Additive loss-of-function proteasome subunit mutations in CANDLE/PRAAS patients promote type I IFN production-Reference-Cited by-同舟云学术

Additive loss-of-function proteasome subunit mutations in CANDLE/PRAAS patients promote type I IFN production

Published:2015-10-20 Issue:11 Volume:125 Page:4196-4211
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:

Author:

Brehm Anja,Liu Yin,Sheikh Afzal,Marrero Bernadette,Omoyinmi Ebun,Zhou Qing,Montealegre Gina,Biancotto Angelique,Reinhardt Adam,Almeida de Jesus Adriana,Pelletier Martin,Tsai Wanxia L.,Remmers Elaine F.,Kardava Lela,Hill Suvimol,Kim Hanna,Lachmann Helen J.,Megarbane Andre,Chae Jae Jin,Brady Jilian,Castillo Rhina D.,Brown Diane,Casano Angel Vera,Gao Ling,Chapelle Dawn,Huang Yan,Stone Deborah,Chen Yongqing,Sotzny Franziska,Lee Chyi-Chia Richard,Kastner Daniel L.,Torrelo Antonio,Zlotogorski Abraham,Moir Susan,Gadina Massimo,McCoy Phil,Wesley Robert,Rother Kristina,Hildebrand Peter W.,Brogan Paul,Krüger Elke,Aksentijevich Ivona,Goldbach-Mansky Raphaela

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Reference46 articles.

1. Autoinflammatory Disease Reloaded: A Clinical Perspective

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3. PSMB8 Encoding the β5i Proteasome Subunit Is Mutated in Joint Contractures, Muscle Atrophy, Microcytic Anemia, and Panniculitis-Induced Lipodystrophy Syndrome

4. Proteasome assembly defect due to a proteasome subunit beta type 8 (PSMB8) mutation causes the autoinflammatory disorder, Nakajo-Nishimura syndrome

5. A mutation in the immunoproteasome subunit PSMB8 causes autoinflammation and lipodystrophy in humans

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