Biological Role of the CCAAT/Enhancer-binding Protein Family of Transcription Factors

Lekstrom-Himes, Julie; Xanthopoulos, Kleanthis G.

doi:10.1074/jbc.273.44.28545

Cited by 733 publications

(582 citation statements)

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“…All known functions of CHOP, including its role in growth arrest and apoptosis, require the presence of the C-terminal basic leucine-zipper heterodimerization domain (bZIP). CHOP forms stable heterodimers with transcription factors of the C/EBP family, and interacts with other early response proteins of the bZIP families (reviewed in Ron and Habener, 1992;Leckstrom-Himes and Xanthopoulos, 1998;Ramji and Foka, 2002). The function of bZIP proteins in the regulation of gene transcription typically requires dimerization of the leucine-zipper domain.…”

Section: Discussionmentioning

confidence: 99%

“…CHOP is a member of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors (reviewed in Ron and Habener, 1992;Leckstrom-Himes and Xanthopoulos, 1998;Ramji and Foka, 2002) and is ubiquitously expressed at low levels in proliferating cells, but strikingly upregulated by oxidative stress, endoplasmatic reticulum (ER) stress and DNA damage in different adult tissues (Ubeda et al, 1996;Wang et al, 1996;Talukder et al, 2002). CHOP induces cell cycle arrest and apoptosis in response to cellular stress factors (Zinszner et al, 1998;Maytin et al, 2001), and was therefore also termed 'growth arrest and DNA damageinducible gene' (GADD153).…”

Section: Introductionmentioning

confidence: 99%

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The C/EBP homologous protein CHOP (GADD153) is an inhibitor of Wnt/TCF signals

et al. 2006

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CHOP (GADD153) is a protein of the C/EBP family of transcriptional regulators, which dimerizes with other C/EBP members and changes their DNA-binding and transactivation properties. It induces growth arrest and apoptosis after endoplasmatic reticulum stress or DNA damage. CHOP is also expressed during early embryogenesis and upregulated in tumour tissues with defective Wnt signals. We report here that CHOP functions as a specific inhibitor of Wnt/T-cell factor (TCF) signalling. CHOP inhibits TCF-dependent transcription in human embryonic and colon cancer cell lines. Injection of CHOP mRNA into early Xenopus laevis embryos suppresses dorsal organizer formation and inhibits secondary axis formation and TCF-dependent transcription in response to Wnt-8, Dishevelled, b-Catenin and TCF-VP16. In embryos and human cells, this inhibition depends on the N-terminal transactivation domain of CHOP, whereas the C-terminal dimerization domain is dispensable. CHOP binds to TCF factors, thereby preventing the binding of TCF to its DNA recognition site. Our findings demonstrate a novel function of CHOP as a Wnt repressor.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The C/EBP homologous protein CHOP (GADD153) is an inhibitor of Wnt/TCF signals

et al. 2006

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“…The CCAAT enhancer binding proteins (C/EBPs) are a family of basic leucine zipper transcription factors involved in the regulation of cellular differentiation and functions [7][8][9] . Six members of the C/EBP family have been described, including C/EBP alpha, beta, gamma, delta, epsilon and zeta [10] .…”

Section: Introductionmentioning

confidence: 99%

C/EBP beta and C/EBP delta expression is elevated in the early phase of ethanol-induced hepatosteatosis in mice

Chen

Yang²,

Chang

et al. 2009

Acta Pharmacol Sin

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Aim: Alcohol, which is predominantly metabolized in the liver, is a major hepatic toxicant that readily induces hepatic steatosis. The expression of CCAAT enhancer binding protein (C/EBP), especially the C/EBP delta variety, is increased in the early phase of adipogenesis. However, the role of C/EBP delta in ethanol-induced hepatosteatosis is unclear. Methods: Male C57BL/6J mice were randomized to one of four groups: a control group, a group receiving orally administered ethanol (4 g ethanol/kg body weight) (EtOH), a high-fat-diet (HF) group and an EtOH+HF group. Mice were sacrifi ced after 5 or 10 weeks for various measurements. The in vitro effect of ethanol on the expression of C/EBP alpha, beta and delta was studied in HepG2 cells. Results: By week 5, ethanol treatment had signifi cantly increased liver C/EBP delta and beta protein expression (by 2.3-and 1.4-fold, respectively), which then returned to the control level by week 10. In contrast, the expression of C/EBP alpha was evident only at week 10. The in vitro study shows that C/EBP delta expression was elevated signifi cantly at 24 h but not at 48 or 72 h. C/EBP beta expression was highest at 48 h, whereas C/EBP alpha expression was highest at 72 h. We also found that a low concentration of ethanol plus oleic acid enhanced C/EBP delta expression in HepG2 cells. Conclusion: C/EBP delta expression appears to play an important role in the early phase of ethanol-induced hepatosteatosis in mice and in ethanol-treated HepG2 cells. In addition, EtOH+HF enhances the expression of C/EBP delta in HepG2 cells. Thus, C/EBP delta might be a therapeutic target in alcoholic hepatosteatosis.

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“…The transcription factor CCAAT/enhancer binding protein alpha (C/EBPα) is a tissuespecific differentiation factor that plays a major role in the terminal differentiation of myeloid cells, hepatocytes, and adipocytes among others (17,18). The association of C/ EBPα and cancer has been elucidated in acute myeloid leukemia (AML) (19), where C/ EBPα expression is reduced in leukemias carrying the t(8;21) translocation (20) and C/ EBPα mutations confer improved prognosis in a small subgroup of AML patients with normal cytogenetics (21,22).…”

Section: Introductionmentioning

confidence: 99%