PXD029689

PXD029689 is an original dataset announced via ProteomeXchange.

Title	Amyloid-like aggregating proteins cause lysosomal defects in neurons via gain-of-function toxicity
Description	Here, we combine cryo-electron tomography, proteomics and cell biology studies to investigate the effects of protein aggregates in primary neurons. We use artificial amyloid-like β-sheet proteins (β proteins) to focus on the gain-of-function aspect of aggregation. These proteins form fibrillar aggregates and cause neurotoxicity. We show that late stages of autophagy are impaired by the aggregates, resulting in lysosomal alterations reminiscent of lysosomal storage disorders.
HostingRepository	PRIDE
AnnounceDate	2021-12-20
AnnouncementXML	Submission_2021-12-20_11:42:11.794.xml
DigitalObjectIdentifier
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Unsupported dataset by repository
PrimarySubmitter	Daniel Hornburg
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	No PTMs are included in the dataset
Instrument	Q Exactive

Revision	Datetime	Status	ChangeLog Entry
0	2021-11-11 05:59:54	ID requested
⏵ 1	2021-12-20 11:42:12	announced

Dataset with its publication pending

submitter keyword: neurodegeneration, protein aggregates, toxic proteins, neurons

Daniel Hornburg
contact affiliation	Stanford
contact email	daniel.dh.hornburg@gmail.com
lab head
Daniel Hornburg
contact affiliation	Stanford
contact email	daniel.dh.hornburg@gmail.com
dataset submitter

Dataset FTP location NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2021/12/PXD029689

PRIDE project URI

• PRIDE
  1. PXD029689
     1. Label: PRIDE project
     2. Name: Amyloid-like aggregating proteins cause lysosomal defects in neurons via gain-of-function toxicity