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Natalie Deuitch
Researcher at National Institutes of Health
Publications - 31
Citations - 1269
Natalie Deuitch is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Medicine & Proinflammatory cytokine. The author has an hindex of 10, co-authored 20 publications receiving 563 citations. Previous affiliations of Natalie Deuitch include Stanford University & University of North Carolina at Chapel Hill.
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Journal ArticleDOI
Somatic Mutations in UBA1 and Severe Adult-Onset Autoinflammatory Disease.
David B. Beck,Marcela A. Ferrada,Keith A. Sikora,Amanda K. Ombrello,Jason C. Collins,Wuhong Pei,Nicholas Balanda,Daron L. Ross,Daniela Ospina Cardona,Zhijie Wu,Bhavisha A Patel,Kalpana Manthiram,Emma M. Groarke,Fernanda Gutierrez-Rodrigues,Patrycja Hoffmann,Sofia Rosenzweig,Shuichiro Nakabo,Laura W. Dillon,Christopher S. Hourigan,Wanxia L. Tsai,Sarthak Gupta,Carmelo Carmona-Rivera,Anthony J. Asmar,Lisha Xu,Hirotsugu Oda,Wendy Goodspeed,Karyl S. Barron,Michele Nehrebecky,Anne Jones,Ryan S. Laird,Natalie Deuitch,Dorota Rowczenio,Emily Rominger,Kristina V. Wells,Chyi-Chia Richard Lee,Weixin Wang,Megan Trick,James C. Mullikin,Gustaf Wigerblad,Stephen R. Brooks,Stefania Dell'Orso,Zuoming Deng,Jae Jin Chae,Alina Dulau-Florea,May Christine V. Malicdan,Danica Novacic,Robert A. Colbert,Mariana J. Kaplan,Massimo Gadina,Sinisa Savic,Helen J. Lachmann,Mones Abu-Asab,Benjamin D. Solomon,Kyle Retterer,William A. Gahl,Shawn M. Burgess,Ivona Aksentijevich,Neal S. Young,Katherine R. Calvo,Achim Werner,Daniel L. Kastner,Peter C. Grayson +61 more
TL;DR: Using a genotype-driven approach, this disorder is identified that connects seemingly unrelated adult-onset inflammatory syndromes and is named the VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome.
Journal ArticleDOI
Biallelic hypomorphic mutations in a linear deubiquitinase define otulipenia, an early-onset autoinflammatory disease
Qing Zhou,Xiaomin Yu,Erkan Demirkaya,Natalie Deuitch,Deborah L. Stone,Wanxia Li Tsai,Hye Sun Kuehn,Hongying Wang,Dan Yang,Yong Hwan Park,Amanda K. Ombrello,Mary Blake,Tina Romeo,Elaine F. Remmers,Jae Jin Chae,James C. Mullikin,Ferhat Guzel,Joshua D. Milner,Manfred Boehm,Sergio D. Rosenzweig,Massimo Gadina,Steven B. Welch,Seza Ozen,Rezan Topaloglu,Mario Abinun,Daniel L. Kastner,Ivona Aksentijevich +26 more
TL;DR: An autoinflammatory disease caused by loss-of-function mutations in OTULIN (FAM105B), encoding a deubiquitinase with linear linkage specificity is reported, adding to the emerging spectrum of human diseases caused by defects in the ubiquitin pathway and suggests a role for targeted cytokine therapies.
Journal ArticleDOI
A dominant autoinflammatory disease caused by non-cleavable variants of RIPK1
Panfeng Tao,Jinqiao Sun,Zheming Wu,Shihao Wang,Jun Wang,Wanjin Li,Heling Pan,Renkui Bai,Jiahui Zhang,Ying Wang,Pui Y. Lee,Wenjing Ying,Qinhua Zhou,Jia Hou,Wenjie Wang,Bijun Sun,Mi Yang,Danru Liu,Ran Fang,Huan Han,Zhaohui Yang,Xin Huang,Haibo Li,Natalie Deuitch,Yuan Zhang,Dilan Dissanayake,Katrina Haude,Kirsty McWalter,Chelsea Roadhouse,Jennifer MacKenzie,Jennifer MacKenzie,Ronald M. Laxer,Ivona Aksentijevich,Xiaomin Yu,Xiaochuan Wang,Junying Yuan,Qing Zhou,Qing Zhou +37 more
TL;DR: Two families with variants in RIPK1 (D324V and D324H) that lead to distinct symptoms of recurrent fevers and lymphadenopathy in an autosomal-dominant manner are identified andRIPK1 mutations that prevent caspase-8 cleavage sensitize cells to apoptosis, necroptosis and inflammation are identified.
Journal ArticleDOI
Treatment Strategies for Deficiency of Adenosine Deaminase 2.
Amanda K. Ombrello,Jing Qin,Patrycja Hoffmann,Parag Kumar,Deborah L. Stone,Anne Jones,Tina Romeo,Beverly K. Barham,Gineth Pinto-Patarroyo,Camilo Toro,Ariane Soldatos,Qing Zhou,Natalie Deuitch,Ivona Aksentijevich,Sherry L. Sheldon,Susan J. Kelly,Ada Man,Karyl S. Barron,Michael S. Hershfield,Willy A. Flegel,Daniel L. Kastner +20 more
TL;DR: In a series of 15 patients with a deficiency of adenosine deaminase 2, a genetic disease, early-onset lacunar stroke and TNF Inhibition, patients were diagnosed with atypical central giant cell granuloma.
Journal ArticleDOI
Aberrant tRNA processing causes an autoinflammatory syndrome responsive to TNF inhibitors.
Angeliki Giannelou,Hongying Wang,Qing Zhou,Yong Hwan Park,Mones Abu-Asab,Kris Ylaya,Deborah L. Stone,Anna Sediva,Rola Sleiman,Lucie Sramkova,Deepika Bhatla,Elisavet Serti,Wanxia Li Tsai,Dan Yang,Kevin Bishop,Blake Carrington,Wuhong Pei,Natalie Deuitch,Stephen R. Brooks,Jehad H. Edwan,Sarita Joshi,Seraina Prader,Daniela Kaiser,William Owen,Abdullah Al Sonbul,Yu Zhang,Julie E. Niemela,Shawn M. Burgess,Manfred Boehm,Barbara Rehermann,JaeJin Chae,Martha Quezado,Amanda K. Ombrello,Rebecca H. Buckley,A. Grom,Elaine F. Remmers,Jana M. Pachlopnik,Helen C. Su,Gustavo Gutierrez-Cruz,Stephen M. Hewitt,Raman Sood,Kimberly A. Risma,Katherine R. Calvo,Sergio D. Rosenzweig,Massimo Gadina,Markus Hafner,Hong-Wei Sun,Daniel L. Kastner,Ivona Aksentijevich +48 more
TL;DR: Characterise the clinical features, immune manifestations and molecular mechanisms in a recently described autoinflammatory disease caused by mutations in TRNT1, a tRNA processing enzyme, and to explore the use of cytokine inhibitors in suppressing the inflammatory phenotype.