a particularly important methyltransferase in leukemias with Mixed Lineage Leukemia (MLL) rearrangements. Leukemogenic MLL fusion proteins transform primarily through upregulation of A-cluster HOX genes, including HOXA9 and the HOX cofactor MEIS1. Many of the most common MLL translocation partners including the AF4 family members, AF9, ENL, and AF10, form the Elongation Assisting Proteins (EAP) complex that includes DOT1L. DOT1L is the onl

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16

Wan, Shanshan, Yiwen Zhou, Qiong Huang, and Yanning Yang. "Dot1l Aggravates Keratitis Induced by Herpes Simplex Virus Type 1 in Mice via p38 MAPK-Mediated Oxidative Stress." Oxidative Medicine and Cellular Longevity 2021 (February 15, 2021): 1–14. http://dx.doi.org/10.1155/2021/6612689.

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Background. Disruptor of telomeric silencing 1-like (Dot1l) plays a vital role in biological processes as a well-known methyltransferase. However, its role in herpes simplex virus type 1- (HSV-1-) infected keratitis remains unclear. Methods. In vitro and in vivo models were assessed to investigate the role of Dot1l in HSV-1 induced keratitis. C57BL/6 mice corneas were infected with HSV-1 for different days, with or without Dot1l inhibitor, to demonstrate the regulation of Dot1l in herpes simplex keratitis (HSK). Human corneal epithelial (HCE) cells were cultured and infected with HSV-1 to iden

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17

Malcom, Carrie A., Joanna Piasecka-Srader, Nehemiah S. Alvarez, and Patrick E. Fields. "Identifying the Molecular Mechanisms By Which Disruptor of Telomere Silencing 1-like (DOT1L), a Histone 3, Lysine 79 (H3K79) Methyltransferase, Regulates Mammalian Hematopoiesis." Blood 128, no. 22 (2016): 2654. http://dx.doi.org/10.1182/blood.v128.22.2654.2654.

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Abstract Disruptor of Telomere silencing 1-Like (DOT1L), is a histone 3, lysine 79 (H3K79) methyltransferase that has been implicated in multiple processes, including activation of transcription, regulation of the cell cycle, leukemogenesis, and mouse embryonic development. In previous studies, we found that Dot1L deficiency results in an erythropoietic defect, leading to lethal anemia at around mid-gestation (Feng et al., 2010, Blood). The precise molecular mechanism(s) by which DOT1L regulates embryonic hematopoiesis has not yet been elucidated and is the overall objective of this study. DOT

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18

Bernt, Kathrin M., Nan Zhu, Joerg Faber, et al. "Demonstration of a Role for Dot1l In MLL-Rearranged Leukemia Using a Conditional Loss of Function Model." Blood 116, no. 21 (2010): 62. http://dx.doi.org/10.1182/blood.v116.21.62.62.

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Abstract Abstract 62 Leukemias associated with translocations of the Mixed Lineage Leukemia (MLL) gene account for a significant percentage of both AML and ALL, and often carry a poor prognosis. The exact molecular mechanisms by which MLL-fusion proteins transform cells are incompletely understood. One proposed model involves the aberrant activation of transcriptional programs through epigenetic changes that ultimately lead to leukemogenesis. The histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been shown to be recruited by the most common MLL fusion proteins, and MLL fusion protein tar

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19

Chen, Chun-Wei, Lu Yang, Xi Wang, et al. "High-Density CRISPR Scan Identifies Functional Regions of DOT1L That Mediate Therapeutic Response in MLL-r Leukemia." Blood 132, Supplement 1 (2018): 179. http://dx.doi.org/10.1182/blood-2018-179.

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Abstract Leukemias containing Mixed Lineage Leukemiagene rearrangement (MLL-r) account for 5-10% of human acute leukemia cases and are associated with a poor prognosis. The unmet clinical need and the lack of an effective targeted therapy emphasizes the need for novel approaches for these malignancies.Recent studies have discovered an essential role for the histone H3 lysine 79 (H3K79) methyltransferase DOT1L in the maintenance of MLL-r leukemias. Phase-I clinical trials (NCT01684150 and NCT02141828) have demonstrated the safety and clinical activity of the DOT1L-specific small molecule inhibi

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20

Nguyen, Anh Tram, Olena Taranova, Jin He, and Yi Zhang. "DOT1L, the H3K79 methyltransferase, is required for MLL-AF9–mediated leukemogenesis." Blood 117, no. 25 (2011): 6912–22. http://dx.doi.org/10.1182/blood-2011-02-334359.

