The role of Y132‐ in Tyrosine‐Kinase dependent suppression of homomeric Kv1.2: Implications for Alzheimer's Disease

Phosphorylation at site Y132 may be a critical mediator of Aβ based suppression of Kv1.2 current, particularly through endocytotic methods. Suppression of these channels may lead to increased excitotoxicity via increased Ca2+ influx into excitatory neurons and glutamate release.

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Publication Details

Journal
Alzheimer s & Dementia
Published
2025-12-01
DOI
https://doi.org/10.1002/alz70855_107170
Primary Topic
Alzheimer's disease research and treatments
Type
article
Field-Weighted Citation Impact
0.00
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article

The role of Y132‐ in Tyrosine‐Kinase dependent suppression of homomeric Kv1.2: Implications for Alzheimer's Disease

Kristi DeBoeuf, Joseph Farley, Dina Jamshidi, Jack Hyatt et al.
Alzheimer s & Dementia
Alzheimer's disease research and treatments
article

The role of Y132‐ in Tyrosine‐Kinase dependent suppression of homomeric Kv1.2: Implications for Alzheimer's Disease

Kristi DeBoeuf, Joseph Farley, Dina Jamshidi, Jack Hyatt, Logen Yaklin, Sebastian Burch
article en

Abstract

Phosphorylation at site Y132 may be a critical mediator of Aβ based suppression of Kv1.2 current, particularly through endocytotic methods. Suppression of these channels may lead to increased excitotoxicity via increased Ca2+ influx into excitatory neurons and glutamate release.

Alzheimer s & DementiaVol. 21(S1)
Indiana University Bloomington (US)
Quality Education
Openalex Percentile: Top 33%
Alzheimer's disease research and treatments
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The role of Y132‐ in Tyrosine‐Kinase dependent suppression of homomeric Kv1.2: Implications for Alzheimer's Disease — Kristi DeBoeuf, Joseph Farley, et al. · Alzheimer s & Dementia (2025) | TGRS Research Map | TGRS