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Cloning and analysis of small cytoplasmic leucine-rich repeat protein (SCLP), a novel, phylogenetically-conserved protein that is dramatically up-regulated during the programmed death of moth skeletal muscle
Export of virulence proteins by malaria-infected erythrocytes involves remodeling of host actin cytoskeleton
Following invasion of human red blood cells (RBCs) by the malaria parasite, Plasmodium falciparum, a remarkable process of remodeling occurs in the host cell mediated by trafficking of several hundred effector proteins to the RBC compartment. The exported virulence protein, P falciparum erythrocyte membrane protein 1 (PfEMP1), is responsible for cytoadherence of infected cells to host endothelial receptors. Maurer clefts are organelles essential for protein trafficking, sorting, and assembly of protein complexes. Here we demonstrate that disruption of PfEMP1 trafficking protein 1 (PfPTP1) function leads to severe alterations in the architecture of Maurer's clefts. Furthermore, 2 major surface antigen families, PfEMP1 and STEVOR, are no longer displayed on the host cell surface leading to ablation of cytoadherence to host receptors. PfPTP1 functions in a large complex of proteins and is required for linking of Maurer's clefts to the host actin cytoskeleton
Atrophy and programmed cell death of skeletal muscle
Striated skeletal is subject to nonlethal cycles of atrophy in response to a variety of physiological and pathological stimuli, including: starvation, disuse, denervation and inflammation. These cells can also undergo cell death in response to appropriate developmental signals or specific pathological insults. Most of the insights gained into the control of vertebrate skeletal muscle atrophy and death have resulted from experimental interventions rather than natural processes. In contrast, the intersegmental muscles (ISMs) of moths are giant cells that initiate sequential and distinct programs of atrophy and death at the end of metamorphosis as a normal component of development. This model has provided fundamental information about the control, biochemistry, molecular biology and anatomy of naturally occurring atrophy and death in vivo. The ISMs have provided a good complement to studies in vertebrates and may provide insights into clinically relevant disorders