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CSCs: Cancer stem cells MVBs: Multivesicular bodies ILVs: Luminal vesicles ESCRT: Endoprotein sorting and transferring device PM: Plasma membrane HSPs: Heat shock proteins PBMCs: Peripheral blood mononuclear cells DCs: Dendritic cells CICs: Cancer-initiating cells NSCs: Normal stem cells AML: Acute myelocytic leukemia MSCs: Mesenchymal stem cells CAFs: Cancer-associated fibroblasts HGF: Hepatocyte growth factors EMT: Epithelial-mesenchymal transition EVs: Extracellular vesicles CRC: Colorectal cancer TGF-beta: Transforming growth factor beta aSMase: Acid sphingomyelinase HSPGs: Heparin proteoglycans.
Overexpression of the heparanase gene revealed the importance of HSPGs for the uptake of triglyceride rich lipoproteins (TRPs) and their protective effect on fatty streak formation and potentially atherosclerosis initiation .
[sup], The Hsulf-1 protein is an arylsulfatase that has been shown to remove specific sulfate groups from cell surface HSPGs, which results in a down-regulation of receptor tyrosine kinase signaling.
It is not known if perlecan is associated with islet amyloid because in vivo amyloid fibers are long-lived structures that present HSPG binding sites, or because HSPGs directly promote amyloid formation, but it is well documented that the glycosaminoglycan (GAG) chains of HSPGs catalyze hIAPP amyloid formation in vitro [64, 104].
Also, for reasons already partially explained, the CNS is particularly susceptible to Al toxic damage, especially considering the critical role of biosulfates, both the HSPGs and, especially, the sulfoglycolipids such as sulfatide [57, 117, 118, 177] in the CNS.
Diamond, MD, the David Clayson Professor of Neurology, said that many of the enzymes that create HSPGs or otherwise help them function are good targets for drug treatments.
One of them is genetic engineering of BMPs to increase binding capacity to the extracellular matrix components such as heparin and heparan sulfate proteoglycans (HSPGs) (8).
In the exogenous pathway, lipoprotein lipase (LPL), held on the vascular endothelium by heparan sulphate proteoglycans (HSPGs), hydrolyses triglycerides (in the presence of apoprotein C2 (apo C2)), releasing FAs and CM-remnants in the process.
HSPGs, which constitute approximately 95% of all proteoglycans , are present in all tissues and comprise five types of protein core, including the cell surface syndecan and the ECM perlecan, the latter being a major constituent of pancreatic islet amyloids .
This effect is dependent on the ability of PTX3 to bind with high affinity and selectivity FGF-2 [51, 54] which in turn results in the inhibition of the interaction of FGF2 with tyrosine-kinase receptors (FGFRs) and heparin sulphate proteoglycans (HSPGs) on the surface of ECs and SMCs, thus dampening the generation of the proangiogenic complex HSPG/FGF2/FGFR .
Heparan sulfate proteoglycans (HSPGs) comprise a reduced and specific group of proteins covalently linked to heparan sulfate (HS) GAG chains.
Syndecan-1 (SDC-1) is a transmembrane heparan sulfate proteoglycan (HSPG).
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