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Abstract Chromosomal translocations of the mixed lineage leukemia (MLL) gene are a common cause of acute leukemias. The oncogenic function of MLL fusion proteins is, in part, mediated through aberrant activation of Hoxa genes and Meis1, among others. Here we demonstrate using a tamoxifen-inducible Cre-mediated loss of function mouse model that DOT1L, an H3K79 methyltransferase, is required for both initiation and maintenance of MLL-AF9–induced leukemogenesis in vitro and in vivo. Through gene expression and chromatin immunoprecipitation analysis we demonstrate that mistargeting of DOT1L, subse

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21

Song, Xiaosheng, Liuliu Yang, Mingzhu Wang, et al. "A higher-order configuration of the heterodimeric DOT1L–AF10 coiled-coil domains potentiates their leukemogenenic activity." Proceedings of the National Academy of Sciences 116, no. 40 (2019): 19917–23. http://dx.doi.org/10.1073/pnas.1904672116.

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Chromosomal translocations of MLL1 (Mixed Lineage Leukemia 1) yield oncogenic chimeric proteins containing the N-terminal portion of MLL1 fused with distinct partners. The MLL1–AF10 fusion causes leukemia through recruiting the H3K79 histone methyltransferase DOT1L via AF10’s octapeptide and leucine zipper (OM-LZ) motifs. Yet, the precise interaction sites in DOT1L, detailed interaction modes between AF10 and DOT1L, and the functional configuration of MLL1–AF10 in leukeomogenesis remain unknown. Through a combined approach of structural and functional analyses, we found that the LZ domain of A

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22

Riedel, Simone, Kathrin M. Bernt, Jessica Haladyna, et al. "Targeting Meningeoma-1 Driven AML through Epigenetic Modulation of the Cell of Origin." Blood 124, no. 21 (2014): 838. http://dx.doi.org/10.1182/blood.v124.21.838.838.

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Abstract Meningeoma-1 (MN1) overexpression in AML is common and predicts a poor prognosis. Forced expression of MN1 in early murine hematopoietic progenitors (CMP and LSK) but not hematopoietic stem cells (HSC) or committed progenitors (GMP) induces an aggressive myeloid leukemia as a single hit. This leukemia is strictly dependent on the high-level expression of a defined gene expression program in the cell of origin, which includes the key component HoxA9. This “susceptibility program” has been proposed as a therapeutic target in MN1high AML, but means to modulate this program have so far re

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23

Yi, Joanna S., Alex Federation, Jun Qi, et al. "Structure-Guided Design of DOT1L Methyltransferase Inhibitors By a Novel, Label Free Assay Platform." Blood 124, no. 21 (2014): 4811. http://dx.doi.org/10.1182/blood.v124.21.4811.4811.

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Abstract Cooperation between several epigenetic modulators defines MLL-rearranged leukemia as an epigenomic-driven cancer. Wild type MLL catalyzes trimethylation of lysine 4 on histone 3 from the methyl donor S-adenosylmethionine (SAM) at homeobox and other genes important for hematopoiesis, promoting their expression during development. However, in MLL-rearrangements, its methyltransferase domain is ubiquitously lost and replaced with >70 known fusion partners. Many of these fusion partners recruit DOT1L, the only known SAM-dependent lysine methyltransferase responsible for the methylation

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Steger, David J., Martina I. Lefterova, Lei Ying, et al. "DOT1L/KMT4 Recruitment and H3K79 Methylation Are Ubiquitously Coupled with Gene Transcription in Mammalian Cells." Molecular and Cellular Biology 28, no. 8 (2008): 2825–39. http://dx.doi.org/10.1128/mcb.02076-07.

