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Cited by 19Protein Kinase Regulation and GTPase SignalingGenetics and Neurodevelopmental DisordersNeurogenesis and neuroplasticity mechanisms

Of rings and spines: The multiple facets of Citron proteins in neural development

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Bianchi, Federico T., Gai, Marta, Berto, Gaia E., Di Cunto, Ferdinando·2020·Small GTPases
DOI 10.1080/21541248.2017.1374325PMC PMC7053930
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Abstract

The Citron protein was originally identified for its capability to specifically bind the active form of RhoA small GTPase, leading to the simplistic hypothesis that it may work as a RhoA downstream effector in actin remodeling. More than two decades later, a much more complex picture has emerged. In particular, it has become clear that in animals, and especially in mammals, the functions of the Citron gene (CIT) are intimately linked to many aspects of central nervous system (CNS) development and function, although the gene is broadly expressed. More specifically, CIT encodes two main isoforms, Citron-kinase (CIT-K) and Citron-N (CIT-N), characterized by complementary expression pattern and different functions. Moreover, in many of their activities, CIT proteins act more as upstream regulators than as downstream effectors of RhoA. Finally it has been found that, besides working through actin, CIT proteins have many crucial functional interactions with the microtubule cytoskeleton and may directly affect genome stability. In this review, we will summarize these advances and illustrate their actual or potential relevance for CNS diseases, including microcephaly and psychiatric disorders.

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  • Citron N is expressed only in postmitotic and fully differentiated neurons.

    “While citron kinase is ubiquitously expressed in proliferating cells, the isoform citron N, which is also a scaffold protein for RhoA, is expressed only in postmitotic and fully differentiated neurons [124].”

    From RhoA Signaling in Neurodegenerative Diseases (2022) · cites this paper as [124]

    The “Expression and localization of CIT proteins” section says CIT-N expression begins when cells become post-mitotic and reaches its highest levels in fully differentiated neurons. It does not say CIT-N is expressed only in neurons or only after full differentiation: the same section describes CIT-N in astrocytes and in early post-mitotic neurons. (LLM, conf=0.90)

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Cited by

Sorted by citations

Authors
Bianchi, F. T., Gai, M., Berto, G. E., & Di Cunto, F.
Affiliations
  • Neuroscience Institute Cavalieri Ottolenghi (IT)
  • University of Turin (IT)
  • Neuroscience Institute Cavalieri Ottolenghi, Regione Golzole 10, Orbassano, TO, Italy
ORCID
Venue
Small GTPases
Publisher
Informa UK Limited
Published
2017-11-29
Volume
11
Issue
2
Pages
122-130
ISSN
  • 2154-1248 (ISSN-L)
  • 2154-1256
DOI
10.1080/21541248.2017.1374325
PMC
PMC7053930
OpenAlex
W2770880042
Cited by
19
References
2
Citations by year
2026: 4 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 3
FWCI
0.16
Type
journal article
Language
en
Open access
Licence
Locations
  • Small GTPases (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Institutional Research Information System University of Turin (University of Turin) (submittedVersion, other-oa)
Funders
Associazione Italiana per la Ricerca sul Cancro (IG17527)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
RhoA, actin cytoskeleton remodeling, microtubule cytoskeleton, citron kinase, central nervous system development, genome stability, microcephaly, mental illness
MeSH terms
Animals, Humans, Nervous System, Neurons, Phenotype, Genetic Variation, Gene Expression Regulation, Enzymologic, Protein Serine-Threonine Kinases, Intracellular Signaling Peptides and Proteins

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