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1 ne its relationship to mammalian Golgi alpha-mannosidase II.
2 localized with the medial-Golgi marker alpha-mannosidase II.
3 emical similarities to mammalian Golgi alpha-mannosidase II.
4 the Sf9 enzyme is distinct from Golgi alpha-mannosidase II.
5 es originating from the Golgi and containing mannosidase II.
7 ndoplasmic reticulum, as well as that due to mannosidase II, a marker for the trans-Golgi network.
12 development consistent with increasing alpha-mannosidase II and core fucosyl-transferase enzyme activ
13 cDNA encoding a protein homologous to alpha-mannosidase II and designated it alpha-mannosidase IIx.
15 ra and antisera against known Golgi markers (mannosidase-II and furin) revealed that the staining of
16 -GFP fusion colocalized with a Golgi marker, mannosidase II, and retained catalytic activity compared
17 Swainsonine, an inhibitor of Golgi alpha-mannosidase II, blocked beta1,6GlcNAc N-glycan expressio
18 e associated with the Golgi apparatus marker mannosidase II but not with markers to early endosomes (
22 reen et al. now show that mice lacking alpha-mannosidase II develop an autoimmune disease similar to
23 nnose trimming enzyme drosophila Golgi alpha-mannosidase II (dGMII) complexed with the inhibitors man
25 of the RER (ribophorin I) and GA (p58, alpha-mannosidase II, galactosyltransferase, and TGN38/41).
27 aminyltransferase I, Arabidopsis Golgi alpha-mannosidase II (GMII), and Arabidopsis beta1,2-xylosyltr
30 tegral membrane Golgi proteins called GEARs (mannosidase II, GOS-28, GS15, GPP130, CASP, giantin, and
35 nto small punctate structures at a time when mannosidase II is still largely localized to Golgi struc
40 several Golgi and vesicle markers, including mannosidase II, p58, trans-Golgi network (TGN)38, and be
42 ed oligosaccharides by endoplasmic reticulum mannosidase II partitions variant PI Z away from the con
45 on is temporally and spatially distinct from mannosidase II relocation and that FTCD provides a novel
47 onsisting of the first 117 residues of alpha-mannosidase II tagged with a fluorescent protein and a t
48 Swainsonine, an inhibitor of Golgi alpha-mannosidase II that causes abnormal N-glycosylation, str
51 taining pattern was similar to that of alpha-mannosidase II which is a known resident enzyme of the G
52 at mutation of a single gene, encoding alpha-mannosidase II, which regulates the hybrid to complex br
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