ArticleBMB reports2017
C-terminally mutated tubby protein accumulates in aggresomes.
Article in BMB reports, 2017. 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, 13 citations in OpenAlex.
- A novel homozygous TUB mutation associated with autosomal recessive retinitis pigmentosa in a consanguineous Chinese family.BMC medical genomics · 2023Article
- Acute exercise reduces feeding by activating IL-6/Tubby axis in the mouse hypothalamus.Frontiers in physiology · 2022Article
- Genome-wide identification of the Tubby-Like Protein (TLPs) family in medicinal model plantPeerJ · 2021Article
- Decrypting tubby-like protein gene family of multiple functions in starch root crop cassava.AoB PLANTS · 2019Article
- TheeLife · 2019Article
- Primary cilia proteins: ciliary and extraciliary sites and functions.Cellular and molecular life sciences : CMLS · 2018Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tubby protein (Tub), a putative transcription factor, plays important roles in the maintenance and function of neuronal cells. A splicing defect-causing mutation in the 3'-end of the tubby gene, which is predicted to disrupt the carboxy-terminal region of the Tub protein, causes maturity-onset obesity, blindness, and deafness in mice. Although this pathological Tub mutation leads to a loss of function, the precise mechanism has not yet been investigated. Here, we found that the mutant Tub proteins were mostly localized to puncta found in the perinuclear region and that the C-terminus was important for its solubility. Immunocytochemical analysis revealed that puncta of mutant Tub co-localized with the aggresome. Moreover, whereas wild-type Tub was translocated to the nucleus by extracellular signaling, the mutant forms failed to undergo such translocation. Taken together, our results suggest that the malfunctions of the Tub mutant are caused by its misfolding and subsequent localization to aggresomes. [BMB Reports 2017; 50(1): 37-42].
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