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LSD1

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https://www.readbyqxmd.com/read/29765516/selective-dissociation-between-lsd1-and-gfi1b-by-a-lsd1-inhibitor-ncd38-induces-the-activation-of-erg-super-enhancer-in-erythroleukemia-cells
#1
Ryusuke Yamamoto, Masahiro Kawahara, Shinji Ito, Junko Satoh, Goichi Tatsumi, Masakatsu Hishizawa, Takayoshi Suzuki, Akira Andoh
Lysine-specific demethylase 1 (LSD1) is a histone modifier for transcriptional repression involved in the regulation of hematopoiesis. We previously reported that a LSD1 inhibitor NCD38 induces transdifferentiation from erythroid lineage to granulomonocytic lineage and exerts anti-leukemia effect through de-repression of the specific super-enhancers of hematopoietic regulators including ERG in a human erythroleukemia cell line, HEL. However, the mechanistic basis for this specificity of NCD38 has remained unclear...
April 20, 2018: Oncotarget
https://www.readbyqxmd.com/read/29760584/lsd1-inhibition-attenuates-androgen-receptor-v7-splice-variant-activation-in-castration-resistant-prostate-cancer-models
#2
Sergio Regufe da Mota, Sarah Bailey, Rosemary A Strivens, Annette L Hayden, Leon R Douglas, Patrick J Duriez, M Teresa Borrello, Hanae Benelkebir, A Ganesan, Graham Packham, Simon J Crabb
Background: Castrate resistant prostate cancer (CRPC) is often driven by constitutively active forms of the androgen receptor such as the V7 splice variant (AR-V7) and commonly becomes resistant to established hormonal therapy strategies such as enzalutamide as a result. The lysine demethylase LSD1 is a co-activator of the wild type androgen receptor and a potential therapeutic target in hormone sensitive prostate cancer. We evaluated whether LSD1 could also be therapeutically targeted in CRPC models driven by AR-V7...
2018: Cancer Cell International
https://www.readbyqxmd.com/read/29749504/lsd1-negatively-regulates-autophagy-through-the-mtor-signaling-pathway-in-ovarian-cancer-cells
#3
Ye Wei, Tiantian Han, Ranran Wang, Jing Wei, Ke Peng, Qiong Lin, Genbao Shao
Lysine-specific demethylase 1 (LSD1) plays a key role in cell proliferation, differentiation and carcinogenesis. In the present study we revealed that LSD1 functioned as an autophagy suppressor in ovarian cancer HO8910 cells. Pharmacological inhibition or genetic knockdown of LSD1 resulted in the elevation of the LC3‑II protein, enhancement of autophagosomal formation and stimulation of the autophagic flux. In addition, knockdown of LSD1 further promoted the serum starvation- and rapamycin-induced autophagy...
May 10, 2018: Oncology Reports
https://www.readbyqxmd.com/read/29741645/lsd1-coordinates-with-the-sin3a-hdac-complex-and-maintains-sensitivity-to-chemotherapy-in-breast-cancer
#4
Yang Yang, Wei Huang, Rongfang Qiu, Ruiqiong Liu, Yi Zeng, Jie Gao, Yu Zheng, Yongqiang Hou, Shuang Wang, Wenqian Yu, Shuai Leng, Dandan Feng, Yan Wang
Lysine-specific demethylase 1 (LSD1) was the first histone demethylase identified as catalysing the removal of mono- and di-methylation marks on histone H3-K4. Despite the potential broad action of LSD1 in transcription regulation, recent studies indicate that LSD1 may coordinate with multiple epigenetic regulatory complexes including CoREST/HDAC complex, NuRD complex, SIRT1, and PRC2, implying complicated mechanistic actions of this seemingly simple enzyme. Here, we report that LSD1 is also an integral component of the SIN3A/HDAC complex...
May 7, 2018: Journal of Molecular Cell Biology
https://www.readbyqxmd.com/read/29734782/design-synthesis-and-in-vitro-evaluation-of-novel-histone-h3-peptide-based-lsd1-inactivators-incorporating-%C3%AE-%C3%AE-disubstituted-amino-acids-with-%C3%AE-turn-inducing-structures
#5
Yosuke Ota, Taeko Kakizawa, Yukihiro Itoh, Takayoshi Suzuki
Lysine-specific demethylase 1 (LSD1) mainly removes methyl groups of mono- or di-methylated lysine residues at the fourth position of histone H3 to epigenetically regulate the expression of genes associated with several diseases, such as cancer. Therefore, LSD1 inactivators are expected to be used as therapeutic agents. In this study, to identify novel peptide-based LSD1 inactivators, we focused on the X-ray structure of LSD1 complexed with a H3 peptide-based suicide substrate. It has been proposed that a methylated histone substrate forms three consecutive γ-turn structures in the active pocket of LSD1...
