Disruption of the Cereblon Gene Enhances Hepatic AMPK Activity and Prevents High-Fat Diet–Induced Obesity and Insulin Resistance in Mice
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A nonsense mutation in cereblon (CRBN) causes a mild type of mental retardation in humans. An earlier study showed that CRBN negatively regulates the functional activity of AMP-activated protein kinase (AMPK) in vitro by binding directly to the α1-subunit of the AMPK complex. However, the in vivo role of CRBN was not studied. For elucidation of the physiological functions of Crbn, a mouse strain was generated in which the Crbn gene was deleted throughout the whole body. In Crbn-deficient mice fed a normal diet, AMPK in the liver showed hyperphosphorylation, which indicated the constitutive activation of AMPK. Since Crbn-deficient mice showed significantly less weight gain when fed a high-fat diet and their insulin sensitivity was considerably improved, the functions of Crbn in the liver were primarily investigated. These results provide the first in vivo evidence that Crbn is a negative modulator of AMPK, which suggests that Crbn may be a potential target for metabolic disorders of the liver.
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Crbn knock-out mice have been reported to exhibit normal morphology.
“Crbn knock-out mice have been reported to exhibit normal morphology (Lee et al., 2013)”
From Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray syndrome (2018) · cites this paper as Lee et al., 2013
Aryl sulfonamides have produced modest response rates as monotherapy in clinical trials involving patients with advanced-stage solid tumours.
“which to date have produced modest response rates as monotherapy in clinical trials involving patients with advanced-stage solid tumours173–176.”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [174]
The first class of additional molecular glue degraders comprises aryl sulfonamides, including indisulam, tasisulam, E7820 and chloroquinoxaline.
“The first class comprises aryl sulfonamides, including indisulam, tasisulam, E7820 and chloroquinoxaline”
From Cancer therapies based on targeted protein degradation — lessons learned with lenalidomide (2021) · cites this paper as [174]
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References 33 · Cited by 77
- Authors
- Lee, K. M., Yang, S.-J., Kim, Y. D., Choi, Y. D., Nam, J. H., Choi, C. S., Choi, H.-S., & Park, C.-S.
- Affiliations
- Gwangju Institute of Science and Technology (KR)
- Chonnam National University (KR)
- Gachon University (KR)
- Corresponding author
- Park, Chul-Seung
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2013-05-17
- Volume
- 62
- Issue
- 6
- Pages
- 1855-1864
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC3661653
- OpenAlex
- W2024857098
- Cited by
- 77
- References
- 33
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 2 · 2022: 10 · 2021: 12 · 2020: 8 · 2019: 4 · 2018: 10 · 2017: 5 · 2016: 5 · 2015: 3 · 2014: 3 · 2013: 4
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Keywords
- cereblon, AMPK, high-fat diet-induced obesity, insulin resistance, metabolic liver disease, nonsense mutation
- MeSH terms
- Animals, Female, Insulin Resistance, Liver, Male, Obesity, Peptide Hydrolases, Mice, Knockout, Ubiquitin-Protein Ligases, Adaptor Proteins, Signal Transducing, Mice, AMP-Activated Protein Kinases, Diet, High-Fat
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