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ABSTRACT The histone H3 lysine 79 methyltransferase DOT1L/KMT4 can promote an oncogenic pattern of gene expression through binding with several MLL fusion partners found in acute leukemia. However, the normal function of DOT1L in mammalian gene regulation is poorly understood. Here we report that DOT1L recruitment is ubiquitously coupled with active transcription in diverse mammalian cell types. DOT1L preferentially occupies the proximal transcribed region of active genes, correlating with enrichment of H3K79 di- and trimethylation. Furthermore, Dot1l mutant fibroblasts lacked H3K79 di- and tr

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25

Ho, Li-Lun, Amit Sinha, Michael Verzi, Kathrin M. Bernt, Scott A. Armstrong, and Ramesh A. Shivdasani. "DOT1L-Mediated H3K79 Methylation in Chromatin Is Dispensable for Wnt Pathway-Specific and Other Intestinal Epithelial Functions." Molecular and Cellular Biology 33, no. 9 (2013): 1735–45. http://dx.doi.org/10.1128/mcb.01463-12.

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Methylation of H3K79 is associated with chromatin at expressed genes, though it is unclear if this histone modification is required for transcription of all genes. Recent studies suggest that Wnt-responsive genes depend particularly on H3K79 methylation, which is catalyzed by the methyltransferase DOT1L. Human leukemias carrying MLL gene rearrangements show DOT1L-mediated H3K79 methylation and aberrant expression of leukemogenic genes. DOT1L inhibitors reverse these effects, but their clinical use is potentially limited by toxicity in Wnt-dependent tissues such as intestinal epithelium. Genome

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Tian, Yuanyuan, Lijun Meng, Hongshuang Yu, et al. "Graft-Versus-Host Disease Impairs the Histone Methyltransferase Dot1l-Regulated Reconstitution of Plasmacytoid Dendritic Cells in Mice Undergoing Allo-HSCT." Blood 132, Supplement 1 (2018): 477. http://dx.doi.org/10.1182/blood-2018-99-118751.

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Abstract Plasmacytoid dendritic cells (pDCs) derived either from adoptive transfer from the donor graft or stem cell reconstitution can attenuate and prevent graft-versus-host disease (GVHD) in both pre-clinical and clinical settings. However, the reconstitution of donor pDCs is severely impaired during GVHD via an unknown mechanism. Here we demonstrate that the histone methyltransferase Dot1l, which specifically catalyzes methylation of histone H3 at lysine 79 (H3K79me), is critical for regulating the commitment and differentiation of pDCs from hematopoietic stem cells (HSCs) and we observed

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Zhang, Xi, Qiaoling Zhou, Lihe Chen та ін. "Mineralocorticoid receptor antagonizes Dot1a-Af9 complex to increase αENaC transcription". American Journal of Physiology-Renal Physiology 305, № 10 (2013): F1436—F1444. http://dx.doi.org/10.1152/ajprenal.00202.2013.

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Aldosterone is a major regulator of Na+ absorption and acts by activating the mineralocorticoid receptor (MR) to stimulate the epithelial Na+ channel (ENaC). MR −/− mice exhibited pseudohypoaldosteronism type 1 (hyponatremia, hyperkalemia, salt wasting, and high levels of aldosterone) and died around postnatal day 10. However, if and how MR regulates ENaC transcription remain incompletely understood. Our earlier work demonstrated that aldosterone activates αENaC transcription by reducing expression of Dot1a and Af9 and by impairing Dot1a-Af9 interaction. Most recently, we reported identificati

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Reisenauer, Mary Rose, Steven W. Wang, Yang Xia, and Wenzheng Zhang. "Dot1a contains three nuclear localization signals and regulates the epithelial Na+ channel (ENaC) at multiple levels." American Journal of Physiology-Renal Physiology 299, no. 1 (2010): F63—F76. http://dx.doi.org/10.1152/ajprenal.00105.2010.

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We have previously reported that Dot1a is located in the cytoplasm and nucleus (Reisenauer MR, Anderson M, Huang L, Zhang Z, Zhou Q, Kone BC, Morris AP, Lesage GD, Dryer SE, Zhang W. J Biol Chem 284: 35659–35669, 2009), widely expressed in the kidney as detected by its histone H3K79 methyltransferase activity (Zhang W, Hayashizaki Y, Kone BC. Biochem J 377: 641–651, 2004), and involved in transcriptional control of the epithelial Na+ channel subunit-α gene ( αENaC) (Zhang W, Xia X, Jalal DI, Kuncewicz T, Xu W, Lesage GD, Kone BC. Am J Physiol Cell Physiol 290: C936–C946, 2006). Aldosterone rel

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Deshpande, Anagha, Benson Chen, Parham Ramezani-Rad, et al. "Targeting MYC-Driven B-Cell Lymphoma By Inhibition of the Histone Methyltransferase DOT1L." Blood 132, Supplement 1 (2018): 2839. http://dx.doi.org/10.1182/blood-2018-99-115475.

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Abstract Aberrant activation of the MYC proto-oncogene is a recurrent feature in human B-cell lymphomas of diverse sub-types, correlating with adverse prognosis and therapy resistance. Direct pharmacological MYC-targeting has proved difficult, but recent studies have shown that targeting chromatin regulators critical for MYC-driven oncogenesis may provide alternative avenues for therapeutic intervention. Recently, it has been demonstrated that MYC-driven oncogenesis in certain solid tumors is dependent on the histone 3 lysine 79 (H3K79) methyltransferase DOT1L. We hypothesized that B-cell lymp

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Yu, Zhiyuan, Qun Kong, and Bruce C. Kone. "CREB trans-activation of disruptor of telomeric silencing-1 mediates forskolin inhibition of CTGF transcription in mesangial cells." American Journal of Physiology-Renal Physiology 298, no. 3 (2010): F617—F624. http://dx.doi.org/10.1152/ajprenal.00636.2009.

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Connective tissue growth factor (CTGF) participates in diverse fibrotic processes including glomerulosclerosis. The adenylyl cyclase agonist forskolin inhibits CTGF expression in mesangial cells by unclear mechanisms. We recently reported that the histone H3K79 methyltransferase disruptor of telomeric silencing-1 (Dot1) suppresses CTGF gene expression in collecting duct cells ( J Clin Invest 117: 773–783, 2007) and HEK 293 cells ( J Biol Chem In press). In the present study, we characterized the involvement of Dot1 in mediating the inhibitory effect of forskolin on CTGF transcription in mouse

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Chen, Chun-Wei David, Christopher Delaney, Haiming Xu, et al. "An Epigenetic Regulator Screen Identifies Novel Targets That Sensitize MLL-Rearranged Leukemia to DOT1L Inhibition." Blood 128, no. 22 (2016): 571. http://dx.doi.org/10.1182/blood.v128.22.571.571.

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Abstract Mixed Lineage Leukemia gene rearrangements (MLL-r) account for nearly 10% of human acute leukemia cases and are generally associated with poor prognosis. Previous studies have revealed an essential role of the histone H3K79 methyltransferase Disruptor of Telomeric Silencing-1 Like (DOT1L) in MLL-r leukemogenesis. Our recent report (Chen et al. 2015 Nature Medicine) further identified a role for histone acetylation in DOT1L dependent gene expression driven by MLL-fusion proteins including MEIS1 and HOXA cluster genes. A first-in-human Phase I clinical trial demonstrated clinical activi

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David Chen, Chun-Wei, Amit U. Sinha, Jun Qi, et al. "Genome-Wide RNAi Screen Identifies The Mechanistic Role For DOT1L In MLL-Rearranged Leukemia." Blood 122, no. 21 (2013): 598. http://dx.doi.org/10.1182/blood.v122.21.598.598.

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Abstract Rearrangement of Mixed-Lineage Leukemia (MLL) gene defines a genetically distinguishable subset of aggressive leukemias with poor prognosis. Recent studies exhibit promising activity of small-molecule inhibitors of the H3K79 methyltransferase DOT1L (disruptor of telomeric silencing-1 like) against leukemias bearing MLL-translocations (Daigle et. al. 2011 Cancer Cell). However, the mechanisms underlying the epigenetic addiction of MLL-fusion oncogenic program to H3K79-methylation remain unclear. A number of labs have recently shown the expression of MLL-fusion target genes including HO

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Byun, Woong Sub, Gyu Ho Lee, Hyeung-geun Park, and Sang Kook Lee. "Inhibition of DOT1L by Half-Selenopsammaplin A Analogs Suppresses Tumor Growth and EMT-Mediated Metastasis in Triple-Negative Breast Cancer." Pharmaceuticals 14, no. 1 (2020): 18. http://dx.doi.org/10.3390/ph14010018.