May 6, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29709037/correction-histone-demethylase-lsd1-restricts-influenza-a-virus-infection-by-erasing-ifitm3-k88-monomethylation
#6
Jiaoyu Shan, Binbin Zhao, Zhao Shan, Jia Nie, Rong Deng, Rui Xiong, Andy Tsun, Weiqi Pan, Hanzhi Zhao, Ling Chen, Ying Jin, Zhikang Qian, Kawing Lui, Rui Liang, Dan Li, Bing Sun, Dimitri Lavillette, Ke Xu, Bin Li
[This corrects the article DOI: 10.1371/journal.ppat.1006773.].
April 2018: PLoS Pathogens
https://www.readbyqxmd.com/read/29707403/histone-demethylase-lsd1-regulates-bone-mass-by-controlling-wnt7b-and-bmp2-signaling-in-osteoblasts
#7
Jun Sun, Joerg Ermann, Ningning Niu, Guang Yan, Yang Yang, Yujiang Shi, Weiguo Zou
Multiple regulatory mechanisms control osteoblast differentiation and function to ensure unperturbed skeletal formation and remodeling. In this study we identify histone lysine-specific demethylase 1(LSD1/KDM1A) as a key epigenetic regulator of osteoblast differentiation. Knockdown of LSD1 promoted osteoblast differentiation of human mesenchymal stem cells (hMSCs) in vitro and mice lacking LSD1 in mesenchymal cells displayed increased bone mass secondary to accelerated osteoblast differentiation. Mechanistic in vitro studies revealed that LSD1 epigenetically regulates the expression of WNT7B and BMP2...
2018: Bone Research
https://www.readbyqxmd.com/read/29704660/genetic-and-epigenetic-control-of-adipose-development
#8
REVIEW
Olga Gulyaeva, Jon Dempersmier, Hei Sook Sul
White adipose tissue (WAT) is the primary energy storage organ and its excess contributes to obesity, while brown adipose tissue (BAT) and inducible thermogenic (beige/brite) adipocytes in WAT dissipate energy via Ucp1 to maintain body temperature. BAT and subcutaneous WAT develop perinatally while visceral WAT forms after birth from precursors expressing distinct markers, such as Myf5, Pref-1, Wt1, and Prx1, depending on the anatomical location. In addition to the embryonic adipose precursors, a pool of endothelial cells or mural cells expressing Pparγ, Pdgfrβ, Sma and Zfp423 may become adipocytes during WAT expansion in adults...
April 25, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29691401/methylated-dnmt1-and-e2f1-are-targeted-for-proteolysis-by-l3mbtl3-and-crl4-dcaf5-ubiquitin-ligase
#9
Feng Leng, Jiekai Yu, Chunxiao Zhang, Salvador Alejo, Nam Hoang, Hong Sun, Fei Lu, Hui Zhang
Many non-histone proteins are lysine methylated and a novel function of this modification is to trigger the proteolysis of methylated proteins. Here, we report that the methylated lysine 142 of DNMT1, a major DNA methyltransferase that preserves epigenetic inheritance of DNA methylation patterns during DNA replication, is demethylated by LSD1. A novel methyl-binding protein, L3MBTL3, binds the K142-methylated DNMT1 and recruits a novel CRL4DCAF5 ubiquitin ligase to degrade DNMT1. Both LSD1 and PHF20L1 act primarily in S phase to prevent DNMT1 degradation by L3MBTL3-CRL4DCAF5 ...
April 24, 2018: Nature Communications
https://www.readbyqxmd.com/read/29666280/lsd1-a-single-target-to-combat-lineage-plasticity-in-lethal-prostate-cancer
#10
Leigh Ellis, Massimo Loda
No abstract text is available yet for this article.
April 16, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29642935/sp1-induced-upregulation-of-lncrna-spry4-it1-exerts-oncogenic-properties-by-scaffolding-ezh2-lsd1-dnmt1-and-sponging-mir-101-3p-in-cholangiocarcinoma
#11
Yi Xu, Yue Yao, Xingming Jiang, Xiangyu Zhong, Zhidong Wang, Chunlong Li, Pengcheng Kang, Kaiming Leng, Daolin Ji, Zhenglong Li, Lining Huang, Wei Qin, Yunfu Cui
BACKGROUND: Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) behave as a novel class of transcription products during multiple cancer processes. However, the mechanisms responsible for their alteration in cholangiocarcinoma (CCA) are not fully understood. METHODS: The expression of SPRY4-IT1 in CCA tissues and cell lines was determined by RT-qPCR, and the association between SPRY4-IT1 transcription and clinicopathologic features was analyzed...
