The University of Tokyo · Medicine
Professor Shinsuke Yasuda's research lab focuses on the molecular and immunological mechanisms underlying autoimmune and thrombotic disorders, particularly systemic lupus erythematosus (SLE) and antiphiphospholipid syndrome (APS). The lab investigates genetic and post-translational modifications of key proteins such as RasGRP1 and beta(2)-glycoprotein I (beta(2)-GPI), exploring their roles in immune cell signaling and autoantibody development. Recent work also examines novel therapeutic targets, such as GLP-1 receptor agonists, for autoimmune myopathies. The lab integrates molecular biology, immunology, and translational research to identify biomarkers and develop innovative treatments for autoimmune and thrombotic diseases.
Figures are computed from collected data and may differ slightly.
Dysregulation of Ras guanyl nucleotide-releasing protein 1 (RasGRP1) in mice results in a systemic lupus erythematosus (SLE)-like disorder. We therefore looked for defective isoforms and/or diminished levels of human RasGRP1 in a cohort of SLE patients. PBMCs were collected from twenty healthy individuals and thirty-two patients with SLE. mRNA was isolated and five RasGRP1 cDNAs from each subject were sequenced. T cell lysates from healthy controls and SLE patients also were evaluated for their
BEta(2)-glycoprotein I (beta(2)-GPI) is proteolytically cleaved by plasmin in domain V (nicked beta(2)-GPI), being unable to bind to phospholipids. This cleavage may occur in vivo and elevated plasma levels of nicked beta(2)-GPI were detected in patients with massive plasmin generation and fibrinolysis turnover. In this study, we report higher prevalence of elevated ratio of nicked beta(2)-GPI against total beta(2)-GPI in patients with ischemic stroke (63%) and healthy subjects with lacunar infa
The Val(247) beta(2)GPI allele was associated with both a high frequency of anti-beta(2)GPI antibodies and stronger reactivity with anti-beta(2)GPI antibodies compared with the Leu(247) beta(2)GPI allele, suggesting that the Val(247) beta(2)GPI allele may be one of the genetic risk factors for development of APS.
GLP-1R agonist could be a novel therapy for PM that recovers muscle weakness and suppresses muscle inflammation through inhi biting muscle fibre necroptosis.
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