Amyloid precursor-like protein 2 increases the endocytosis, instability, and turnover of the H2-K(d) MHC class I molecule.

Amyloid Precursor-Like Protein 2 Increases the Endocytosis, Instability, and Turnover of the H2-K MHC Class I Molecule

The amyloid precursor-like protein 2 associates with the major histocompatibility complex class I molecule K(d).

Amyloid precursor-like protein 2 (APLP2) is a member of a protein family related to the amyloid precursor protein, which is implicated in Alzheimer's disease. Little is known about the physiological function of this protein family. The adenovirus E3/19K protein binds to major histocompatibility complex (MHC) class I antigens in the endoplasmic reticulum, thereby preventing their transport to th...

The amyloid precursor-like protein 2 and the adenoviral E3/19K protein both bind to a conformational site on H-2Kd and regulate H-2Kd expression.

A protein of unknown physiological function, called amyloid precursor-like protein 2 (APLP2), forms an association with the murine class I molecule K(d) that is up-regulated by the presence of the adenoviral protein E3/19K. We have extended these findings to show that APLP2 and E3/19K associate preferentially with folded K(d) and not with the open form. APLP2 was detectable at the cell surface,...

LOX-1 protein, A Biomarker in the Prognosis of Atherosclerosis

LOX-1 is a class E scavenger receptor that mediates the uptake of oxLDL by vascular cells. LOX-1 is involved in endothelial dysfunctions, monocyte adhesion, the proliferation, migration, and apoptosis of smooth muscle cells, foam cell formation, platelet activation, as well as plaque instability; all of these events are critical in the pathogenesis of atherosclerosis. These LOX-1-dependent bio...

Cholinergic neuropathology in a mouse model of Alzheimer's disease

Transgenic mice over-expressing mutant human amyloid precursor protein (PDAPP mouse) develop several Alzheimer’s disease (AD)-like lesions including an age-related accumulation of amyloid-?-containing neuritic plaques. Although aged, heterozygous PDAPP mice also exhibit synaptic and glial cell changes, that is characteristic of AD pathology, no evidence of neurodegeneration has been observed. T...