Neuroprogenitor Cells From Patients With TBCK Encephalopathy Suggest Deregulation of Early Secretory Vesicle Transport Article Swipe
Danielle de Paula Moreira
,
Ângela May Suzuki
,
André Luíz Teles e Silva
,
Elisa Varella‐Branco
,
Maria Cecília Zorél Meneghetti
,
Gerson Shigeru Kobayashi
,
Mariana Soares Fogo
,
Merari de Fátima Ramires Ferrari
,
Rafaela R. Cardoso
,
Naila Cristina Vilaça Lourenço
,
Karina Griesi‐Oliveira
,
Elaine Cristina Zachi
,
Débora Romeo Bertola
,
Karina Weinmann
,
Marcelo A. Lima
,
Helena B. Nader
,
Andréa L. Sertié
,
Maria Rita Passos‐Bueno
·
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.3389/fncel.2021.803302
YOU?
·
· 2022
· Open Access
·
· DOI: https://doi.org/10.3389/fncel.2021.803302
Biallelic pathogenic variants in TBCK cause encephaloneuropathy, infantile hypotonia with psychomotor retardation, and characteristic facies 3 (IHPRF3). The molecular mechanisms underlying its neuronal phenotype are largely unexplored. In this study, we reported two sisters, who harbored biallelic variants in TBCK and met diagnostic criteria for IHPRF3. We provided evidence that TBCK may play an important role in the early secretory pathway in neuroprogenitor cells (iNPC) differentiated from induced pluripotent stem cells (iPSC). Lack of functional TBCK protein in iNPC is associated with impaired endoplasmic reticulum-to-Golgi vesicle transport and autophagosome biogenesis, as well as altered cell cycle progression and severe impairment in the capacity of migration. Alteration in these processes, which are crucial for neurogenesis, neuronal migration, and cytoarchitecture organization, may represent an important causative mechanism of both neurodevelopmental and neurodegenerative phenotypes observed in IHPRF3. Whether reduced mechanistic target of rapamycin (mTOR) signaling is secondary to impaired TBCK function over other secretory transport regulators still needs further investigation.
Related Topics
Concepts
Biology
Neurogenesis
Cell biology
Phenotype
Endoplasmic reticulum
Neuroscience
Golgi apparatus
Biogenesis
Vesicular transport protein
Genetics
Vesicle
Gene
Membrane
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.3389/fncel.2021.803302
- OA Status
- gold
- Cited By
- 11
- References
- 61
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4205418581
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4205418581Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.3389/fncel.2021.803302Digital Object Identifier
- Title
-
Neuroprogenitor Cells From Patients With TBCK Encephalopathy Suggest Deregulation of Early Secretory Vesicle TransportWork title
- Type
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articleOpenAlex work type
- Language
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enPrimary language
- Publication year
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2022Year of publication
- Publication date
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2022-01-13Full publication date if available
- Authors
-
Danielle de Paula Moreira, Ângela May Suzuki, André Luíz Teles e Silva, Elisa Varella‐Branco, Maria Cecília Zorél Meneghetti, Gerson Shigeru Kobayashi, Mariana Soares Fogo, Merari de Fátima Ramires Ferrari, Rafaela R. Cardoso, Naila Cristina Vilaça Lourenço, Karina Griesi‐Oliveira, Elaine Cristina Zachi, Débora Romeo Bertola, Karina Weinmann, Marcelo A. Lima, Helena B. Nader, Andréa L. Sertié, Maria Rita Passos‐BuenoList of authors in order
- Landing page
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https://doi.org/10.3389/fncel.2021.803302Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.3389/fncel.2021.803302Direct OA link when available
- Concepts
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Biology, Neurogenesis, Cell biology, Phenotype, Endoplasmic reticulum, Neuroscience, Golgi apparatus, Biogenesis, Vesicular transport protein, Genetics, Vesicle, Gene, MembraneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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11Total citation count in OpenAlex
- Citations by year (recent)
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2025: 6, 2024: 1, 2023: 4Per-year citation counts (last 5 years)
- References (count)
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61Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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