Output Catalog
ASAP is committed to accelerating the pace of discovery and informing a path to a cure for Parkinson’s disease through collaboration, research-enabling resources, and data sharing. We’ve created this catalog to showcase the research outputs and tools developed by ASAP-funded programs.
-
Output Type
-
Program
-
CRN Team Name
-
Theme
Image Processing and 3D Reconstruction – Chen et al. 2025 NSMB
Image processing and 3D reconstruction applied in Chen et al. 2025 NSMB
Plasmid construction – Chen et al. 2025 NSMB
Standard cloning procedure.
Available ASAP-related hPSC collection from Team Studer
Collection of human pluripotent stem cell lines consisting of isogenic GBA, LRRK2, SNCA series, KI-reporter lines for TOMM20, b-actin, LAMB1, LAMP1, a-synuclein overexpression lines, and other hPSC resources.
Collection of protocols of Team Deleidi used in the publication: “”LRRK2 kinase activity regulates GCase level and enzymatic activity differently depending on cell type in Parkinson’s disease””
Collection of protocols of Team Deleidi used in the publication: ""LRRK2 kinase activity regulates GCase level and enzymatic activity differently depending on cell type in Parkinson’s disease""
Team Science Approaches to Unravel Monogenic Parkinson’s Disease on a Global Scale
In this article, we describe combining both efforts in a merger project resulting in a global monogenic PD cohort with the buildup of a sustainable infrastructure to identify the multi-ancestry spectrum of monogenic PD and enable studies of factors…
LRRK2 G2019S mutation suppresses differentiation of Th9 and Treg cells via JAK/STAT3
The Leucine-rich repeat kinase-2 (LRRK2) G2019S mutation, resulting in aberrantly enhanced kinase activity, is one of the well-recognized genetic risk factors in Parkinson’s Disease (PD). Increased LRRK2 activity was also observed in immune…
Bidirectional regulation of glycoprotein nonmetastatic melanoma protein B by β-glucocerebrosidase deficiency in GBA1 isogenic dopaminergic neurons from a patient with Gaucher disease and parkinsonism
GBA1 variants increase risk for synucleinopathies due to misfolded GCase and lipid accumulation from reduced enzyme activity. Our Study using iPSCs links lipid levels to PD risk marker GPNMB, refining GBA1 pathogenicity.
CRISPR/Cas9-Based Functional Genomics in Human Induced Pluripotent Stem Cell–Derived Models: Can “the Stars Align” for Neurodegenerative Diseases?
The article discusses the use of CRISPR/Cas9 in studying human diseases using stem cell models, highlighting its potential for advancing functional genomics research.
Lyso-IP: Uncovering Pathogenic Mechanisms of Lysosomal Dysfunction
Lysosomes are ubiquitous membrane-bound organelles found in all eukaryotic cells. Outside of their well-known degradative function, lysosomes are integral in maintaining cellular homeostasis. Growing evidence has shown that lysosomal dysfunction…
Mechanism of human PINK1 activation at the TOM complex in a reconstituted system
The authors demonstrate an essential role of the pore-containing subunit TOM40 and its structurally associated subunits TOM7 and TOM22 for PINK1 activation.
Soluble Immune Factor Profiles in Blood and CSF Associated with LRRK2 Mutations and Parkinson’s Disease
This preprint explores immune factors in Parkinson's disease linked to LRRK2 mutations. Serum showed elevated SDF-1 alpha and TNF-RII levels in LRRK2 carriers, while CSF had reduced immune markers. PD patients displayed reduced CSF inflammation.
Structure of human ULK1 complex core (2:1:1 stoichiometry)
Structure of human ULK1 complex core (2:1:1 stoichiometry)
Structure of human ULK1 complex core (2:2:2 stoichiometry) in the PI3KC3-C1 mixture
Structure of human ULK1 complex core (2:2:2 stoichiometry) in the PI3KC3-C1 mixture (Method: ELECTRON MICROSCOPY, Resolution: 5.85 Å, Aggregation State: PARTICLE, Reconstruction Method: SINGLE PARTICLE).
Structure of human ULK1 complex core (2:2:2 stoichiometry) of the ATG13(450-517) mutant
Structure of human ULK1 complex core (2:2:2 stoichiometry) of the ATG13(450-517) mutant
Structure of human ULK1C:PI3KC3-C1 supercomplex
Structure of human ULK1C:PI3KC3-C1 supercomplex
