Back to search

Article

Conditional ATXN2L-Null in Adult Frontal Cortex CamK2a+ Neurons Does Not Cause Cell Death, but Restricts Spontaneous Mobility, and Affects the Alternative Splicing Pathway

2025-09-10

Abstract excerpt

Ataxin-2-like (ATXN2L) protein is required to survive embryonic development, as documented in mice with constitutive absence of ATXN2L Lsm, LsmAD and PAM2 domains, due to knockout (KO) of exons 5-8 with frameshift. Its less abundant paralog Ataxin-2 (ATXN2) has an extended N-terminus, where a polyglutamine domain is prone to expansions, which mediate vulnerability to the polygenic adult motor neuron disease ALS (A...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
6b37e387-5cc8-5bf0-9859-eaff72d9fa96
DOI
10.20944/preprints202509.0886.v1
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
Conditional ATXN2L-Null in Adult Frontal Cortex CamK2a+ Neurons Does Not Cause Cell Death, but Restricts Spontaneous Mobility, and Affects the Alternative Splicing PathwayDOI 10.20944/preprints202509.0886.v1
Select a neighboring publication to make it the new centre.