C 2023

Omics Analyses in a Neural Stem Cell Model of Familial Parkinson’s Disease

NOTOPOULOU, Sofia; Ioannis GKEKAS a Spyros PETRAKIS

Základní údaje

Originální název

Omics Analyses in a Neural Stem Cell Model of Familial Parkinson’s Disease

Autoři

NOTOPOULOU, Sofia; Ioannis GKEKAS a Spyros PETRAKIS

Vydání

GEWERBESTRASSE 11, CHAM CH-6330, SWITZER, Advances in Experimental Medicine and Biology, od s. 149 - 160, 12 s. Advances in Experimental Medicine and Biology, 1423, 2023

Nakladatel

Springer, Cham

Další údaje

Jazyk

angličtina

Typ výsledku

Kapitola resp. kapitoly v odborné knize

Obor

30103 Neurosciences

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Forma vydání

elektronická verze "online"

Odkazy

Označené pro přenos do RIV

Ano

Kód RIV

RIV/00216224:90127/23:00143875

Organizační jednotka

CIISB II

ISBN

978-3-031-31977-8

EID Scopus

Klíčová slova anglicky

NPCs; Parkinson’s disease; PIP5K1A; Proteomics; Systems biology; UBA52; α-synuclein

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 5. 3. 2026 09:16, Mgr. Eva Dubská

Anotace

V originále

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, affecting millions of people worldwide. Despite considerable efforts, the underlying pathological mechanisms remain elusive, and yet, no treatment has been developed to efficiently reverse or modify disease progression. Thus, new experimental models are required to provide insights into the pathology of PD. Small-molecule neural precursor cells (smNPCs) are ideal for the study of neurodegenerative disorders due to their neural identity and stem cell properties. Cytoplasmic aggregates of α-synuclein (αSyn) are considered a hallmark of PD and a point mutation in the gene encoding p.A53T is responsible for a familial PD form with earlier and robust symptom onset. In order to study the cellular pathology of PD, we genetically modified smNPCs to inducibly overexpress EYFP-SNCA A53T. This cellular model was biochemically characterized, while dysregulated biological pathways and key regulators of PD pathology were identified by computational analyses. Our study indicates three novel genes, UBA52, PIP5K1A, and RPS2, which may mediate PD cellular pathology. © 2023, The Author(s), under exclusive license to Springer Nature Switzerland AG.

Návaznosti

90127, velká výzkumná infrastruktura
Název: CIISB II