April 11, 2018: Journal of Experimental & Clinical Cancer Research: CR
https://www.readbyqxmd.com/read/29618057/lsd1-mediates-metabolic-reprogramming-by-glucocorticoids-during-myogenic-differentiation
#12
Kotaro Anan, Shinjiro Hino, Noriaki Shimizu, Akihisa Sakamoto, Katsuya Nagaoka, Ryuta Takase, Kensaku Kohrogi, Hirotaka Araki, Yuko Hino, Shingo Usuki, Shinya Oki, Hirotoshi Tanaka, Kimitoshi Nakamura, Fumio Endo, Mitsuyoshi Nakao
The metabolic properties of cells are formed under the influence of environmental factors such as nutrients and hormones. Although such a metabolic program is likely initiated through epigenetic mechanisms, the direct links between metabolic cues and activities of chromatin modifiers remain largely unknown. In this study, we show that lysine-specific demethylase-1 (LSD1) controls the metabolic program in myogenic differentiation, under the action of catabolic hormone, glucocorticoids. By using transcriptomic and epigenomic approaches, we revealed that LSD1 bound to oxidative metabolism and slow-twitch myosin genes, and repressed their expression...
March 29, 2018: Nucleic Acids Research
https://www.readbyqxmd.com/read/29616052/the-role-of-programmed-cell-death-regulator-lsd1-in-nematode-induced-syncytium-formation
#13
Mateusz Matuszkiewicz, Miroslaw Sobczak, Javier Cabrera, Carolina Escobar, Stanislaw Karpiński, Marcin Filipecki
Cyst-forming plant-parasitic nematodes are common pests of many crops. They inject secretions into host cells to induce the developmental and metabolic reprogramming that leads to the formation of a syncytium, which is the sole food source for growing nematodes. As in other host-parasite models, avirulence leads to rapid and local programmed cell death (PCD) known as the hypersensitive response (HR), whereas in the case of virulence, PCD is still observed but is limited to only some cells. Several regulators of PCD were analyzed to understand the role of PCD in compatible plant-nematode interactions...
2018: Frontiers in Plant Science
https://www.readbyqxmd.com/read/29610759/molecular-signature-of-the-imprintosome-complex-at-the-mating-type-locus-in-fission-yeast
#14
Célia Raimondi, Bernd Jagla, Caroline Proux, Hervé Waxin, Serge Gangloff, Benoit Arcangioli
Genetic and molecular studies have indicated that an epigenetic imprint at mat1 , the sexual locus of fission yeast, initiates mating type switching. The polar DNA replication of mat1 generates an imprint on the Watson strand. The process by which the imprint is formed and maintained through the cell cycle remains unclear. To understand better the mechanism of imprint formation and stability, we characterized the recruitment of early players of mating type switching at the mat1 region. We found that the switch activating protein 1 (Sap1) is preferentially recruited inside the mat1M allele on a sequence ( SS13 ) that enhances the imprint...
January 16, 2018: Microbial Cell
https://www.readbyqxmd.com/read/29606613/far-upstream-element-binding-protein-1-regulates-lsd1-alternative-splicing-to-promote-terminal-differentiation-of-neural-progenitors
#15
Inah Hwang, Dongqing Cao, Yoonmi Na, Do-Yeon Kim, Tuo Zhang, Jun Yao, Hwanhee Oh, Jian Hu, Hongwu Zheng, Yu Yao, Jihye Paik
Loss of a cell's ability to terminally differentiate because of mutations is a selected genetic event in tumorigenesis. Genomic analyses of low-grade glioma have reported recurrent mutations of far upstream element-binding protein 1 (FUBP1). Here, we show that FUBP1 expression is dynamically regulated during neurogenesis and that its downregulation in neural progenitors impairs terminal differentiation and promotes tumorigenesis collaboratively with expression of IDH1R132H . Mechanistically, collaborative action between SRRM4 and FUBP1 is necessary for mini-exon splicing of the neurospecific LSD1+8a isoform...
March 21, 2018: Stem Cell Reports
https://www.readbyqxmd.com/read/29593255/stress-induced-phosphoprotein-1-acts-as-a-scaffold-protein-for-glycogen-synthase-kinase-3-beta-mediated-phosphorylation-of-lysine-specific-demethylase-1
#16
Chia-Lung Tsai, An-Shine Chao, Shih-Ming Jung, Chiao-Yun Lin, Angel Chao, Tzu-Hao Wang
Stress-induced phosphoprotein 1 (STIP1)-a co-chaperone of heat shock proteins-promotes cell proliferation and may act as an oncogenic factor. Similarly, glycogen synthase kinase-3 beta (GSK3β)-mediated phosphorylation of lysine-specific demethylase 1 (LSD1)-an epigenetic regulator-can contribute to the development of an aggressive cell phenotype. Owing to their ability to tether different molecules into functional complexes, scaffold proteins have a key role in the regulation of different signaling pathways in tumorigenesis...
