Scholarship 22/13424-2 - Deficiência intelectual, Interação proteína-proteína - BV FAPESP
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Identification of E3 ligases interaction partners of ubiquitin-conjugating enzyme UBE2A

Grant number: 22/13424-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date until: January 01, 2023
End date until: December 31, 2023
Field of knowledge:Biological Sciences - Genetics - Human and Medical Genetics
Principal Investigator:Ângela Saito
Grantee:Estefanny Guimarães de Abreu
Host Institution: Centro Nacional de Pesquisa em Energia e Materiais (CNPEM). Ministério da Ciência, Tecnologia e Inovação (Brasil). Campinas , SP, Brazil

Abstract

Ubiquitination is a post-translational modification involved in many cellular processes, like mitophagy, DNA-damage repair, protein degradation by the ubiquitin-proteasome system, and synaptic transmission. UBE2A, an ubiquitin-conjugating enzyme (E2), may perform these described functions by interacting with other proteins, such as E3 ligases RAD18 and Parkin. Due to cellular functions dependent of the action of this enzyme, mutations in its gene are related to several diseases, like some cancers, neurodegenerative diseases, and X-linked intellectual disability (ID) type Nascimento. Preliminary studies demonstrated that Q93E mutation in UBE2A, found in a Brazilian family with ID type Nascimento, is associated with neuronal cytoarchitecture and synaptic transmission alterations. However, there is no knowledge about the cellular and molecular mechanisms which lead to these alterations and interaction partners involved, in special E3 ligases which act with UBE2A. Thus, the project's objective is to identify possible E3 ligases interaction partners of UBE2A in neuronal cells using TurboID and mass spectrometry. After the identification of candidates, validation and functional studies with them will be performed, like immunoprecipitation followed by Western Blot and PLA (Proximity Ligation Assay). Thereby, this project will contribute to a better understanding of molecular mechanisms associated with the UBE2A deficiency syndrome in patients with ID.

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