14-3-3 η ETA protein as a potential marker of joint damage in gout.

[1]  Lingjiang Zhu,et al.  Recent Insights Into the Role of Macrophages in Acute Gout , 2022, Frontiers in Immunology.

[2]  Qian Wang,et al.  Distinct macrophage polarization in acute and chronic gout , 2022, Laboratory Investigation.

[3]  A. Reiff,et al.  Prevalence and significance of serum 14–3-3η in juvenile idiopathic arthritis , 2021, Pediatric Rheumatology.

[4]  T. Moore,et al.  14-3-3η Protein as a Potential Biomarker in Juvenile Idiopathic Arthritis , 2021, Pediatric reports.

[5]  C. Ottmann,et al.  14-3-3 Modulation of the Inflammatory Response. , 2020, Pharmacological research.

[6]  B. Mo,et al.  Diagnostic accuracy of 14‐3‐3 η protein in rheumatoid arthritis: A meta‐analysis , 2020, International journal of rheumatic diseases.

[7]  Le Shi,et al.  Matrix Metalloproteinase-3 induces proteoglycan degradation in gouty arthritis model. , 2020, Gene.

[8]  A. Marotta,et al.  14-3-3η Protein in serum and synovial fluid correlates with radiographic damage and progression in a longitudinal evaluation of patients with established rheumatoid arthritis , 2020, Modern rheumatology.

[9]  N. Hammam,et al.  Serum 14-3-3η protein is associated with clinical and serologic features of Sjögren’s syndrome in patients with systemic lupus erythematosus: a cross-sectional analysis , 2020, Clinical Rheumatology.

[10]  Lin-feng Xie,et al.  Association between musculoskeletal ultrasonography and bone remodelling markers and its role in disease monitoring of gout and hyperuricaemia. , 2019, Clinical and Experimental Rheumatology.

[11]  Y. Sertdemir,et al.  Importance of 14-3-3eta, anti-CarP, and anti-Sa in the diagnosis of seronegative rheumatoid arthritis , 2019, Turkish journal of medical sciences.

[12]  Zhi Li,et al.  Mean Platelet Volume: A Novel Predictor for Bone Erosion in Gouty Arthritis? , 2019, Annals of Clinical and Laboratory Science.

[13]  C. Malemud Inhibition of MMPs and ADAM/ADAMTS. , 2019, Biochemical pharmacology.

[14]  Hyon K. Choi,et al.  Contemporary Prevalence of Gout and Hyperuricemia in the United States and Decadal Trends: The National Health and Nutrition Examination Survey, 2007–2016 , 2019, Arthritis & rheumatology.

[15]  R. Cordtz,et al.  Secular trends in the incidence and prevalence of gout in Denmark from 1995 to 2015: a nationwide register-based study. , 2019, Rheumatology.

[16]  Yanping Han,et al.  Blocking Matrix Metalloproteinase-9 Abrogates Collagen-Induced Arthritis via Inhibiting Dendritic Cell Migration , 2018, The Journal of Immunology.

[17]  Ji‐Won Kim,et al.  Prevalence and incidence of gout in Korea: data from the national health claims database 2007–2015 , 2017, Rheumatology International.

[18]  Xiaofeng Li,et al.  The Immunological Basis in the Pathogenesis of Gout. , 2017, Iranian journal of immunology : IJI.

[19]  Yuqiong Liang,et al.  Traditional Chinese Medicine Formula "Xiaofeng granules" suppressed gouty arthritis animal models and inhibited the proteoglycan degradation on chondrocytes induced by monosodium urate. , 2016, Journal of ethnopharmacology.

[20]  Li-Dong Wu,et al.  Trichostatin A increases the TIMP-1/MMP ratio to protect against osteoarthritis in an animal model of the disease , 2016, Molecular medicine reports.

[21]  M. Boers,et al.  A prospective cohort study of 14-3-3η in ACPA and/or RF-positive patients with arthralgia , 2016, Arthritis Research & Therapy.

[22]  I. Reid,et al.  Path Analysis Identifies Receptor Activator of Nuclear Factor-κB Ligand, Osteoprotegerin, and Sclerostin as Potential Mediators of the Tophus-bone Erosion Relationship in Gout , 2016, The Journal of Rheumatology.

[23]  A. Ogdie,et al.  2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative , 2015, Annals of the rheumatic diseases.

[24]  C. Allaart,et al.  14-3-3η is a novel mediator associated with the pathogenesis of rheumatoid arthritis and joint damage , 2014, Arthritis Research & Therapy.

[25]  M. Doherty,et al.  Rising burden of gout in the UK but continuing suboptimal management: a nationwide population study , 2014, BDJ.

[26]  P. Tak,et al.  SAT0309 Serum 14-3-3 ETA: An independent biomarker associated with joint damage in psoriatic arthritis , 2013 .

[27]  D. Seelow,et al.  Faulty initiation of proteoglycan synthesis causes cardiac and joint defects. , 2011, American journal of human genetics.

[28]  W. Taylor,et al.  Validation of a radiographic damage index in chronic gout. , 2007, Arthritis and rheumatism.

[29]  A. Aitken,et al.  Detection of high levels of 2 specific isoforms of 14-3-3 proteins in synovial fluid from patients with joint inflammation. , 2007, The Journal of rheumatology.

[30]  J Günter Grossmann,et al.  Structural basis for protein–protein interactions in the 14-3-3 protein family , 2006, Proceedings of the National Academy of Sciences.

[31]  T. Pawson,et al.  Proteomic, Functional, and Domain-Based Analysis of In Vivo 14-3-3 Binding Proteins Involved in Cytoskeletal Regulation and Cellular Organization , 2004, Current Biology.

[32]  G. Burmester,et al.  Macrophages in rheumatoid arthritis , 2000, Arthritis research.