نتایج جستجو برای: 3805 gm2

تعداد نتایج: 775  

Journal: :Glycobiology 1998
G Zhu M L Allende E Jaskiewicz R Qian D S Darling C A Worth K J Colley W W Young

Many Golgi glycosyltransferases are type II membrane proteins which are cleaved to produce soluble forms that are released from cells. Cho and Cummings recently reported that a soluble form of alpha1, 3-galactosyltransferase was comparable to its membrane bound counterpart in its ability to galactosylate newly synthesized glycoproteins (Cho,S.K. and Cummings,R.D. (1997) J. Biol. Chem., 272, 136...

2018
Aleksandra Somogyi Anton Petcherski Benedikt Beckert Mylene Huebecker David A Priestman Antje Banning Susan L Cotman Frances M Platt Mika O Ruonala Ritva Tikkanen

Juvenile neuronal ceroid lipofuscinosis (JNCL) is caused by mutations in the CLN3 gene. Most JNCL patients exhibit a 1.02 kb genomic deletion removing exons 7 and 8 of this gene, which results in a truncated CLN3 protein carrying an aberrant C-terminus. A genetically accurate mouse model (Cln3Δex7/8 mice) for this deletion has been generated. Using cerebellar precursor cell lines generated from...

2011
Karen M. Ashe Dinesh Bangari Lingyun Li Mario A. Cabrera-Salazar Scott D. Bercury Jennifer B. Nietupski Christopher G. F. Cooper Johannes M. F. G. Aerts Edward R. Lee Diane P. Copeland Seng H. Cheng Ronald K. Scheule John Marshall

The neuropathic glycosphingolipidoses are a subgroup of lysosomal storage disorders for which there are no effective therapies. A potential approach is substrate reduction therapy using inhibitors of glucosylceramide synthase (GCS) to decrease the synthesis of glucosylceramide and related glycosphingolipids that accumulate in the lysosomes. Genz-529468, a blood-brain barrier-permeant iminosugar...

Journal: :BMJ case reports 2017
Kaushik Maulik Santhosh Kumar Paramjeet Singh Arushi Gahlot Saini

Maulik K, et al. BMJ Case Rep 2017. doi:10.1136/bcr-2017-220912 Description We evaluated a boy aged 16 months with developmental arrest at the age of 6 months followed by neuroregression and recurrent generalised seizures. Perinatal and family history was not contributory. He was first born to non-consanguineous parents by term, uncomplicated vaginal delivery and weighed 2.8 kg at birth. On exa...

Journal: :Journal of Biological Chemistry 2000

Journal: :Arquivos de neuro-psiquiatria 2009
Clecio Godeiro-Junior Andre C Felicio Vinicius Benites Marco Antonio Chieia Acary S B Oliveira

The GM2 gangliosidosis are a group of metabolic disorders in which deficiency of a lysosomal enzyme, hexosaminidase A (Hex A), leads to an abnormal intracellular accumulation of lipids in neurons and glia. Total deficiency is responsible for a fatal infantile disorder, Tay-Sachs disease, characterized by involution in motor abilities, hypotonia, seizures and cortical blindness, with death aroun...

2015
Z.K. Timur S. Akyildiz Demir C. Marsching R. Sandhoff V. Seyrantepe

Tay–Sachs disease is a severe lysosomal storage disorder caused by mutations in the HEXA gene coding for α subunit of lysosomal β-Hexosaminidase A enzyme, which converts GM2 to GM3 ganglioside. HexA−/− mice, depleted of the β-Hexosaminidase A iso-enzyme, remain asymptomatic up to 1 year of age because of a metabolic bypass by neuraminidase(s). These enzymes remove a sialic acid residue converti...

Journal: :The Journal of biological chemistry 1973
Y T Li M Y Mazzotta C C Wan R Orth S C Li

A crude /I-hexosaminidase fraction prepared by (NH,),SO( fractionation of human liver extract or urine was found to convert Tay-Sachs ganglioside, GalNAcPl -+ 4(NANcrZ -+ 3)Gal/31 --f 4Glc + ceramide (G& into NAN& + 3Galfil -+ 4 Glc + ceramide (GMM3). After separation of hexosaminidase A and B by DEAE-cellulose chromatography, only freshly prepared fi-hexosaminidase A hydrolyzed GM2 although bo...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید