High impact information on Man2a1

• Muscle fibers in vivo resembled myotubes except that the ER occupied a smaller volume of cytoplasm and no staining was found for one of the Golgi complex markers, the enzyme alpha-mannosidase II [1].
• In contrast, swainsonine, an inhibitor of the processing alpha-mannosidase-II, had no effect [2].
• Similar trans-first scattering kinetics was seen with the HeLa GalT/alpha-mannosidase II pairing [3].
• Evidence is presented for a functional association of GlcNAc transferases I, II, and alpha-mannosidase II, with separation from GlcNAc transferase IV and/or V [4].
• Receptor-mediated uptake of mannose-terminated glycoproteins by macrophages is blocked by treating the cells with swainsonine, an inhibitor of alpha-mannosidase II, and by castanospermine, an inhibitor of the endoplasmic reticulum processing enzyme alpha-glucosidase [5].

Anatomical context of Man2a1

• The endoplasmic reticulum alpha-mannosidase activity toward p-nitrophenyl-alpha-D-mannoside is relatively insensitive to swainsonine, an inhibitor of both the lysosomal alpha-mannosidase and Golgi alpha-mannosidase II [6].
• However, whereas Abi4 immunoreactivity was mainly concentrated within nerve cell bodies and extensively colocalized with the Golgi marker alpha-mannosidase II, Abi3 immunoreactivity was predominantly located along neuronal processes [7].
• Also, an unexpected lack of immunoreactivity with the TGN38 and alpha-mannosidase II antibodies points to biochemical differentiation of the subneural Golgi apparatus at the adult motor endplate [8].
• In the epididymis, principal cells were unreactive for alpha-mannosidase II, but they expressed alpha-mannosidase IB in the initial segment and caput regions, and alpha-mannosidase IA in the corpus and cauda regions [9].
• When microsomes were subfractionated into Golgi (light) and rough ER (heavy) fractions on sucrose density gradients, greater than 65% of alpha-mannosidase II and galactosyltransferase activities were found in light fractions (1.14-1.16 g/ml) in both control and BFA-treated lobules [10].

Associations of Man2a1 with chemical compounds

• Tunicamycin inhibited secretion of glycoprotein A. Swainsonine, which inhibits Golgi alpha-mannosidase II, completely inhibited synthesis of the fully sialylated molecule [11].
• Beta-Hexosaminidase, the high mannose oligosaccharide processing enzyme, alpha-mannosidase II, the two enzymes involved in the biosynthesis of the phosphomannosyl recognition marker, and the phosphomannosyl receptor itself decreased in specific activity or amount from cis to trans [12].

Analytical, diagnostic and therapeutic context of Man2a1

• Microinjection of wild-type rab1a protein or a variety of negative controls (injection buffer alone or activated ras protein) did not affect the appearance of the Golgi, as visualized by immunofluorescence of alpha-mannosidase II (Man II), used as a Golgi marker [13].

References