Erin Heinzen
@eheinzen.bsky.social
Happy to share our latest manuscript!
We created an isogenic human stem cell model that showed loss-of-function SLC35A2 variants disrupt glycosylation, accelerate neurodevelopment, skew neuronal fate, and lead to hypoactive, asynchronous neural networks with altered synaptic function.
We created an isogenic human stem cell model that showed loss-of-function SLC35A2 variants disrupt glycosylation, accelerate neurodevelopment, skew neuronal fate, and lead to hypoactive, asynchronous neural networks with altered synaptic function.
SLC35A2 loss-of-function variants affect glycomic signatures, neuronal fate and network dynamics
Lai et al. have used human stem cell-derived neurons to model SLC35A2-associated epilepsy. They show that loss-of-function variants disrupt glycosylation,
academic.oup.com
May 28, 2025 at 9:08 PM
Happy to share our latest manuscript!
We created an isogenic human stem cell model that showed loss-of-function SLC35A2 variants disrupt glycosylation, accelerate neurodevelopment, skew neuronal fate, and lead to hypoactive, asynchronous neural networks with altered synaptic function.
We created an isogenic human stem cell model that showed loss-of-function SLC35A2 variants disrupt glycosylation, accelerate neurodevelopment, skew neuronal fate, and lead to hypoactive, asynchronous neural networks with altered synaptic function.