High impact information on BT 325

• In a yeast two-hybrid screen, we discovered that pallidin interacts with syntaxin 13, a t-SNARE protein that mediates vesicle-docking and fusion [1].
• The receptor is identified in an aqueous extract of crude P. pallidum membranes as a potent inhibitor of the hemagglutination activity of pallidin [2].
• The coat-color phenotype of young homozygous double-mutant mice deficient in subunits of BLOC-3 (HPS1) and BLOC-1 (pallidin) was indistinguishable from that of BLOC-1 single mutants [3].
• BLOC-1, a novel complex containing the pallidin and muted proteins involved in the biogenesis of melanosomes and platelet-dense granules [4].
• Steady-state pallidin protein levels were reduced in fibroblasts derived from muted and reduced pigmentation mice, suggesting that the genes defective in these two mutant strains could encode components of BLOC-1 that are required for pallidin stability [4].

Biological context of BT 325

• Proceedings: Influence of psychic stress on the intestinal absorption of methylsulfadiazin [5].
• As SNARE proteins mediate fusion of intracellular membranes, pallidin may play a role in membrane fusion events required for melanosome biogenesis [6].
• We also show that pallidin can be phosphorylated by a red-cell membrane kinase which partially co-purifies with it, and has properties similar to the catalytic subunit of cAMP-dependent kinase [7].
• Structural domain mapping and phosphorylation of human erythrocyte pallidin (band 4.2) [7].
• Based on previous studies on the rapid, nongenomic actions of glucocorticoid (GC) and the G-protein-protein kinase pathways involved, including our own studies on PC12, SK-N-SH, BT-325 cells, and synaptosomes, in this review we will discuss the issue of multiple signal transduction pathways involved in the rapid, nongenomic effects of GC [8].

Anatomical context of BT 325

• Human erythrocyte dematin and protein 4.2 (pallidin) are ATP binding proteins [9].
• Pallidin is a component of a multi-protein complex involved in the biogenesis of lysosome-related organelles [10].

Associations of BT 325 with other chemical compounds

• The result showed that 27 EST clones are expressed at different level in control and all-trans retinoic acid treated BT-325 cells [11].

Gene context of BT 325

• This review focuses on the product of the pallidin (Pldn) gene, one of a number of genes that in mice are associated with pigmentation defects and platelet dense granule deficiency [6].
• This review discusses the biochemical and functional properties of the products of identified HPS genes, which include subunits of the AP-3 complex and the novel proteins HPS1p, HPS3p, HPS4p, pallidin and muted [12].
• Cappuccino, a mouse model of Hermansky-Pudlak syndrome, encodes a novel protein that is part of the pallidin-muted complex (BLOC-1) [13].
• Human erythrocyte membrane protein band 4.2 (pallidin) [14].
• Within BLOC-1, dysbindin is engaged in interactions with three other subunits, named pallidin, snapin and muted [15].

Analytical, diagnostic and therapeutic context of BT 325

• Immunofluorescence studies corroborate that the cellular distribution of pallidin overlaps that of syntaxin 13 [1].
• Size-exclusion chromatography and sedimentation velocity analyses indicated that the bulk of cytosolic pallidin is a component of an asymmetric protein complex with a molecular mass of approximately 200 kDa [4].
• Immunoprecipitation of endogenous dysbindin from brain or muscle resulted in robust co-immunoprecipitation of the pallidin subunit of BLOC-1 but no specific co-immunoprecipitation of dystrobrevin isoforms [15].

References