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Due to a lack of hormone receptors, current treatment strategies for triple-negative breast cancer (TNBC) are limited with frequent disease recurrence and metastasis. Recent findings have suggested that aberrant methylation of histone H3 lysine 79 residue (H3K79me) by the histone methyltransferase disruptor of telomeric silencing 1-like (DOT1L) is a potential therapeutic target for TNBC clinical management. Therefore, we developed DOT1L inhibitors as potential antitumor agents against TNBC cells. We reveal that a synthetic half-selenopsammaplin A analog 9l (subsequently known as 9l) exhibited

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Liu, Chaohua, Qiaoyan Yang, Qian Zhu, et al. "CBP mediated DOT1L acetylation confers DOT1L stability and promotes cancer metastasis." Theranostics 10, no. 4 (2020): 1758–76. http://dx.doi.org/10.7150/thno.39013.

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Park, Geunyeong, Zihua Gong, Junjie Chen, and Ja-Eun Kim. "Characterization of the DOT1L Network: Implications of Diverse Roles for DOT1L." Protein Journal 29, no. 3 (2010): 213–23. http://dx.doi.org/10.1007/s10930-010-9242-8.

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Nassa, Giovanni, Annamaria Salvati, Roberta Tarallo та ін. "Inhibition of histone methyltransferase DOT1L silences ERα gene and blocks proliferation of antiestrogen-resistant breast cancer cells". Science Advances 5, № 2 (2019): eaav5590. http://dx.doi.org/10.1126/sciadv.aav5590.

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Breast cancer (BC) resistance to endocrine therapy results from constitutively active or aberrant estrogen receptor α (ERα) signaling, and ways to block ERα pathway in these tumors are sought after. We identified the H3K79 methyltransferase DOT1L as a novel cofactor of ERα in BC cell chromatin, where the two proteins colocalize to regulate estrogen target gene transcription. DOT1L blockade reduces proliferation of hormone-responsive BC cells in vivo and in vitro, consequent to cell cycle arrest and apoptotic cell death, with widespread effects on ER-dependent gene transcription, including ERα

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Lonetti, Annalisa, Valentina Indio, Maria Antonella Laginestra, et al. "Inhibition of Methyltransferase DOT1L Sensitizes to Sorafenib Treatment AML Cells Irrespective of MLL-Rearrangements: A Novel Therapeutic Strategy for Pediatric AML." Cancers 12, no. 7 (2020): 1972. http://dx.doi.org/10.3390/cancers12071972.

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Pediatric acute myeloid leukemia (AML) is an aggressive malignancy with poor prognosis for which there are few effective targeted approaches, despite the numerous genetic alterations, including MLL gene rearrangements (MLL-r). The histone methyltransferase DOT1L is involved in supporting the proliferation of MLL-r cells, for which a target inhibitor, Pinometostat, has been evaluated in a clinical trial recruiting pediatric MLL-r leukemic patients. However, modest clinical effects have been observed. Recent studies have reported that additional leukemia subtypes lacking MLL-r are sensitive to D

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Riedel, Simone, Jessica Haladyna, Brett Stevens, et al. "Meningeoma-1 Cooperates with MLL and DOT1L to Induce Leukemia." Blood 126, no. 23 (2015): 2428. http://dx.doi.org/10.1182/blood.v126.23.2428.2428.

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Abstract Meningioma-1 (MN1) is frequently overexpressed in AML, and associated with a poor prognosis. In addition, MN1-TEL fusions are found in AML, underscoring the importance and possible driver function of MN1 in AML. Forced expression of MN1 in murine hematopoietic progenitors induces a highly aggressive leukemia as a single hit. The mechanism by which MN1 induces AML is unclear. MN1 is a transcriptional co-activator with almost no sequence or structural similarity to any other protein, and no targeted approaches to MN1-high AML are currently available. We sought to understand the mechanis

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Chen, Liying, Aniruddha J. Deshpande, Deepti Banka, et al. "Abrogation of MLL-AF10 and CALM-AF10 Mediated Transformation Through Genetic Inactivation or Pharmacological Inhibition of the H3K79 Methyltransferase DOT1L." Blood 120, no. 21 (2012): 2384. http://dx.doi.org/10.1182/blood.v120.21.2384.2384.

