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Cited by 262

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Deficit of tRNALys modification by Cdkal1 causes the development of type 2 diabetes in mice

Open access
Wei, Fan-Yan, Suzuki, Takeo, Watanabe, Sayaka, Kimura, Satoshi, Kaitsuka, Taku, Fujimura, Atsushi, Matsui, Hideki, Atta, Mohamed, Michiue, Hiroyuki, Fontecave, Marc, Yamagata, Kazuya, Suzuki, Tsutomu, Tomizawa, Kazuhito·2011·Journal of Clinical Investigation
DOI 10.1172/jci58056
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Abstract

The worldwide prevalence of type 2 diabetes (T2D), which is caused by a combination of environmental and genetic factors, is increasing. With regard to genetic factors, variations in the gene encoding Cdk5 regulatory associated protein 1-like 1 (Cdkal1) have been associated with an impaired insulin response and increased risk of T2D across different ethnic populations, but the molecular function of this protein has not been characterized. Here, we show that Cdkal1 is a mammalian methylthiotransferase that biosynthesizes 2-methylthio-N6-threonylcarbamoyladenosine (ms2t6A) in tRNA(Lys)(UUU) and that it is required for the accurate translation of AAA and AAG codons. Mice with pancreatic β cell-specific KO of Cdkal1 (referred to herein as β cell KO mice) showed pancreatic islet hypertrophy, a decrease in insulin secretion, and impaired blood glucose control. In Cdkal1-deficient β cells, misreading of Lys codon in proinsulin occurred, resulting in a reduction of glucose-stimulated proinsulin synthesis. Moreover, expression of ER stress-related genes was upregulated in these cells, and abnormally structured ER was observed. Further, the β cell KO mice were hypersensitive to high fat diet-induced ER stress. These findings suggest that glucose-stimulated translation of proinsulin may require fully modified tRNA(Lys)(UUU), which could potentially explain the molecular pathogenesis of T2D in patients carrying cdkal1 risk alleles.

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Metadata

Authors
Wei, F.-Y., Suzuki, T., Watanabe, S., Kimura, S., Kaitsuka, T., Fujimura, A., Matsui, H., Atta, M., Michiue, H., Fontecave, M., Yamagata, K., Suzuki, T., & Tomizawa, K.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2011-09-01
Volume
121
Issue
9
Pages
3598-3608
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci58056
OpenAlex
W1980089198
Cited by
262
References
6
FWCI
19.29
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Deficit of tRNALys modification by Cdkal1 causes the development of type 2 diabetes in mice. https://app.cochat.ai/papers/10.1172/jci58056
The paper
Wei, F.-Y., Suzuki, T., Watanabe, S., Kimura, S., Kaitsuka, T., Fujimura, A., Matsui, H., Atta, M., Michiue, H., Fontecave, M., Yamagata, K., Suzuki, T., & Tomizawa, K. (2011). Deficit of tRNALys modification by Cdkal1 causes the development of type 2 diabetes in mice. Journal of Clinical Investigation. https://doi.org/10.1172/jci58056

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.