Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

mTOR hyperactivation in Down Syndrome underlies deficits in autophagy induction, autophagosome formation, and mitophagy

22 Jul 2019

Abstract excerpt

Down syndrome (DS), a complex genetic disorder caused by chromosome 21 trisomy, is associated with mitochondrial dysfunction leading to the accumulation of damaged mitochondria. Here we report that mitophagy, a form of selective autophagy activated to clear damaged mitochondria is deficient in primary human fibroblasts derived from individuals with DS leading to accumulation of damaged mitochondria with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy in Disease and Therapy
Share to Endoplasmic Reticulum Stress and Disease
Share to Ubiquitin and proteasome pathways

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31332166
DOI: 10.1038/s41419-019-1752-5

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

mTOR hyperactivation in Down Syndrome underlies deficits in autophagy induction, autophagosome formation, and mitophagyPMID 31332166Read ↗

Autophagy is a promising process for linking inflammation and redox homeostasis in Down syndromeSemantic proximity Read ↗

Down syndrome fibroblasts exhibit diminished autophagic clearance and endosomal dysfunction after serum starvationSemantic proximity Read ↗

Loss of Proteostasis and Abnormal Aging in Down Syndrome: From Mechanisms to InterventionsSemantic proximity Read ↗

RUNX1 Upregulation Causes Mitochondrial Dysfunction via Regulating the PI3K-Akt Pathway in iPSC from Patients with Down SyndromeSemantic proximity Read ↗

Targeting Mitochondrial Network Architecture in Down Syndrome and AgingSemantic proximity Read ↗

Mitochondrial dysfunction in down syndrome: molecular mechanisms and therapeutic targetsSemantic proximity Read ↗

Parkin-dependent mitophagy occurs via proteasome-dependent steps sequentially targeting separate mitochondrial sub-compartments for autophagySemantic proximity Read ↗

Metformin restores the mitochondrial network and reverses mitochondrial dysfunction in Down syndrome cellsSemantic proximity Read ↗

NRIP1/RIP140 siRNA-mediated attenuation counteracts mitochondrial dysfunction in Down syndromeSemantic proximity Read ↗

The burden of trisomy 21 disrupts the proteostasis network in Down syndromeSemantic proximity Read ↗

Parkin ubiquitinates mTOR to regulate mTORC1 activity under mitochondrial stressSemantic proximity Read ↗

Impaired mitophagy links mitochondrial disease to epithelial stress in methylmalonyl-CoA mutase deficiencySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.