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atherosclerosis/arabidopsis
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Phylogeny and evolution of plant macrophage migration inhibitory factor/D-dopachrome tautomerase-like proteins.
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BACKGROUND
The human (Homo sapiens) chemokine-like protein macrophage migration inhibitory factor (HsMIF) is a pivotal mediator of inflammatory, infectious and immune diseases including septic shock, colitis, malaria, rheumatoid arthritis, and atherosclerosis, as well as tumorigenesis. HsMIF has
The autophagy-lysosome pathway: a novel mechanism involved in the processing of oxidized LDL in human vascular endothelial cells.
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Oxidized low-density lipoprotein (ox-LDL) is involved in the pathogenesis of atherosclerosis and atherosclerotic plaque rupture by promoting lipid accumulation, proinflammatory responses, and cell death. LDL is mainly oxidized in the subendothelial layer of the vascular wall and then can be taken up
Studying Plant MIF/D-DT-Like Genes and Proteins (MDLs).
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Human macrophage migration inhibitory factor (MIF) is an inflammatory cytokine with chemokine-like characteristics and an upstream regulator of host innate immunity. It is a critical mediator of a variety of human diseases, such as acute and chronic inflammatory diseases, autoimmunity,
Diverse Role of SNARE Protein Sec22 in Vesicle Trafficking, Membrane Fusion, and Autophagy.
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Protein synthesis begins at free ribosomes or ribosomes attached with the endoplasmic reticulum (ER). Newly synthesized proteins are transported to the plasma membrane for secretion through conventional or unconventional pathways. In conventional protein secretion, proteins are transported from the
Cross-kingdom mimicry of the receptor signaling and leukocyte recruitment activity of a human cytokine by its plant orthologs.
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Human macrophage migration-inhibitory factor (MIF) is an evolutionarily conserved protein that has both extracellular immune-modulating and intracellular cell-regulatory functions. MIF plays a role in various diseases including inflammatory diseases, atherosclerosis, autoimmunity, and cancer. It
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