PFB-FDGlu (5-(Pentafluorobenzoylamino)Fluorescein Di-β-D-Glucopyranoside)
Invitrogen™

PFB-FDGlu (5-(Pentafluorobenzoylamino)Fluorescein Di-β-D-Glucopyranoside)

ß-グルコシダーゼ基質 5-(ペンタフルオロベンゾイルアミノ)フルオレセイン、di-ß-D-グルコピラノシド(PFB-FDGlu)は、ピノサイトーシスにより細胞にロードする際に、エンドソーム細胞やリソソーム細胞に局在するように見える緑色蛍光PFB-F色素(励起/最大発光約492/516詳細を見る
製品番号(カタログ番号)数量
P11947
または、製品番号P-11947
5 mg
製品番号(カタログ番号) P11947
または、製品番号P-11947
価格(JPY)
137,000
Each
数量:
5 mg
ß-グルコシダーゼ基質

5-(ペンタフルオロベンゾイルアミノ)フルオレセイン、di-ß-D-グルコピラノシド(PFB-FDGlu

)は、ピノサイトーシスにより細胞にロードする際に、エンドソーム細胞やリソソーム細胞に局在するように見える緑色蛍光PFB-F色素(励起/最大発光約492/516 nm)を生成します。
研究用にのみ使用できます。診断用には使用いただけません。
仕様
細胞透過性細胞透過性
Green
励起/発光492⁄516
使用対象 (装置)フローサイトメーター
標識または色素Fluorescein
製品タイプSubstrate
数量5 mg
出荷条件室温
保存要件Freezer (-5°C to -30°C)
基質β‐グルコシダーゼ基質
検出法蛍光
形状Powder
Substrate Properties化学基質
基質タイプBeta-Glucosidase Substrate
Target EnzymeBeta-Glucosidase
Unit SizeEach
組成および保存条件
冷凍庫(-5~-30℃)に保存。

引用および参考文献 (16)

引用および参考文献
Abstract
Activation and Purification of ß-Glucocerebrosidase by Exploiting its Transporter LIMP-2 - Implications for Novel Treatment Strategies in Gaucher's and Parkinson's Disease.
Authors:Dobert JP,Bub S,Mächtel R,Januliene D,Steger L,Regensburger M,Wilfling S,Chen JX,Dejung M,Plötz S,Hehr U,Moeller A,Arnold P,Zunke F
Journal:Advanced science (Weinheim, Baden-Wurttemberg, Germany)
PubMed ID:38666485
Genetic variants of GBA1 can cause the lysosomal storage disorder Gaucher disease and are among the highest genetic risk factors for Parkinson's disease (PD). GBA1 encodes the lysosomal enzyme beta-glucocerebrosidase (GCase), which orchestrates the degradation of glucosylceramide (GluCer) in the lysosome. Recent studies have shown that GluCer accelerates α-synuclein aggregation, ... More
Late-onset Krabbe disease presenting as spastic paraplegia - implications of GCase and CTSB/D.
Authors:Mächtel R,Dobert JP,Hehr U,Weiss A,Kettwig M,Laugwitz L,Groeschel S,Schmidt M,Arnold P,Regensburger M,Zunke F
Journal:Annals of clinical and translational neurology
PubMed ID:38837642
Krabbe disease (KD) is a multisystem neurodegenerative disorder with severe disability and premature death, mostly with an infancy/childhood onset. In rare cases of late-onset phenotypes, symptoms are often milder and difficult to diagnose. We here present a translational approach combining diagnostic and biochemical analyses of a male patient with a ... More
Tau accumulation in degradative organelles is associated to lysosomal stress.
Authors:Piovesana E,Magrin C,Ciccaldo M,Sola M,Bellotto M,Molinari M,Papin S,Paganetti P
Journal:Scientific reports
PubMed ID:37865674
Neurodegenerative disorders are characterized by the brain deposition of insoluble amyloidogenic proteins, such as α-synuclein or Tau, and the concomitant deterioration of cell functions such as the autophagy-lysosomal pathway (ALP). The ALP is involved in the degradation of intracellular macromolecules including protein aggregates. ALP dysfunction due to inherited defects in ... More
Dysregulation of mitochondria-lysosome contacts by GBA1 dysfunction in dopaminergic neuronal models of Parkinson's disease.
Authors:Kim S,Wong YC,Gao F,Krainc D
Journal:Nature communications
PubMed ID:33753743
Mitochondria-lysosome contacts are recently identified sites for mediating crosstalk between both organelles, but their role in normal and diseased human neurons remains unknown. In this study, we demonstrate that mitochondria-lysosome contacts can dynamically form in the soma, axons, and dendrites of human neurons, allowing for their bidirectional crosstalk. Parkinson's disease ... More
Development of screening strategies for the identification of paramylon-degrading enzymes.
Authors:Gissibl A,Care A,Sun A,Hobba G,Nevalainen H,Sunna A
Journal:Journal of industrial microbiology & biotechnology
PubMed ID:30806871
Enzymatic degradation of the β-1,3-glucan paramylon could enable the production of bioactive compounds for healthcare and renewable substrates for biofuels. However, few enzymes have been found to degrade paramylon efficiently and their enzymatic mechanisms remain poorly understood. Thus, the aim of this work was to find paramylon-degrading enzymes and ways ... More