M
Massimo Gadina
Researcher at National Institutes of Health
Publications - 125
Citations - 17441
Massimo Gadina is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Janus kinase & Cytokine. The author has an hindex of 51, co-authored 113 publications receiving 14198 citations. Previous affiliations of Massimo Gadina include Queen's University Belfast.
Papers
More filters
Journal ArticleDOI
Germline mutations in the extracellular domains of the 55 kda tnf receptor, tnfr1, define a family of dominantly inherited autoinflammatory syndromes
Michael F. McDermott,Ivona Aksentijevich,Jérôme Galon,Elizabeth M. McDermott,B. William Ogunkolade,Michael Centola,Elizabeth Mansfield,Massimo Gadina,Leena Karenko,Tom Pettersson,John McCarthy,David M. Frucht,Martin Aringer,Yelizaveta Torosyan,Anna-Maija Teppo,Meredith Wilson,H.Mehmet Karaarslan,Ying Wan,Ian Todd,Geryl Wood,Ryan Schlimgen,Thisum R. Kumarajeewa,Sheldon M. Cooper,John P. Vella,Christopher I. Amos,John C. Mulley,Kathleen A. Quane,Michael G. Molloy,Annamari Ranki,Richard J. Powell,Graham A. Hitman,John J. O'Shea,Daniel L. Kastner +32 more
TL;DR: It is proposed that the autoinflammatory phenotype results from impaired downregulation of membrane TNFR1 and diminished shedding of potentially antagonistic soluble receptor inTNFR1-associated periodic syndromes.
Journal ArticleDOI
Cytokine signaling in 2002: new surprises in the Jak/Stat pathway.
TL;DR: This review focuses on recent advances in the field and highlights some of the most active areas of Jak-Stat pathway research.
Journal ArticleDOI
The JAK-STAT Pathway: Impact on Human Disease and Therapeutic Intervention*
John J. O'Shea,Daniella M. Schwartz,Alejandro V. Villarino,Massimo Gadina,Iain B. McInnes,Arian Laurence +5 more
TL;DR: The Janus kinase (JAK)-signal transducer of activators of transcription (STAT) pathway is now recognized as an evolutionarily conserved signaling pathway employed by diverse cytokines, interferons, growth factors, and related molecules.
Journal ArticleDOI
Activated STING in a Vascular and Pulmonary Syndrome
Yongmei Liu,A Almeida de Jesus,B Marrero,Dan Yang,Suzanne E. Ramsey,Suzanne E. Ramsey,G.A. Montealegre Sanchez,Klaus Tenbrock,Klaus Tenbrock,Helmut Wittkowski,Helmut Wittkowski,Olcay Y. Jones,Olcay Y. Jones,Hye Sun Kuehn,Chyi-Chia Richard Lee,Michael A. DiMattia,Edward W. Cowen,Benito Gonzalez,Ira Palmer,J.J. DiGiovanna,Angelique Biancotto,H. Kim,Wanxia L. Tsai,Anna M. Trier,Yhu Chering Huang,Deborah L. Stone,S Hill,Hanna Kim,C. St. Hilaire,Shakuntala Gurprasad,Nicole Plass,D. Chapelle,Iren Horkayne-Szakaly,Iren Horkayne-Szakaly,Dirk Foell,Dirk Foell,Andrei Barysenka,Andrei Barysenka,Fabio Candotti,Steven M. Holland,Jason D. Hughes,Jason D. Hughes,Huseyin Mehmet,Huseyin Mehmet,Andrew C. Issekutz,Andrew C. Issekutz,Mark Raffeld,Joshua J McElwee,Joshua J McElwee,Joseph R. Fontana,Caterina P. Minniti,Susan Moir,Daniel L. Kastner,Massimo Gadina,A.C. Steven,Paul T. Wingfield,Stephen R. Brooks,Sofia Rosenzweig,Thomas A. Fleisher,Zuoming Deng,Manfred Boehm,Amy S. Paller,Amy S. Paller,Raphaela Goldbach-Mansky +63 more
TL;DR: STING-associated vasculopathy with onset in infancy (SAVI) is an autoinflammatory disease caused by gain-of-function mutations in TMEM173, the stimulator of interferon genes (STING), andConstitutive up-regulation of phosphorylated STAT1 in patients' lymphocytes was reduced by JAK inhibitors.
Journal ArticleDOI
An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist
Ivona Aksentijevich,Seth L. Masters,Polly J. Ferguson,Paul Dancey,Joost Frenkel,Annet van Royen-Kerkhoff,R. M. Laxer,Ulf Tedgård,Edward W. Cowen,Tuyet-Hang Pham,Matthew G. Booty,Jacob D. Estes,Netanya G. Sandler,Nicole Plass,Deborah L. Stone,Maria L. Turner,Suvimol Hill,John A. Butman,Rayfel Schneider,Paul Babyn,Hatem El-Shanti,Elena Pope,Karyl S. Barron,Xinyu Bing,Arian Laurence,Chyi-Chia Richard Lee,Dawn Chapelle,Gillian I. Clarke,Kamal Ohson,Marc Nicholson,Massimo Gadina,Barbara Yang,Benjamin D. Korman,Peter K. Gregersen,P. Martin van Hagen,A. Elisabeth Hak,Marjan Huizing,Proton Rahman,Daniel C. Douek,Elaine F. Remmers,Daniel L. Kastner,Raphaela Goldbach-Mansky +41 more
TL;DR: The term deficiency of the interleukin-1-receptor antagonist, or DIRA, is proposed to denote this autosomal recessive autoinflammatory disease caused by mutations affecting IL1RN, resulting in life-threatening systemic inflammation with skin and bone involvement.