Relevant bibliographies by topics / Complexo LSD1/CoREST

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Academic literature on the topic 'Complexo LSD1/CoREST'

Author: Grafiati
Published: 4 September 2021
Last updated: 29 July 2025

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Journal articles on the topic "Complexo LSD1/CoREST"

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Ladaika, Christopher A., Ahmed H. Ghobashi, William C. Boulton, and Heather M. O'Hagan. "Abstract 1690: LSD1 and CoREST2 demethylate STAT3 to promote enteroendocrine cell differentiation in mucinous colorectal cancer." Cancer Research 84, no. 6_Supplement (2024): 1690. http://dx.doi.org/10.1158/1538-7445.am2024-1690.

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Abstract Across different cancer types, tumor heterogeneity has been shown to drive tumor progression, metastasis, and therapeutic resistance. Adenocarcinoma to neuroendocrine lineage transition is an emergent mechanism of targeted therapy resistance in several cancer types, including lung and prostate cancer. Therefore, understanding the dynamics and mechanisms driving neuroendocrine cell fates in cancer is critical. Mucinous colorectal cancer accounts for upwards of 20% of colorectal cancer cases and is characterized by tumors with mucous accounting for at least 50% of the tumor volume. The
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Fiskus, Warren, Christopher Peter Mill, Christine Birdwell, et al. "Pre-Clinical Efficacy of Co-Targeting GFI1/KDM1A and BRD4 or JAK1/2 Against AML and Post-MPN Secondary AML Blast Progenitor Cells." Blood 136, Supplement 1 (2020): 27. http://dx.doi.org/10.1182/blood-2020-140212.

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Transcriptional regulators (TFs) involved in cell-growth, differentiation and survival of AML stem/progenitor cells (LSCs) include RUNX1, PU.1, CEBPα, c-Myb and c-Myc. LSD1 (KDM1A) is an FAD-dependent amine-oxidase that demethylates mono and dimethyl histone H3 lysine 4 (H3K4Me1 and H3K4Me2). LSD1 is part of the repressor complexes involving GFI1, CoREST and HDAC1/2, that regulate active super-enhancers/enhancers (SEs/Es) and their target genes, mediating transcriptional repression and differentiation block in LSCs. GFI1 is a zinc-finger transcriptional repressor involved in AML development an
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Foster, Charles T., Oliver M. Dovey, Larissa Lezina, et al. "Lysine-Specific Demethylase 1 Regulates the Embryonic Transcriptome and CoREST Stability." Molecular and Cellular Biology 30, no. 20 (2010): 4851–63. http://dx.doi.org/10.1128/mcb.00521-10.

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ABSTRACT Lysine-specific demethylase 1 (LSD1), which demethylates mono- and dimethylated histone H3-Lys4 as part of a complex including CoREST and histone deacetylases (HDACs), is essential for embryonic development in the mouse beyond embryonic day 6.5 (e6.5). To determine the role of LSD1 during this early period of embryogenesis, we have generated loss-of-function gene trap mice and conditional knockout embryonic stem (ES) cells. Analysis of postimplantation gene trap embryos revealed that LSD1 expression, and therefore function, is restricted to the epiblast. Conditional deletion of LSD1 i
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Haase, Rebecca, Andrew Groves, Hafsa Mire, Jun Qi, and Mariella Filbin. "DIPG-53. LSD1 DEGRADATION SYNERGIZES WITH HDAC INHIBITION IN PEDIATRIC H3K27M DIFFUSE MIDLINE GLIOMA." Neuro-Oncology 25, Supplement_1 (2023): i25. http://dx.doi.org/10.1093/neuonc/noad073.100.

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Abstract H3K27M-mutated diffuse midline glioma (H3K27M DMG) is an aggressive, lethal pediatric brain tumor which resists conventional cancer treatments. To identify new therapeutic targets, our lab executed a focused CRISPR negative selection screen in patient-derived H3K27M cell lines after treatment with the histone deacetylase (HDAC) inhibitor panobinostat, and discovered a strong co-dependence with the histone demethylase LSD1. We further explored the therapeutic potential of this synergistic interaction with a screen of HDAC- and LSD1- targeting drugs to identify synergistic combinations,
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Subramaniam, Agatheeswaran, Kristijonas Žemaitis, Mehrnaz Safaee Talkhoncheh, et al. "Lysine-specific demethylase 1A restricts ex vivo propagation of human HSCs and is a target of UM171." Blood 136, no. 19 (2020): 2151–61. http://dx.doi.org/10.1182/blood.2020005827.

