Human immunodeficiency virus type 1 gp120-mediated disruption of tight junction proteins by induction of proteasome-mediated degradation of zonula occludens-1 and -2 in human brain microvascular endothelial cells.

The infiltration of human immunodeficiency virus (HIV)-1, such as by HIV-infected leukocytes, across an injured blood-brain barrier (BBB) is a characteristic pathologic manifestation of HIV-1-associated dementia. HIV-1 gp120 has been implicated as a cause of breakdown of tight junctions between endothelial cells of the BBB, though the disrupting molecular mechanisms are unexplained. This study offers a new explanation for the increased BBB microvascular permeability, due to the degradation of tight junction proteins by the proteasome induced by gp120, and the negative regulation of this process by the scaffold protein, 14-3-3tau.

Specific regional distribution of protein arginine methyltransferase 8 (PRMT8) in the mouse brain.

The regional distribution of PRMT8 transcript was examined in mouse brain using in situ hybridization (ISH) histochemistry. The PRMT8 cRNA probe was specifically hybridized with CNS and the signals were observed only in the neurons. The distribution of the neurons expressing PRMT8 mRNA was not even throughout the brain.