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MAN1B1 encodes an enzyme belonging to the glycosyl hydrolase 47 family. De plus, nous expédions MAN1B1 Protéines (9) et beaucoup plus de produits pour cette protéine.
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Results show that MAN1B1 expression was higher in bladder cancer (BC) tissues than those in normal tissues. Its overexpression was associated with poor prognosis. Furthermore, MAN1B1 seems to act as an oncogene (Montrer RAB1A Anticorps) in BC, which improved the likelihood of MAN1B1 taking on a promising prognostic biomarker.
The two genetic associations with severe liver disease that had been suspected previously (one SNP for SERPINA1 (Montrer SERPINA1 Anticorps) and another for MAN1B1) were not confirmed in our cohort. For MAN1B1, four major haplotypes were identified but the prevalence of PHT did not significantly differ between them.
in the bound substrate complex, hydrophobic stacking interactions between Trp (Montrer TBPL1 Anticorps) residues and the glycan core anchor the base of the glycan structure to the enzyme cleft
MAN1B1 defective congenital disorder of glycosylation is reviewed.
Data show that HIV-1 env (Montrer ERVW-1 Anticorps) protein interacts with alpha-mannosidases ERManI (MAN1B1) and initiates endoplasmic reticulum (ER)-associated protein degradation (ERAD) pathway degradation process.
The properties of ERMAN1 enable rapid selection of endoplasmic reticulum-associated degradation substrates in the endoplasmic reticulum.ERMAN1 digests mono-, di- and tri (Montrer VANGL2 Anticorps)-glucosylated N-glycans.
we linked mutations in MAN1B1 to a Golgi glycosylation disorder. Additionally, our results support the recent findings on MAN1B1 localization
MAN1B1 deficiency appeared to be a frequent cause in our cohort of patients with unsolved congenital disorder of glycosylation type II.
A novel post-transcriptional regulatory mechanism for ERManI via miR (Montrer MLXIP Anticorps)-125b and this molecule contributes to the regulation of carcinogenesis in hepatocellular carcinoma.
ERManI and gamma-COP contribute to a golgi-based quality control module that facilitates the retrieval of captured ERAD substrates back to the endoplasmic reticulum.
This gene encodes an enzyme belonging to the glycosyl hydrolase 47 family. This enzyme functions in N-glycan biosynthesis, and is a class I alpha-1,2-mannosidase that specifically converts Man9GlcNAc to Man8GlcNAc isomer B. It is required for N-glycan trimming to Man5-6GlcNAc2 in the endoplasmic-reticulum-associated degradation pathway. Mutations in this gene cause autosomal-recessive intellectual disability. Alternative splicing results in multiple transcript variants. A related pseudogene has been identified on chromosome 11.
mannosidase, alpha, class 1B, member 1
, alpha 1,2-mannosidase
, ER alpha 1,2-mannosidase
, Man9GlcNAc2-specific processing alpha-mannosidase
, endoplasmic reticulum mannosyl-oligosaccharide 1,2-alpha-mannosidase
, endoplasmic reticulum mannosyl-oligosaccharide 1,2-alpha-mannosidase 1
, ER alpha-1,2-mannosidase
, ER mannosidase 1
, man9GlcNAc2-specific-processing alpha-mannosidase