Inhibition of glucose trimming with castanospermine reduces calnexin association and promotes proteasome degradation of the alpha-subunit of the nicotinic acetylcholine receptor.
about
The chaperone protein 14-3-3eta interacts with the nicotinic acetylcholine receptor alpha 4 subunit. Evidence for a dynamic role in subunit stabilizationLocalization of the lectin, ERp57 binding, and polypeptide binding sites of calnexin and calreticulinCell surface expression of GluR5 kainate receptors is regulated by an endoplasmic reticulum retention signalThe molecular basis of oculocutaneous albinism type 1 (OCA1): sorting failure and degradation of mutant tyrosinases results in a lack of pigmentationBiosynthesis of inositol trisphosphate receptors: selective association with the molecular chaperone calnexinExocytic trafficking is required for nicotine-induced up-regulation of alpha 4 beta 2 nicotinic acetylcholine receptorsComorbid alcohol and nicotine dependence: from the biomolecular basis to clinical consequences.Limiting role of protein disulfide isomerase in the expression of collagen-tailed acetylcholinesterase forms in muscle.The anatomy and cell biology of peripheral myelin protein-22.Role of N-oligosaccharide endoplasmic reticulum processing reactions in glycoprotein folding and degradationGlucose residues as key determinants in the biosynthesis and quality control of glycoproteins with N-linked oligosaccharides.Early postnatal death and motor disorders in mice congenitally deficient in calnexin expression.Voltage sensor mutations differentially target misfolded K+ channel subunits to proteasomal and non-proteasomal disposal pathways.Dodecyl maltopyranoside enabled purification of active human GABA type A receptors for deep and direct proteomic sequencingEstrogen regulation of duodenal bicarbonate secretion and sex-specific protection of human duodenumResistance to Inhibitors of Cholinesterase 3 (Ric-3) Expression Promotes Selective Protein Associations with the Human α7-Nicotinic Acetylcholine Receptor Interactome.Endoplasmic reticulum chaperones stabilize nicotinic receptor subunits and regulate receptor assembly.N-linked glycosylation is required for nicotinic receptor assembly but not for subunit associations with calnexinAn ER-resident membrane protein complex regulates nicotinic acetylcholine receptor subunit composition at the synapse.Single chain variable fragment against nicastrin inhibits the gamma-secretase activity.Regulation of nicotinic receptor expression by the ubiquitin-proteasome systemSorting things out through endoplasmic reticulum quality control.Relationship between calnexin and BiP in suppressing aggregation and promoting refolding of protein and glycoprotein substrates.The lectin chaperone calnexin utilizes polypeptide-based interactions to associate with many of its substrates in vivo.Endoplasmic reticulum (ER)-associated degradation of misfolded N-linked glycoproteins is suppressed upon inhibition of ER mannosidase I.Dissociation from BiP and retrotranslocation of unassembled immunoglobulin light chains are tightly coupled to proteasome activity.Degradation of a short-lived glycoprotein from the lumen of the endoplasmic reticulum: the role of N-linked glycans and the unfolded protein response.Release of polymannose oligosaccharides from vesicular stomatitis virus G protein during endoplasmic reticulum-associated degradation.Adjacent basic amino acid residues recognized by the COP I complex and ubiquitination govern endoplasmic reticulum to cell surface trafficking of the nicotinic acetylcholine receptor alpha-Subunit.Separate roles and different routing of calnexin and ERp57 in endoplasmic reticulum quality control revealed by interactions with asialoglycoprotein receptor chainsN-Linked oligosaccharides on the meprin A metalloprotease are important for secretion and enzymatic activity, but not for apical targeting.The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type Ca2+ currents by altering calnexin-dependent trafficking of Cav3.2 channels.Ion channel assembly: creating structures that functionDeterminants responsible for assembly of the nicotinic acetylcholine receptorEndoplasmic reticulum Ca2+ increases enhance mutant glucocerebrosidase proteostasis.Acetylcholine receptors and nerve terminal distribution at the neuromuscular junction of non-obese diabetic mice.Critical role of the C-terminal segment in the maturation and export to the cell surface of the homopentameric alpha 7-5HT3A receptor.Degradation routes of trafficking-defective VLDLR mutants associated with Dysequilibrium syndrome.
P2860
Q28188947-4DD3CE42-56F9-42E8-BB78-E0D87AD7D535Q28203094-0A1B093A-6EC1-4566-BEF3-BAC04C606E30Q28207435-86B44F6A-2C7A-4D2D-A612-AF345779FC91Q28361790-861095F4-9B6A-491A-9E51-7ABC4AF3545FQ28578579-1373DA87-03A1-46C7-A9A0-81C8A38EEB51Q28589553-764DE8F6-EDE7-4FA7-A02C-DB43ABFC5110Q30438012-84FC223C-BF12-4563-92C0-7ED584BD247DQ33553718-DD306A98-60E0-4C2E-870B-F3ADBA1A9E5BQ33787330-FC43C721-8AC4-4C01-B652-46D328A61179Q33905603-76499492-053F-4BCE-AA4C-A9035F235AB0Q34047041-8A7B710D-96CD-4E25-9E3D-3FE82CA52074Q34325550-82426C69-CFD7-48A7-93C7-188DB8E740FAQ35006046-D75DB6DA-8D1C-4845-9DE0-A905967F3168Q35148408-A050DB59-E3E1-42C0-AA0B-B108974BF85EQ35186576-A253C121-3AFF-4E1D-8BC9-EEE1073F527FQ35741413-C6C3F315-AE9F-4BBE-8638-6596031DCE81Q36627304-DEB9956A-DB19-4DC9-8FE0-E92B857EDF1EQ36638528-1334A549-8DA3-4957-B524-5FB53A14914CQ37334917-F9C1A8EE-3D0D-42CF-A81D-901EDD2AC630Q37459837-3C450FC7-DC4A-4B98-8C43-E3FFDEE377D6Q37592899-231A0F79-5591-40C8-A733-78D3BD9AA5CFQ37765593-8D196BAA-913D-40E0-8FB3-AD4CF82B6CC9Q38297618-A49CA393-1907-4C26-BFBA-AF6B2F192D01Q38301167-DEA9201A-858E-4201-9CCC-E582CD643B84Q38308427-096E98CC-7A53-4B3F-AD1A-ECECE810C9F6Q38477851-5F11BCDD-CFAB-4870-BF06-A9F8A48C9DC1Q38615280-AC2ADB69-B7A1-4542-A80B-E750BD5911E6Q40776579-E9C401E7-9219-41F3-ABA6-AFDF4248C5BAQ40816332-FBF07F1F-7F15-40F8-9E2D-BF6D9EB43E66Q40831389-199EC674-0533-4E90-80C9-2FE93BAB7612Q40876068-D927D15A-4CD8-4C80-A91C-08A30F3F7E52Q41044294-05467C13-F9F5-40FA-92D5-BF356B169333Q41911011-2B0D01C8-676F-466E-AF94-B0A68636D00EQ41911016-30101C34-1ED9-4930-B44D-73092526BA5BQ41976836-55123018-A853-49E8-B2B0-B34DBEBDD95CQ43984747-B81CB4D2-BA11-49DC-8823-5D5A4B750FCFQ45079457-20EB3A37-68C2-423C-A8E2-51F3A5AC0DD1Q47839001-A61F80DC-B7EE-40CF-9AD7-5ED37C99D71F
P2860
Inhibition of glucose trimming with castanospermine reduces calnexin association and promotes proteasome degradation of the alpha-subunit of the nicotinic acetylcholine receptor.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年学术文章
@wuu
1998年学术文章
@zh-cn
1998年学术文章
@zh-hans
1998年学术文章
@zh-my
1998年学术文章
@zh-sg
1998年學術文章
@yue
1998年學術文章
@zh
1998年學術文章
@zh-hant
name
Inhibition of glucose trimming ...... otinic acetylcholine receptor.
@en
type
label
Inhibition of glucose trimming ...... otinic acetylcholine receptor.
@en
prefLabel
Inhibition of glucose trimming ...... otinic acetylcholine receptor.
@en
P2093
P356
P1476
Inhibition of glucose trimming ...... otinic acetylcholine receptor.
@en
P2093
P304
17064-17072
P356
10.1074/JBC.273.27.17064
P407
P577
1998-07-01T00:00:00Z