ArticleFrontiers of medicine2023
GID complex regulates the differentiation of neural stem cells by destabilizing TET2.
Article in Frontiers of medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Targeting Cend1-Atp5f1b interaction rescues mitochondrial dysfunction and ameliorates ischemic brain injury.Communications biology · 2025Article
- GRIN2B alleviates mid-gestational sevoflurane exposure-induced early differentiation of rat neural stem cells by interacting with KIF17.Journal of cell communication and signaling · 2025Article
- Interleukin-18 interacts with NKCC1 to mediate brain injury after intracerebral hemorrhage.Brain, behavior, & immunity - health · 2024Article
- Targeting Nr2e3 to Modulate Tet2 Expression: Therapeutic Potential for Depression Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Skraban-Deardorff intellectual disability syndrome-associated mutations in WDR26 impair CTLH E3 complex assembly.FEBS letters · 2024Article
- The progress of novel strategies on immune-based therapy in relapsed or refractory diffuse large B-cell lymphoma.Experimental hematology & oncology · 2023Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain development requires a delicate balance between self-renewal and differentiation in neural stem cells (NSC), which rely on the precise regulation of gene expression. Ten-eleven translocation 2 (TET2) modulates gene expression by the hydroxymethylation of 5-methylcytosine in DNA as an important epigenetic factor and participates in the neuronal differentiation. Yet, the regulation of TET2 in the process of neuronal differentiation remains unknown. Here, the protein level of TET2 was reduced by the ubiquitin-proteasome pathway during NSC differentiation, in contrast to mRNA level. We identified that TET2 physically interacts with the core subunits of the glucose-induced degradation-deficient (GID) ubiquitin ligase complex, an evolutionarily conserved ubiquitin ligase complex and is ubiquitinated by itself. The protein levels of GID complex subunits increased reciprocally with TET2 level upon NSC differentiation. The silencing of the core subunits of the GID complex, including WDR26 and ARMC8, attenuated the ubiquitination and degradation of TET2, increased the global 5-hydroxymethylcytosine levels, and promoted the differentiation of the NSC. TET2 level increased in the brain of the Wdr26
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