Specific alterations in levels of mannose 6-phosphorylated glycoproteins in different neuronal ceroid lipofuscinoses.
about
Batten's disease: clues to neuronal protein catabolism in lysosomesNeuronal ceroid lipofuscinoses are connected at molecular level: interaction of CLN5 protein with CLN2 and CLN3Increased expression of lysosomal acid phosphatase in CLN3-defective cells and mouse brain tissueNovel interactions of CLN5 support molecular networking between Neuronal Ceroid Lipofuscinosis proteinsA critical tryptophan and Ca2+ in activation and catalysis of TPPI, the enzyme deficient in classic late-infantile neuronal ceroid lipofuscinosisDetermination of the substrate specificity of tripeptidyl-peptidase I using combinatorial peptide libraries and development of improved fluorogenic substrates.A novel interaction of CLN3 with nonmuscle myosin-IIB and defects in cell motility of Cln3(-/-) cellsFlupirtine blocks apoptosis in batten patient lymphoblasts and in human postmitotic CLN3- and CLN2-deficient neurons.Cathepsin deficiency as a model for neuronal ceroid lipofuscinoses.The neuronal ceroid-lipofuscinoses.Significance and prognostic value of lysosomal enzyme activities measured in surgically operated adenocarcinomas of the gastroesophageal junction and squamous cell carcinomas of the lower third of esophagus.Positive lysosomal modulation as a unique strategy to treat age-related protein accumulation diseasesPhotoreceptor phagosome processing defects and disturbed autophagy in retinal pigment epithelium of Cln3Δex1-6 mice modelling juvenile neuronal ceroid lipofuscinosis (Batten disease).Proteomic analysis of mouse models of Niemann-Pick C disease reveals alterations in the steady-state levels of lysosomal proteins within the brain.Human iPSC models of neuronal ceroid lipofuscinosis capture distinct effects of TPP1 and CLN3 mutations on the endocytic pathwayA mutation in the ovine cathepsin D gene causes a congenital lysosomal storage disease with profound neurodegeneration.Neuronal ceroid lipofuscinosis: a common pathway?Loss of the chloride channel ClC-7 leads to lysosomal storage disease and neurodegeneration.S. pombe btn1, the orthologue of the Batten disease gene CLN3, is required for vacuole protein sorting of Cpy1p and Golgi exit of Vps10p.Metabolic changes in the lower esophageal sphincter influencing the result of anti-reflux surgical interventions in chronic gastroesophageal reflux disease.Loss of the Batten disease gene CLN3 prevents exit from the TGN of the mannose 6-phosphate receptor.Proteomic Analysis of Brain and Cerebrospinal Fluid from the Three Major Forms of Neuronal Ceroid Lipofuscinosis Reveals Potential Biomarkers.Loss of CLN7 results in depletion of soluble lysosomal proteins and impaired mTOR reactivation.
P2860
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P2860
Specific alterations in levels of mannose 6-phosphorylated glycoproteins in different neuronal ceroid lipofuscinoses.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Specific alterations in levels ...... euronal ceroid lipofuscinoses.
@en
type
label
Specific alterations in levels ...... euronal ceroid lipofuscinoses.
@en
prefLabel
Specific alterations in levels ...... euronal ceroid lipofuscinoses.
@en
P2093
P2860
P356
P1433
P1476
Specific alterations in levels ...... euronal ceroid lipofuscinoses.
@en
P2093
P S Pullarkat
R K Pullarkat
P2860
P304
P356
10.1042/BJ3340547
P407
P478
334 ( Pt 3)
P577
1998-09-01T00:00:00Z