The University of Tokyo · 의학
Shinsuke Yasuda 교수의 연구실은 자가면역질환, 특히 시스템성 레우마티스성 질환과 관련된 분자 기전을 규명하는 데 초점을 맞추고 있습니다. RasGRP1의 기능 이상이 레우마티스성 관절염 및 홍반성 낭포성 홍반성 피부염과 유사한 병태생리학적 변화를 유도할 수 있음을 밝혀내었으며, beta(2)-GPI의 단백질 가공형태와 유전적 다형성이 항체 생성 및 혈전성 질환 위험에 미치는 영향을 연구하고 있습니다. 또한 GLP-1 수용체 작용제가 근육염과 근육 위축을 개선하는 새로운 치료 전략이 될 수 있음을 제시하며, 염증 반응과 세포 사멸 경로를 타겟으로 한 약물 개발에도 기여하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
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.