March 29, 2018: Oncogenesis
https://www.readbyqxmd.com/read/29590629/enhancer-activation-by-pharmacologic-displacement-of-lsd1-from-gfi1-induces-differentiation-in-acute-myeloid-leukemia
#17
Alba Maiques-Diaz, Gary J Spencer, James T Lynch, Filippo Ciceri, Emma L Williams, Fabio M R Amaral, Daniel H Wiseman, William J Harris, Yaoyong Li, Sudhakar Sahoo, James R Hitchin, Daniel P Mould, Emma E Fairweather, Bohdan Waszkowycz, Allan M Jordan, Duncan L Smith, Tim C P Somervaille
Pharmacologic inhibition of LSD1 promotes blast cell differentiation in acute myeloid leukemia (AML) with MLL translocations. The assumption has been that differentiation is induced through blockade of LSD1's histone demethylase activity. However, we observed that rapid, extensive, drug-induced changes in transcription occurred without genome-wide accumulation of the histone modifications targeted for demethylation by LSD1 at sites of LSD1 binding and that a demethylase-defective mutant rescued LSD1 knockdown AML cells as efficiently as wild-type protein...
March 27, 2018: Cell Reports
https://www.readbyqxmd.com/read/29588287/fanconi-anemia-fancm-fncm-1-and-fancd2-fcd-2-are-required-for-maintaining-histone-methylation-levels-and-interact-with-the-histone-demethylase-lsd1-spr-5-in-caenorhabditis-elegans
#18
Hyun-Min Kim, Sara E Beese-Sims, Monica P Colaiácovo
The histone demethylase LSD1 was originally discovered as removing methyl groups from di- and monomethylated histone H3 lysine 4 (H3K4me2/1). Several studies suggest LSD1 plays roles in meiosis as well as in the epigenetic regulation of fertility given that in its absence there is evidence of a progressive accumulation of H3K4me2 and increased sterility through generations. In addition to the progressive sterility phenotype observed in the mutants, growing evidence for the importance of histone methylation in the regulation of DNA damage repair has attracted more attention to the field in recent years...
March 27, 2018: Genetics
https://www.readbyqxmd.com/read/29581704/targeting-histone-demethylase-lsd1-kdm1a-in-neurodegenerative-diseases
#19
Susanna Ambrosio, Barbara Majello
The autophagy-lysosome pathway sustains cellular homeostasis and is a protective mechanism against neurodegenerative diseases. Recent findings highlight the role of the histone demethylases LSD1/LDM1A as a pivotal regulator of autophagy process, by controlling the mTORC1 cascade, in neuroblastoma cells. LSD1 binds to the promoter region of the SESN2 gene, where LSD1-mediated demethylation leads to the accumulation of repressive histone marks that maintain SESN2 expression at low levels. LSD1 depletion results in enhanced SESN2 expression and consequently mTORC1 inhibition, thereby triggering the induction of autophagy...
2018: Journal of Experimental Neuroscience
https://www.readbyqxmd.com/read/29581250/lsd1-activates-a-lethal-prostate-cancer-gene-network-independently-of-its-demethylase-function
#20
Archana Sehrawat, Lina Gao, Yuliang Wang, Armand Bankhead, Shannon K McWeeney, Carly J King, Jacob Schwartzman, Joshua Urrutia, William H Bisson, Daniel J Coleman, Sunil K Joshi, Dae-Hwan Kim, David A Sampson, Sheila Weinmann, Bhaskar V S Kallakury, Deborah L Berry, Reina Haque, Stephen K Van Den Eeden, Sunil Sharma, Jared Bearss, Tomasz M Beer, George V Thomas, Laura M Heiser, Joshi J Alumkal
Medical castration that interferes with androgen receptor (AR) function is the principal treatment for advanced prostate cancer. However, clinical progression is universal, and tumors with AR-independent resistance mechanisms appear to be increasing in frequency. Consequently, there is an urgent need to develop new treatments targeting molecular pathways enriched in lethal prostate cancer. Lysine-specific demethylase 1 (LSD1) is a histone demethylase and an important regulator of gene expression. Here, we show that LSD1 promotes the survival of prostate cancer cells, including those that are castration-resistant, independently of its demethylase function and of the AR...
May 1, 2018: Proceedings of the National Academy of Sciences of the United States of America
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