Tamara Manuelian

TL;DR: In this article, three mutations (E1172Stop, R1210C, and R1215G) were identified in the C-terminal region of the complement regulator factor H and each of the three mutations caused reduced binding to the central complement component C3b/C3d.

TL;DR: Two novel complement resistance mechanisms of ovarian tumour cells are revealed: production of factor H-like protein and factor H andSecretion of soluble membrane cofactor protein could protect ovarian tumours against humoral immune attack and pose an obstacle for therapy with monoclonal antibodies.

TL;DR: A novel protective and anti‐inflammatory role of the two important complement regulators FHL‐1 and factor H in rheumatoid arthritis is shown and a disease controlling role of these two proteins is suggested.

TL;DR: Factor H is a 150 kDa single-chain plasma glycoprotein that plays a pivotal role in the regulation of the alternative pathway of complement as mentioned in this paper, and has been associated with susceptibility to Hemolytic Uremic Syndrome (HUS), a disease consisting of microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure, caused by platelet thrombi which mainly, but not exclusively, form in the microcirculation of the kidney.

TL;DR: Recent genetic and biochemical data indicate a critical role for factor H in the pathogenesis of HUS and suggest an important role of the most C-terminal domain, i.e. SCR 20, in the disease.