Related Experiment Video
Updated: Feb 10, 2026

Isolation of CD133+ Liver Stem Cells for Clonal Expansion
Published on: October 10, 2011
Clonal expansion mechanisms in paroxysmal nocturnal hemoglobinuria
1Center for Infectious Disease Education and Research, The University of Osaka, 1-10 Yamada-Oka, Suita-City, Osaka, 565-0871, Japan. tkinoshi@biken.osaka-u.ac.jp.
None:
Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by complement-dependent intravascular hemolysis and thrombosis as well as bone marrow failure. Complement dysregulation occurs as a result of defective cell surface expression of two glycosylphosphatidylinositol (GPI)-anchored complement regulators, decay-accelerating factor/CD55 and CD59, caused by somatic mutation of the phosphatidylinositol glycan anchor biosynthesis class A gene (PIGA). Somatic loss-of-function mutation of PIGA generates GPI-anchor-defective hematopoietic stem cell clones, the expansion of which results in large numbers of abnormal erythrocytes, platelets, and other blood cells. The clonal expansion of PIGA mutant hematopoietic stem cells is thought to be mediated by an autoimmune mechanism that suppresses or eliminates normal hematopoietic stem cells while sparing GPI-defective stem cell clones under bone marrow failure environments, the acquisition of a growth phenotype, or both of these mechanisms. This review examines current knowledge and views about the clonal expansion mechanism.
Related Concept Videos
Heat and Free Expansion
T Cell Activation and Clonal Selection
Naive T cells that have not yet encountered an antigen express two primary CD...
Thermal Expansion
Reaction Mechanisms
For instance, the decomposition of ozone appears to follow a mechanism with two steps:
Mechanical Protein Functions
Binomial Expansion Using Pascal's Triangle

