CORDIS Project
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This project investigates the role of the Myt1l protein in maintaining neuronal cell identity by repressing non-neuronal gene programs. It aims to understand how loss of this repression contributes to mental disorders like autism and schizophrenia, utilizing molecular and behavioral studies in human and mouse models.
Cell identity and function requires both induction of desired genes and repression of unwanted programs.
While master regulators that activate gene networks during development are well characterized, the mechanisms that terminally repress alternative fates remain poorly understood.
Within this project, I aim to demonstrate that active terminal repression is a universal mechanism required to prevent loss of cell identity and disease.We recently found that the neuron-specific transcription repress…
DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG
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