The COP9 Signalosome Controls Adipocyte Differentiation by Regulating CHOP Protein Stability

Huang, Xiaohua; Dubiel, Wolfgang

doi:10.4236/eng.2012.410b050

ENG

2012

DOI: 10.4236/eng.2012.410b050

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The COP9 Signalosome Controls Adipocyte Differentiation by Regulating CHOP Protein Stability

Xiaohua Huang¹,

Wolfgang Dubiel²

Abstract: Obesity is a serious health problem of our time. Dysfunction of adipogenesis, the differentiation of adipocytes, is a hallmark of obesity. Therefore here we investigate the role of the COP9 signalosome and of CHOP in the differentiation of LiSa-2 preadipocytes.

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2024

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Neddylation and Its Target Cullin 3 Are Essential for Adipocyte Differentiation

Zhou,

Patel,

Rice

et al. 2024

Cells

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The ongoing obesity epidemic has raised awareness of the complex physiology of adipose tissue. Abnormal adipocyte differentiation results in the development of systemic metabolic disorders such as insulin resistance and diabetes. The conjugation of NEDD8 (neural precursor cell expressed, developmentally downregulated 8) to target protein, termed neddylation, has been shown to mediate adipogenesis. However, much remains unknown about its role in adipogenesis. Here, we demonstrated that neddylation and its targets, the cullin (CUL) family members, are differentially regulated during mouse and human adipogenesis. Inhibition of neddylation by MLN4924 significantly reduced adipogenesis of 3T3-L1 and human stromal vascular cells. Deletion of NAE1, a subunit of the only NEDD8 E1 enzyme, suppressed neddylation and impaired adipogenesis. Neddylation deficiency did not affect mitotic cell expansion. Instead, it disrupted CREB/CEBPβ/PPARγ signaling, essential for adipogenesis. Interestingly, among the neddylation-targeted CUL family members, deletion of CUL3, but not CUL1, CUL2, or CUL4A, largely replicated the adipogenic defects observed with neddylation deficiency. A PPARγ agonist minimally rescued the adipogenic defects caused by the deletion of NAE1 and CUL3. In conclusion, our study demonstrates that neddylation and its targeted CUL3 are crucial for adipogenesis. These findings provide potential targets for therapeutic intervention in obesity and metabolic disorders.

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Neddylation and Its Target Cullin 3 Are Essential for Adipocyte Differentiation

Zhou,

Patel,

Rice

et al. 2024

Cells

View full text Add to dashboard Cite

show abstract

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The COP9 Signalosome Controls Adipocyte Differentiation by Regulating CHOP Protein Stability

Abstract: Obesity is a serious health problem of our time. Dysfunction of adipogenesis, the differentiation of adipocytes, is a hallmark of obesity. Therefore here we investigate the role of the COP9 signalosome and of CHOP in the differentiation of LiSa-2 preadipocytes.

Cited by 1 publication

References 6 publications

Neddylation and Its Target Cullin 3 Are Essential for Adipocyte Differentiation

Neddylation and Its Target Cullin 3 Are Essential for Adipocyte Differentiation

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