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Eliza Joodmardi

Researcher at Ludwig Institute for Cancer Research

Publications -  14
Citations -  1584

Eliza Joodmardi is an academic researcher from Ludwig Institute for Cancer Research. The author has contributed to research in topics: Dopaminergic & Neuron. The author has an hindex of 14, co-authored 14 publications receiving 1341 citations. Previous affiliations of Eliza Joodmardi include Max Planck Society.

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Nurr1 Is Required for Maintenance of Maturing and Adult Midbrain Dopamine Neurons

TL;DR: The results show that developmental pathways play key roles for the maintenance of terminally differentiated neurons and suggest that disrupted function of Nurr1 and other developmental transcription factors may contribute to neurodegenerative disease.
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Single-cell RNA sequencing reveals midbrain dopamine neuron diversity emerging during mouse brain development

TL;DR: Single cell RNA sequencing of isolated mouse neurons expressing the transcription factor Pitx3 (broad mDA neuronal marker) is used to identify and characterize seven neuron subgroups divided in two major branches of developing PitX3-expressing neurons.
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p57(Kip2) cooperates with Nurr1 in developing dopamine cells.

TL;DR: Evidence indicates that p57Kip2 functions by a direct protein–protein interaction with Nurr1, an orphan nuclear receptor that is essential for dopamine neuron development, and reveals a mechanism whereby p57 Kip2 influences postmitotic differentiation of dopamine neurons.
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Transcription factor Nurr1 maintains fiber integrity and nuclear-encoded mitochondrial gene expression in dopamine neurons

TL;DR: It is shown that Nurr1 ablation results in a progressive pathology associated with reduced striatal DA, impaired motor behaviors, and dystrophic axons and dendrites, and that Nur r 1 ablation in mice recapitulates early features of Parkinson's disease.
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NR4A orphan nuclear receptors as mediators of CREB-dependent neuroprotection.

TL;DR: It is demonstrated that NR4A and the transcriptional coactivator PGC-1α independently regulate distinct CREB-dependent neuroprotective gene programs and are identified as essential mediators of neuroprotection after exposure to neuropathological stress.