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Abstract Abstract 2384 The t(10;11)(p12;q23) and the t(10;11)(p12;q14), which encode the MLL-AF10 and CALM-AF10 fusion oncoproteins respectively, are two recurrent chromosomal rearrangements observed in patients with acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL). Patients with AML harboring either MLL-AF10 or CALM-AF10 rearrangements have a particularly poor outcome compared to patients whose leukemia cells do not harbor these translocations. Thus new therapeutic approaches are clearly needed for patients with leukemias bearing rearrangements of the AF10 gene. Previous st

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Kwesi-Maliepaard, Eliza Mari, Muhammad Assad Aslam, Mir Farshid Alemdehy, et al. "The histone methyltransferase DOT1L prevents antigen-independent differentiation and safeguards epigenetic identity of CD8+T cells." Proceedings of the National Academy of Sciences 117, no. 34 (2020): 20706–16. http://dx.doi.org/10.1073/pnas.1920372117.

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Cytotoxic T cell differentiation is guided by epigenome adaptations, but how epigenetic mechanisms control lymphocyte development has not been well defined. Here we show that the histone methyltransferase DOT1L, which marks the nucleosome core on active genes, safeguards normal differentiation of CD8+T cells. T cell-specific ablation ofDot1Lresulted in loss of naïve CD8+T cells and premature differentiation toward a memory-like state, independent of antigen exposure and in a cell-intrinsic manner. Mechanistically, DOT1L controlled CD8+T cell differentiation by ensuring normal T cell receptor d

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Rau, Rachel E., Benjamin A. Rodriguez, Min Luo, et al. "DOT1L as a therapeutic target for the treatment of DNMT3A-mutant acute myeloid leukemia." Blood 128, no. 7 (2016): 971–81. http://dx.doi.org/10.1182/blood-2015-11-684225.

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Key Points Data from Dnmt3a−/− mice implicate Dot1l as a critical mediator of the malignant gene expression program of Dnmt3a-mediated leukemia. Pharmacologic inhibition of DOT1L exerts potent antileukemic activity in DNMT3A-mutant human acute myeloid leukemia in vitro and in vivo.

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Geng, Jingping, Xiangli Guo, Lidan Wang, et al. "Intracellular Delivery of DNA and Protein by a Novel Cell-Permeable Peptide Derived from DOT1L." Biomolecules 10, no. 2 (2020): 217. http://dx.doi.org/10.3390/biom10020217.

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Cellular uptake and intracellular release efficiency of biomacromolecules is low because of hurdles in the cell membrane that result in limited access to intra-cellular targets with few functional effects. Cell-penetrating peptides (CPPs) act as cargo delivery vehicles to promote therapeutic molecule translocation. Here, we describe the novel CPP-Dot1l that not only penetrates by itself, but also mediates cargo translocation in cultured cells, as confirmed by fluorescence microscopy and fluorescence spectrophotometry. We conducted cytotoxicity assays and safety evaluations, and determined pept

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Thomas, Tim. "DOT1L in prostate cancer." Nature Reviews Urology 17, no. 10 (2020): 544. http://dx.doi.org/10.1038/s41585-020-0374-0.

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Kingsley, Molly C., Simone Stefanie Riedel, Hongbo Michael Xie, Sally P. Stabler, Taylor Pastuer, and Kathrin M. Bernt. "Tight Regulation of H3K79 Methylation Levels in KMT2A-Rearranged AML." Blood 132, Supplement 1 (2018): 3884. http://dx.doi.org/10.1182/blood-2018-99-114784.

