|1.||Hill, Anita: 2 articles (09/2013 - 11/2012)|
|2.||Hillmen, Peter: 2 articles (09/2013 - 01/2004)|
|3.||Bessler, M: 2 articles (10/2001 - 09/2001)|
|4.||Keller, P: 2 articles (10/2001 - 09/2001)|
|5.||Tao, Shandong: 1 article (01/2015)|
|6.||Chen, Yue: 1 article (01/2015)|
|7.||Song, Lixiao: 1 article (01/2015)|
|8.||Deng, Yuan: 1 article (01/2015)|
|9.||Yu, Liang: 1 article (01/2015)|
|10.||Canalejo, K: 1 article (04/2014)|
|1.||Paroxysmal Hemoglobinuria (Paroxysmal Nocturnal Hemoglobinuria)
11/01/1999 - "PIGA is somatically mutated in blood cells from patients with paroxysmal nocturnal hemoglobinuria (PNH), leading to deficiency of GPI-linked proteins on the cell surface. "
10/01/1998 - "The PIG-A mutation and absence of glycosylphosphatidylinositol-linked proteins do not confer resistance to apoptosis in paroxysmal nocturnal hemoglobinuria."
09/25/1998 - "The identification of CD59-mediated signaling events may help explain why paroxysmal nocturnal hemoglobinuria patients, who are deficient in glycosylphosphatidylinositol-linked proteins including CD59, are susceptible to proliferative disorders."
04/01/2014 - "Paroxysmal nocturnal hemoglobinuria (PNH) is a hemolytic, clonal and acquired disorder of the hematopoietic stem cell with a deficiency of all glycophosphatidyl-inositol (GPI) linked proteins. "
09/12/2013 - "In paroxysmal nocturnal hemoglobinuria (PNH), hematopoietic cells lacking glycosylphosphatidylinositol (GPI)-linked proteins on their surface (GPI(neg)) exist alongside normal (GPI+) cells. "
06/01/2002 - "These animals have a discrete proportion of blood cells devoid of GPI-linked proteins, and although not anemic, they have evidence of hemolysis. "
01/01/2001 - "Absence of GPI-linked proteins from the surface of blood cells is characteristic of the PIG-A mutant (PNH) clone and is also accountable fo certain manifestations, such as intravascular hemolysis. "
01/01/2015 - "Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hematopoietic stem cell (HSC) disorder arising from a somatic mutation of the X-linked phosphatidylinositol glycan complementation class A gene (PIG-A) which leads to partial or complete deficiency of glycosyl-phosphatidylinositol (GPI)-linked membrane proteins and causes intravascular hemolysis. "
11/25/2008 - "Paroxysmal nocturnal hemoglobinuria is an acquired hematopoietic stem cell (HSC) disorder characterized by the partial or complete deficiency of glycosyl-phosphatidylinositol (GPI)-linked membrane proteins, which leads to intravascular hemolysis. "
11/01/2012 - "However, in patients with PNH, these 2 proteins, along with numerous other GPI-linked proteins, are absent from the cell surface of red cells, granulocytes, monocytes, and platelets, resulting in complement-mediated intravascular hemolysis and other complications. "
01/01/2004 - "In Section I, Dr. Peter Hillmen outlines the recent findings in the pathogenesis of paroxysmal nocturnal hemoglobinuria (PNH), relating the biochemical defect (the lack of glycosylphosphatidylinositol [GPI]-linked proteins on the cell surface) to the clinical manifestations, particularly hemolysis (and its effects) and thrombosis. "
07/01/2007 - "PNH clones then fail to generate glycosylphosphatidylinositol (GPI) or to express a series of GPI-linked membrane proteins including complement-regulatory proteins, resulting in complement-mediated intravascular hemolysis and thrombosis. "
|5.||Rare Diseases (Rare Disease)
|2.||Proteins (Proteins, Gene)
|3.||Complement System Proteins (Complement)
|4.||Scavenger Receptors (Scavenger Receptor)
|5.||Monomeric GTP-Binding Proteins
|6.||GTP-Binding Proteins (G-Protein)