Epithelial cell-specific loss of function of <i>Miz1</i> causes a spontaneous COPD-like phenotype and up-regulates <i>Ace2</i> expression in mice.-论文-万方医学网

作者： Hanh Chi,Do-Umehara ^[1] ; Cong,Chen ^[2] ; Qiao,Zhang ^[2] ; Alexander V,Misharin ^[2] ; Hiam,Abdala-Valencia ^[2] ; S Marina,Casalino-Matsuda ^[2] ; Paul A,Reyfman ^[2] ; Kishore R,Anekalla ^[2] ; Francisco J,Gonzalez-Gonzalez ^[2] ; Marc A,Sala ^[2] ; Chao,Peng ^[3] ; Ping,Wu ^[3] ; Catherine C L,Wong ^[4] ; Ravi,Kalhan ^[2] ; Ankit,Bharat ^[2] ; Harris,Perlman ^[5] ; Karen M,Ridge ^[6] ; Jacob I,Sznajder ^[2] ; Peter H S,Sporn ^[2] ; Navdeep S,Chandel ^[2] ; Jindan,Yu ^[7] ; Xiangdong,Fu ^[2] ; Irina,Petrache ^[8] ; Rubin,Tuder ^[9] ; G R Scott,Budinger ^[10] ; Jing,Liu ^[11]

作者单位： Department of Surgery, College of Medicine and University of Illinois Cancer Center, University of Illinois at Chicago, Chicago, IL 60612, USA. ^[1] Division of Pulmonary and Critical Care Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ^[2] National Facility for Protein Science in Shanghai, Zhangjiang Lab, SARI, CAS, Shanghai 201210, China. ^[3] Peking University School of Pharmaceutical Science, Beijing 100191, China. ^[4] Division of Thoracic Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. ^[5] Division of Rheumatology, Northwestern University Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ^[6] Jesse Brown Veterans Affairs Medical Center, Chicago, IL 60612, USA. ^[7] Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ^[8] Department of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093-0651, USA; Institute of Genomic Medicine, University of California, San Diego, La Jolla, CA 92093-0651, USA. ^[9] National Jewish Health, 1400 Jackson Street, Molly Blank Building, J203, Denver, CO 80206, USA. ^[10] University of Colorado at Denver Health Sciences Center, Department of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Denver, CO 80206, USA. ^[11]

主题词动物(Animals);冠状病毒感染(Coronavirus Infections);上皮细胞(Epithelial Cells);基因敲除技术(Gene Knockout Techniques);人类(Humans);Kruppel样转录因子类(Kruppel-Like Transcription Factors);肺(Lung);小鼠(Mice);小鼠, 近交C57BL(Mice, Inbred C57BL);小鼠, 基因敲除(Mice, Knockout);疾病大流行(Pandemics);肽基二肽酶A(Peptidyl-Dipeptidase A);表型(Phenotype);肺炎, 病毒性(Pneumonia, Viral);活化STAT的蛋白抑制物(Protein Inhibitors of Activated STAT);肺疾病, 慢性阻塞性(Pulmonary Disease, Chronic Obstructive);信号传导(Signal Transduction);吸烟(Smoking);转录因子RelA(Transcription Factor RelA);泛素蛋白连接酶类(Ubiquitin-Protein Ligases);增量调节(Up-Regulation)

DOI 10.1126/sciadv.abb7238

PMID 32851183

发布时间 2024-04-28

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Epithelial cell-specific loss of function of <i>Miz1</i> causes a spontaneous COPD-like phenotype and up-regulates <i>Ace2</i> expression in mice.

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Epithelial cell-specific loss of function of <i>Miz1</i> causes a spontaneous COPD-like phenotype and up-regulates <i>Ace2</i> expression in mice.

Science advances

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Science advances

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