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Strategies that regulate LSD1 for novel therapeutics

Acta Pharmaceutica Sinica B 2024年第4期14卷 1494-1507页

作者： Meng Li Mengge Dai Bing Cheng Shaotong Li Enhui Guo Junwei Fu Ting Ma Bin Yu School of Pharmaceutical Sciences&Key Laboratory of Advanced Drug Preparation Technologies Ministry of EducationZhengzhou UniversityZhengzhou 450001China College of Chemistry Zhengzhou UniversityZhengzhou 450001China Tianjian Laboratory of Advanced Biomedical Sciences Institute of Advanced Biomedical SciencesZhengzhou UniversityZhengzhou 450000China Pingyuan Laboratory State Key Laboratory of Antiviral DrugsHenan Normal UniversityXinxiang 453007China State Key Laboratory of Pharmaceutical Biotechnology Nanjing UniversityNanjing 210023China

Histone methylation plays crucial roles in regulating chromatin structure and gene transcrip-tion in epigenetic modifications.Lysine-specific demethylase 1(LSD1),the first identified histone de-methylase,is universally overexpressed in various diseases.LSD1 dysregulation is closely associated with cancer,viral infections,and neurodegenerative diseases,etc.,making it a promising therapeutic target.Several LSD1 inhibitors and two small-molecule degraders(UM171 and BEA-17)have entered the clinical stage.LSD1 can remove methyl groups from histone 3 at lysine 4 or lysine 9(H3K4 or H3K9),resulting in either transcription repression or activation.While the roles of LSD1 in transcrip-tional regulation are well-established,studies have revealed that LSDl can also be dynamically regulated by other factors.For example,the expression or activity of LSD1 can be regulated by many proteins that form transcriptional corepressor complexes with LSD1.Moreover,some post-transcriptional modifica-tions and cellular metabolites can also regulate LSD1 expression or its demethylase activity.Therefore,in this review,we will systematically summarize how proteins involved in the transcriptional corepressor complex,various post-translational modifications,and metabolites act as regulatory factors for LSD1 ac-tivity.

关键词： LSD1 regulation transcription repression transcription activation the Corepressor complex Post-transcriptional modifications Metabolites

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H19通过干扰hnRNP U-actin复合物抑制RNA聚合酶Ⅱ介导的转录

H19通过干扰hnRNP U-actin复合物抑制RNA聚合酶Ⅱ介导的转录

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第十二次全国医学遗传学学术会议

作者：毕海珊袁继行杨富王芳孙树汉第二军医大学医学遗传学教研室

Background & Aims:H19 is one of the earliest identified and studied long noncoding RNAs.It is presumed that H19 is essential for regulating development and disease conditions,and is associated with ca

关键词： CTD phosphorylation EU incorporation H19 hnRNP U transcription repression

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Zinc finger protein DPZF promotes TLR-triggered innate immunity by repressing IkBa gene transcription in macrophages

Zinc finger protein DPZF promotes TLR-triggered innate immun...

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第九届全国免疫学学术大会

作者： Xingguang Liu Peng Zhang Qian Zhang Zhenzhen Zhan Jun Meng Nan Li Xuetao Cao National Key Laboratory of Medical Immunology & Institute of Immunology Second Military Medical University

Background:The ability of the innate immune system to recognize and eliminate invading microbial pathogens has been largely attributed to Toll-like receptors(TLRs)and TLR-triggered immune response.Although many factors mediate the transduction of TLR signals,the molecular mechanisms involved in the full activation of TLR-triggered innate immunity remain to be fully elucidated.Dendritic cell-derived BTB/POZ zinc finger(DPZF)also named as HOF and ZNF288,belongs to BTB/POZ(broad complex tramtrack bric-a-brac/poxvirus and zinc finger)zinc finger family.DPZF was found to participate in neurogenesis and function as a key transcription repressor of alpha-fetoprotein gene in liver.However,the roles of DPZF in immune system remain unknown.Method:Myeloid cell-specific DPZF knockout mice were generated by repeated mating of DPZFmice with LysMcre mice.The endotoxin shock mouse model was established by intraperitoneal(i.p.)injection of 15 mg/kg LPS.For bacterial infection,mice were given intraperitoneal injection of 1 x 10’E.coli or intravenous injection of 1×10L.monocytogenes.Chromatin was immunoprecipitated according to the toinstructions instructions of the EZ ChIP kit.Results:Here we generated myeloid cell-specific DPZF knockout mice by the LysM-Cre/loxP approach and found these mice were resistant to endotoxin shock and Escherichia co//’-caused sepsis.DPZF deficiency attenuated the TLRtriggered production of proinflammatory’cytokines and type I interferon in macrophages,which attributed to the higher abundance of IkBa and impaired activity of the transcription factor NF-kB.Futhermore,chromatin immunoprecipitation(ChIP)-sequence assay showed that DPZF specifically bound to IkBa gene promoter(+1 to+60 region)after TLR activation.We found that DPZF was a transcriptional repressor capable of specifically inhibiting IkBa promoter-driven transcriptional activity.Therefore,DPZF functions a key regulator governing IkBa gene transcription,inhibits IkBa protein expression and enhances NF-kB activation,which leading to enhanced TLR

关键词： DPZF Toll-like receptor IkBa transcription repression Innate immunity

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