Engineered tRNAs efficiently suppress CDKL5 premature termination codons
Abstract The CDKL5 deficiency disorder (CDD) is a severe neurodevelopmental disorder characterized by early-onset epilepsy, intellectual disability, motor and visual dysfunctions. The causative gene is CDKL5, which codes for a kinase required for brain development. There is no cure for CDD patients;...
Saved in:
Main Authors: | Stefano Pezzini, Aurora Mustaccia, Pierre Aboa, Giorgia Faustini, Alessio Branchini, Mirko Pinotti, Angelisa Frasca, Joseph J. Porter, John D. Lueck, Nicoletta Landsberger |
---|---|
Format: | Article |
Language: | English |
Published: |
Nature Portfolio
2024-12-01
|
Series: | Scientific Reports |
Online Access: | https://doi.org/10.1038/s41598-024-82766-0 |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Similar Items
-
Heterozygous CDKL5 Knockout Female Mice Are a Valuable Animal Model for CDKL5 Disorder
by: Claudia Fuchs, et al.
Published: (2018-01-01) -
Cyclin-Dependent Kinase-Like 5 (CDKL5): Possible Cellular Signalling Targets and Involvement in CDKL5 Deficiency Disorder
by: Syouichi Katayama, et al.
Published: (2020-01-01) -
DDX1 is required for non-spliceosomal splicing of tRNAs but not of XBP1 mRNA
by: Teruhiko Suzuki, et al.
Published: (2025-01-01) -
PDE12 mediated pruning of the poly-A tail of mitochondrial DNA-encoded tRNAs is essential for survival
by: Chenxiao Yu, et al.
Published: (2024-11-01) -
Human TRMT1 and TRMT1L paralogs ensure the proper modification state, stability, and function of tRNAs
by: Kejia Zhang, et al.
Published: (2025-01-01)