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Abstract Rationale: KMT2A-rearrangements (KMT2A-r) in acute myeloid leukemia (AML), encompassing both KMT2a-fusions (KMT2A-F) and KMT2A-partial tandem duplications (KMT2A-PTD), represent a subgroup of AML with a particularly poor prognosis. Both KMT2A-F and KMT2A-PTD share a dependency on the H3K79 methyltransferase DOT1L for proper histone 3 lysine 79 dimethylation (H3K79me2) on target genes such as HOXA9 and MEIS1. Pharmacologic inhibition of DOT1L results in downregulation of KMT2A fusion/PTD target genes. Albeit rare, complete responses observed in patients with relapsed/refractory KMT2A-r

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Deshpande, Aniruddha J., Liying Chen, Maurizio Fazio, et al. "MLL-AF6 Mediated Transformation Is Dependent On the H3K79 Methyl-transferase Dot1l." Blood 120, no. 21 (2012): 3502. http://dx.doi.org/10.1182/blood.v120.21.3502.3502.

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Abstract Abstract 3502 The t(6;11)(q27;q23) produces a chimeric MLL-AF6 oncogene, and is a recurrent chromosomal rearrangement observed in patients with diverse hematologic malignancies such as acute myelogenous leukemia (AML), as well as both B-cell and T-cell acute lymphoblastic leukemias (ALL). The presence of an MLL-AF6 translocation predicts a particularly poor prognosis. Of particular biological interest, the MLL-AF6 translocation is the most common fusion event in which MLL fuses to a predominantly cytoplasmic protein. Very little is known about the molecular mechanisms of transformatio

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Xu, Jie, Wu Zhang, Xiaojing Yan, et al. "NPM1 Mutation Contributes to Hematological Dysfunction By Disrupting H3K79 Methylation." Blood 128, no. 22 (2016): 2702. http://dx.doi.org/10.1182/blood.v128.22.2702.2702.

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Abstract NPM1 is one of the most frequent acquired mutated genes in acute myeloid leukemia (AML). Previous studies have shown that NPM1 mutation (NPMc+) established the distinctive gene expression signatures, which were associated with mixed lineage leukemia (MLL)-target genes, like MEIS1 and HOXA cluster. In AML carrying MLL fusion-oncoproteins, DOT1L-mediated histone 3 lysine 79 (H3K79) methylation is implicated in the regulation of MLL-target genes. Compared with MLL abnormalities, NPM1 variants preserve the similar transcriptional characteristics. However, whether NPM1 mutation could affec

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Bon, Corentin, Yang Si, Melanie Pernak, et al. "Synthesis and Biological Activity of a Cytostatic Inhibitor of MLLr Leukemia Targeting the DOT1L Protein." Molecules 26, no. 17 (2021): 5300. http://dx.doi.org/10.3390/molecules26175300.

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Histone methyltransferase DOT1L catalyzes mono-, di- and trimethylation of histone 3 at lysine residue 79 (H3K79) and hypermethylation of H3K79 has been linked to the development of acute leukemias characterized by the MLL (mixed-lineage leukemia) rearrangements (MLLr cells). The inhibition of H3K79 methylation inhibits MLLr cells proliferation, and an inhibitor specific for DOT1L, pinometostat, was in clinical trials (Phase Ib/II). However, the compound showed poor pharmacological properties. Thus, there is a need to find new potent inhibitors of DOT1L for the treatment of rearranged leukemia

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Dickins, Ross A. "Rerouting DOT1L inhibitors in leukemia." Blood 136, no. 17 (2020): 1900–1901. http://dx.doi.org/10.1182/blood.2020007352.

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Soria-Valles, Clara, Fernando G. Osorio, and Carlos López-Otín. "Reprogramming aging through DOT1L inhibition." Cell Cycle 14, no. 21 (2015): 3345–46. http://dx.doi.org/10.1080/15384101.2015.1093443.

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Barve, Vega, Shah, et al. "Perturbation of Methionine/S-adenosylmethionine Metabolism as a Novel Vulnerability in MLL Rearranged Leukemia." Cells 8, no. 11 (2019): 1322. http://dx.doi.org/10.3390/cells8111322.

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Leukemias bearing mixed lineage leukemia (MLL) rearrangement (MLL-R) resulting in expression of oncogenic MLL fusion proteins (MLL-FPs) represent an especially aggressive disease subtype with the worst overall prognoses and chemotherapeutic response. MLL-R leukemias are uniquely dependent on the epigenetic function of the H3K79 methyltransferase DOT1L, which is misdirected by MLL-FPs activating gene expression, driving transformation and leukemogenesis. Given the functional necessity of these leukemias to maintain adequate methylation potential allowing aberrant activating histone methylation

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