HEИндивидуална стипендия2024–2026

SUMOMyePath · UNVEILING THE ROLE OF SUMOYLATION AS NOVEL MOLECULAR PATHWAY IN MYELIN BIOLOGY; IMPLICATION IN NEURODEVELOPMENT AND DEMYELINATING PATHOPHYSIOLOGY.

„Хоризонт Европа“ — Действия „Мария Склодовска-Кюри“

Период
2024-04-01 → 2026-03-31
Финансиране от ЕС
188 590 €
Участници
2
Схема
HORIZON-TMA-MSCA-PF-EF

Линиите свързват координатора с партньорите.

Накратко на български

СУМОилацията е молекулярен процес, който регулира работата на протеините при образуването на миелина – защитната обвивка на нервните клетки. Разбирането на този механизъм помага при изследването на неврологични заболявания като рассеяното sclerosis и търсенето на начини за възстановяване на миелина.

Този кратък обзор е генериран от изкуствен интелект

Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.

Резултати накратко

UNVEILING THE ROLE OF SUMOYLATION AS NOVEL MOLECULAR PATHWAY IN MYELIN BIOLOGY; IMPLICATION IN NEURODEVELOPMENT AND DEMYELINATING PATHOPHYSIOLOGY.

Myelin is an essential biological structure that allows the nervous system to transmit information rapidly and efficiently. It is produced by specialised glial cells called oligodendrocytes in the central nervous system. When myelin is damaged, lost, or not properly maintained, neurological function can be severely affected. This is relevant to several neurodevelopmental, neurodegenerative and demyelinating conditions, including multiple sclerosis. SUMOMyePath addressed an important knowledge gap in myelin biology: whether SUMOylation, a reversible molecular modification that regulates protein function, localisation and interactions, contributes to oligodendrocyte development, myelin formation and demyelinating pathology. While SUMOylation is known to regulate many cellular processes, its role in oligodendrocyte biology and myelin-related disease mechanisms remains insufficiently understood. The overall objective of the project was to explore SUMOylation as a novel regulatory pathway in myelin biology, with the long-term aim of identifying new molecular mechanisms that may contribute to demyelinating disease and future remyelination-oriented strategies. The project combined molecular and cellular biology, glial-cell models, myelin biology and training in advanced neuroscience approaches. Its pathway to impact was based on generating mechanistic knowledge, developing experimental know-how and enabling resources, and strengthening future research capacity in the field of oligodendrocyte and myelin biology. In the wider European context, the project contributes to the need for better understanding of chronic neurological diseases, improved research capacity in neurobiology, and training of highly skilled researchers able to work across molecular neuroscience, disease modelling, open science, communication and responsible research practice.

Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз

Цел на проекта

SUMOMyePath: a New Pathway to Wrestle Demyelinating diseases.(Re)myelination is the process by which Oligodendrocyte Precursor Cells (OPCs) migrate and differentiate and mature into myelin generating Oligodendrocytes (OLs). Understanding this process is key to cure demyelinating disorders of which, Multiple Sclerosis (MS), is the most prevalent, affecting 2.8 million individuals worldwide and specially women (69%). SUMOylation is a post-translational modification mainly studied in neurons within the central nervous system, however its pathway’s role in oligodendroglia and its relation with myelin (patho)physiology remains to be investigated. Thus, it is an exciting field to explore and SUMOMyePath will address this challenge by synergizing the applicant’s experience in SUMOylation and myelin biology and the expertise of 1) the host group´s (UniTo) in OPCs biology and 2) the secondment group´s (Ubx) in state-of-art live-imaging of OL lineage cells, opening novel avenues of research and, as consequence, new diagnostic and therapeutic strategies.

Оригинален текст от CORDIS (на английски).

Участници

Връзки

Данни: CORDIS, © Европейски съюз