Proteomics

Dataset Information

0

Gonatopoulos-Pournatzis _eIF4Gmicroexon_P105_Lumos


ABSTRACT: A This dataset consists of 24 raw MS files, acquired on Orbitrap Fusion Lumos Tribrid mass spectrometer operated in Data Dependent Acquisition mode. B Mouse samples were generated by Thomas Gonatopoulos-Pournatzis. Proteomics sample preparation and mass spectrometric acquisition was performed by Shen Zhang. Analysis was performed by Shen Zhang and Robert J. Weatheritt. C The files are associated with a manuscript submitted for publication by Thomas Gonatopoulos-Pournatzis et al. The main goal of this paper was to reveal a critical role for alternative splicing in the functional specialization of the translational machinery, and further uncover an autism-disrupted mechanism by which microexons reprogram the synaptic proteome to control neuronal activity and higher-order cognitive functions. D Benjamin J. Blencowe (b.blencowe@utoronto.ca), Sabine P. Cordes (cordes@lunenfeld.ca) and Thomas Gonatopoulos-Pournatzis (thomas.gonatopoulos@utoronto.ca) are the corresponding authors of the manuscript; Anne-Claude Gingras should be contacted for questions on this dataset (gingras@lunenfeld.ca). This submission is associated with 2 Supplementary Files (in addition to this README file) Table 1 describes the composition of this dataset Table 2 lists all the protein and peptide identification evidence

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Anne-Claude Gingras  

PROVIDER: MSV000084658 | MassIVE | Wed Dec 04 14:17:00 GMT 2019

REPOSITORIES: MassIVE

Dataset's files

Source:
Action DRS
Other
Items per page:
1 - 1 of 1
altmetric image

Publications


Microexons represent the most highly conserved class of alternative splicing, yet their functions are poorly understood. Here, we focus on closely related neuronal microexons overlapping prion-like domains in the translation initiation factors, eIF4G1 and eIF4G3, the splicing of which is activity dependent and frequently disrupted in autism. CRISPR-Cas9 deletion of these microexons selectively upregulates synaptic proteins that control neuronal activity and plasticity and further triggers a gene  ...[more]

Similar Datasets

2022-02-17 | MSV000088855 | MassIVE
2022-02-17 | MSV000088854 | MassIVE
2022-02-17 | MSV000088853 | MassIVE
2022-02-17 | MSV000088852 | MassIVE
2022-02-18 | MSV000088862 | MassIVE
2022-02-17 | MSV000088858 | MassIVE
2022-02-17 | MSV000088856 | MassIVE
2022-06-13 | MSV000089642 | MassIVE
2021-10-08 | MSV000088204 | MassIVE
2020-02-25 | MSV000085005 | MassIVE