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

A Soft Mechanical Phenotype of SH-SY5Y Neuroblastoma and Primary Human Neurons Is Resilient to Oligomeric Aβ(1-42) Injury.

ACS chemical neuroscience - 18 Mar 2020

Kruger Terra M, Bell Kendra J, Lansakara Thiranjeewa I, Tivanski Alexei V, Doorn Jonathan A, Stevens Lewis L

Abstract excerpt

Aggregated amyloid beta (Aβ) is widely reported to cause neuronal dystrophy and toxicity through multiple pathways: oxidative stress, disrupting calcium homeostasis, and cytoskeletal dysregulation. The neuro-cytoskeleton is a dynamic structure that reorganizes to maintain cell homeostasis in response to varying soluble and physical cues presented from the extracellular matrix (ECM). Due this relationship between...

Read the complete abstract on PubMed

Topics

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

Share to Amyloid beta-Peptides
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cellular Mechanics and Interactions

Share to Neuroblastoma

Share to Neurons

Share to Peptide Fragments

Share to Phenotype

Share to Skin and Cellular Biology Research

Source

Open in PubMed Open full text

Identifiers

PMID: 32058688
DOI: 10.1021/acschemneuro.9b00401
PMCID: PMC7958432

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A Soft Mechanical Phenotype of SH-SY5Y Neuroblastoma and Primary Human Neurons Is Resilient to Oligomeric Aβ(1-42) Injury.PMID 32058688Read ↗

The Beta-Amyloid Protein of Alzheimer’s Disease: Communication Breakdown by Modifying the Neuronal CytoskeletonSemantic proximity Read ↗

Investigating Connectivity Deficits in Alzheimer’s Disease Using a Novel 3D Bioprinted Model Designed to Quantify Neurite OutgrowthSemantic proximity Read ↗

Neuropathy-Associated HSPB1 Mutant Impairs Neuronal Mechanoadaptation and Axonal Regeneration.Semantic proximity Read ↗

β/A4‐evoked degeneration of differentiated SH‐SY5Y human neuroblastoma cellsSemantic proximity Read ↗

The expression of amyloid beta protein precursor protects nerve cells from β-amyloid and glutamate toxicity and alters their interaction with the extracellular matrixSemantic proximity Read ↗

Impact of four common hydrogels on amyloid-β (Aβ) aggregation and cytotoxicity: Implications for 3D models of Alzheimer’s diseaseSemantic proximity Read ↗

The structure of an Amyloid Precursor Protein/talin complex indicates a mechanical basis of Alzheimer's Disease.Semantic proximity Read ↗

Effects of amyloid-β-mimicking peptide hydrogel matrix on neuronal progenitor cell phenotype.Semantic proximity Read ↗

Tau-Mediated Cytoskeletal Stabilization Modulates Cell Mechanics and Vulnerability to Mechanical StrainSemantic proximity Read ↗

Optimizing the <i>In Vitro</i> Neuronal Microenvironment to Mitigate Phototoxicity in Live-cell ImagingSemantic proximity Read ↗

Cytoskeletal adaptation following long-term dysregulation of actomyosin in neuronal processesSemantic proximity Read ↗

Increased Substrate Stiffness Elicits a Myofibroblastic Phenotype in Human Lamina Cribrosa Cells.Semantic proximity Read ↗

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