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Abstract Culture conditions in which hematopoietic stem cells (HSCs) can be expanded for clinical benefit are highly sought after. Here, we report that inhibition of the epigenetic regulator lysine-specific histone demethylase 1A (LSD1) induces a rapid expansion of human cord blood–derived CD34+ cells and promotes in vitro propagation of long-term repopulating HSCs by preventing differentiation. The phenotype and molecular characteristics of cells treated with LSD1 inhibitors were highly similar to cells treated with UM171, an agent promoting expansion of HSCs through undefined mechanisms and
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Barnes, Claire E., David M. English, Megan Broderick, Mark O. Collins, and Shaun M. Cowley. "Proximity-dependent biotin identification (BioID) reveals a dynamic LSD1–CoREST interactome during embryonic stem cell differentiation." Molecular Omics 18, no. 1 (2022): 31–44. http://dx.doi.org/10.1039/d1mo00236h.

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Barnes, Claire E., David M. English, Megan Broderick, Mark O. Collins, and Shaun M. Cowley. "Proximity-dependent biotin identification (BioID) reveals a dynamic LSD1–CoREST interactome during embryonic stem cell differentiation." Molecular Omics 18, no. 1 (2022): 31–44. http://dx.doi.org/10.1039/d1mo00236h.

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8

Groves, Andrew, Rebecca Poetschke, Hafsa Mire, et al. "DIPG-26. Targeted Protein Degradation of LSD1 synergizes with HDAC inhibitors in Diffuse Intrinsic Pontine Glioma." Neuro-Oncology 24, Supplement_1 (2022): i24. http://dx.doi.org/10.1093/neuonc/noac079.083.

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Abstract Diffuse intrinsic pontine glioma (DIPG) remains one of the most lethal brain tumors in all of childhood with no effective treatments besides radiation, which only extends survival a few months. Against this backdrop, our lab recently executed a focused CRISPR negative selection screen in DIPG cell lines after treatment with the histone deacetylase (HDAC) inhibitor panobinostat and discovered a strong co-dependence with the histone demethylase LSD1. To further explore the therapeutic potential of this synergistic interaction, we tested a drug library of HDAC- and LSD1- targeting drugs
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9

Gu, Haidong, and Bernard Roizman. "Engagement of the Lysine-Specific Demethylase/HDAC1/CoREST/REST Complex by Herpes Simplex Virus 1." Journal of Virology 83, no. 9 (2009): 4376–85. http://dx.doi.org/10.1128/jvi.02515-08.

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ABSTRACT Among the early events in herpes simplex virus 1 replication are localization of ICP0 in ND10 bodies and accumulation of viral DNA-protein complexes in structures abutting ND10. ICP0 degrades components of ND10 and blocks silencing of viral DNA, achieving the latter by dislodging HDAC1 or -2 from the lysine-specific demethylase 1 (LSD1)/CoREST/REST repressor complex. The role of this process is apparent from the observation that a dominant-negative CoREST protein compensates for the absence of ICP0 in a cell-dependent fashion. HDAC1 or -2 and the CoREST/REST complex are independently
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Wasson, Christopher W., Esther Perez Barreiro, Francesco Del Galdo, and Natalia A. Riobo-Del Galdo. "Lysine Demethylase 1 Has Demethylase-Dependent and Non-Canonical Functions in Myofibroblast Activation in Systemic Sclerosis." Cells 14, no. 6 (2025): 433. https://doi.org/10.3390/cells14060433.

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Systemic sclerosis (SSc) is an autoimmune disease of unknown aetiology characterised by vasculopathy with progressive fibrosis of the skin and internal organs. Tissue fibrosis is driven by activated fibroblasts (myofibroblasts) with exacerbated contractile and secretory properties. We previously reported that the long non-coding RNA HOTAIR is a key driver of SSc fibroblast activation. HOTAIR interacts with the chromatin modifiers, the polycomb repressor complex (PRC2) and coREST complex, promoting expression of pro-fibrotic genes. In this study, we show that acute activation of dermal fibrobla
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Dissertations / Theses on the topic "Complexo LSD1/CoREST"

1

Santos, Ana Raquel Pereira. "The role of LSD1/CoREST during hemogenic reprogramming." Master's thesis, 2018. http://hdl.handle.net/10316/82432.

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Dissertação de Mestrado em Investigação Biomédica apresentada à Faculdade de Medicina<br>As células estaminais hematopoiéticas (HSCs) são capazes de se auto-renovar e diferenciar em todos os tipos de células sanguíneas. Estas características fazem com que a transplantação de HSCs seja o principal tratamento contra doenças hematológicas. A incompatibilidade entre dador-paciente e o número insuficiente de HSCs que são obtidas para transplantação limitam o sucesso deste tipo de terapia celular. De forma a ultrapassar estas limitações, a expansão destas células in vitro seria a solução, mas este p
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