Clinical case of proteasome-associated autoinflammatory syndrome-2 (PRAAS2)
暂无分享,去创建一个
E. Viktorova | N. Kuzmenko | V. Burlakov | A. Kozlova | E. Raikina | D. Konovalov | V. Zaharova | A. Terentieva | J. Rodina
[1] E. Krüger,et al. Novel proteasome assembly chaperone mutations in PSMG2/PAC2 cause the autoinflammatory interferonopathy CANDLE/PRAAS4. , 2019, The Journal of allergy and clinical immunology.
[2] Lisa T. Emrick,et al. Heterozygous Truncating Variants in POMP Escape Nonsense-Mediated Decay and Cause a Unique Immune Dysregulatory Syndrome. , 2018, American journal of human genetics.
[3] U. Pannicke,et al. MCM3AP and POMP Mutations Cause a DNA‐Repair and DNA‐Damage‐Signaling Defect in an Immunodeficient Child , 2016, Human mutation.
[4] E. Remmers,et al. Erratum: Additive loss-of-function proteasome subunit mutations in CANDLE/PRAAS patients promote type i IFN production (Journal of Clinical Investigation (2015) 125:11 (4196-4211) DOI: 10.1172/JCI81260) , 2016 .
[5] E. Remmers,et al. Additive loss-of-function proteasome subunit mutations in CANDLE/PRAAS patients promote type I IFN production. , 2015, The Journal of clinical investigation.
[6] N. Dahl,et al. siRNA Silencing of Proteasome Maturation Protein (POMP) Activates the Unfolded Protein Response and Constitutes a Model for KLICK Genodermatosis , 2012, PloS one.
[7] Neha Tiwari,et al. A single-nucleotide deletion in the POMP 5' UTR causes a transcriptional switch and altered epidermal proteasome distribution in KLICK genodermatosis. , 2010, American journal of human genetics.