A5014752837- Cellular transport and secretion
- Alzheimer's disease research and treatments
- Retinal Development and Disorders
- Spinal Cord Injury Research
- ATP Synthase and ATPases Research
- Autophagy in Disease and Therapy
- Nerve injury and regeneration
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Calcium signaling and nucleotide metabolism
- Blood Coagulation and Thrombosis Mechanisms
- Machine Learning in Bioinformatics
- Advanced biosensing and bioanalysis techniques
- DNA and Nucleic Acid Chemistry
- Chemical Reaction Mechanisms
- Zebrafish Biomedical Research Applications
- Cholinesterase and Neurodegenerative Diseases
- Congenital heart defects research
- Cancer Research and Treatment
Liaoning Normal University
2024
Dalian Polytechnic University
2024
Nathan Kline Institute for Psychiatric Research
2001-2023
New York University
2001-2023
Syracuse University
1991
Lysosome dysfunction arises early and propels Alzheimer's disease (AD). Herein, we show that amyloid precursor protein (APP), linked to early-onset AD in Down syndrome (DS), acts directly via its β-C-terminal fragment (βCTF) disrupt lysosomal vacuolar (H+)-adenosine triphosphatase (v-ATPase) acidification. In human DS fibroblasts, the phosphorylated 682YENPTY internalization motif of APP-βCTF binds selectively within a pocket v-ATPase V0a1 subunit cytoplasmic domain competitively inhibits...
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCoupled kinetic analysis of cleavage DNA by esperamicin and calicheamicinHiroko Kishikawa, Ying Ping Jiang, Jerry Goodisman, James C. DabrowiakCite this: J. Am. Chem. Soc. 1991, 113, 14, 5434–5440Publication Date (Print):July 1, 1991Publication History Published online1 May 2002Published inissue 1 July 1991https://pubs.acs.org/doi/10.1021/ja00014a040https://doi.org/10.1021/ja00014a040research-articleACS PublicationsRequest reuse permissionsArticle...
Abstract Dysfunction of the endolysosomal system within neurons is a prominent feature Alzheimer’s disease (AD) pathology. Multiple AD-risk factors are known to cause hyper-activity early-endosome small GTPase rab5, resulting in neuronal endosomal pathway disruption. APPL1, an important rab5 effector protein, interface between and function through rab5-activating interaction with BACE1-generated C-terminal fragment (βCTF or C99) amyloid precursor protein (APP), pathogenic APP generated...