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@ARTICLE{Mestres:164668,
author = {Mestres, Ivan and Houtman, Judith and Calegari, Federico
and Toda, Tomohisa},
title = {{A} {N}uclear {B}elt {F}astens on {N}eural {C}ell {F}ate},
journal = {Cells},
volume = {11},
number = {11},
issn = {2073-4409},
address = {Basel},
publisher = {MDPI},
reportid = {DZNE-2022-01198},
pages = {1761},
year = {2022},
note = {(CC BY)},
abstract = {Successful embryonic and adult neurogenesis require
proliferating neural stem and progenitor cells that are
intrinsically and extrinsically guided into a neuronal fate.
In turn, migration of new-born neurons underlies the complex
cytoarchitecture of the brain. Proliferation and migration
are therefore essential for brain development, homeostasis
and function in adulthood. Among several tightly regulated
processes involved in brain formation and function, recent
evidence points to the nuclear envelope (NE) and
NE-associated components as critical new contributors.
Classically, the NE was thought to merely represent a
barrier mediating selective exchange between the cytoplasm
and nucleoplasm. However, research over the past two decades
has highlighted more sophisticated and diverse roles for NE
components in progenitor fate choice and migration of their
progeny by tuning gene expression via interactions with
chromatin, transcription factors and epigenetic factors.
Defects in NE components lead to neurodevelopmental
impairments, whereas age-related changes in NE components
are proposed to influence neurodegenerative diseases. Thus,
understanding the roles of NE components in brain
development, maintenance and aging is likely to reveal new
pathophysiological mechanisms for intervention. Here, we
review recent findings for the previously underrepresented
contribution of the NE in neuronal commitment and migration,
and envision future avenues for investigation. View
Full-Text},
keywords = {Cell Differentiation: physiology / Cell Nucleus /
Neurogenesis: genetics / Neurons: metabolism / Nuclear
Envelope: metabolism},
cin = {AG Toda},
ddc = {570},
cid = {I:(DE-2719)1710014},
pnm = {352 - Disease Mechanisms (POF4-352)},
pid = {G:(DE-HGF)POF4-352},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC9179901},
pubmed = {pmid:35681456},
doi = {10.3390/cells11111761},
url = {https://pub.dzne.de/record/164668},
}