Biological roles of CCAAT/enhancer-binding protein delta during inflammation

Chiung Yuan Ko, Wen Chang Chang, Ju-Ming Wang

Research output: Contribution to journalReview article

24 Citations (Scopus)

Abstract

CCAAT/enhancer-binding protein delta (CEBPD) belongs to the CCAAT/enhancer-binding protein family, and these proteins function as transcription factors in many biological processes, including cell differentiation, motility, growth arrest, proliferation, cell death, metabolism and immune responses. The functional diversity of CEBPD depends, in part, on the cell type and cellular context, which indicates that CEBPD could interpret a variety of cues to adjust cellular responses in specific situations. Here, we review the regulation of the CEBPD gene and its function in response to inflammatory stimuli. We also address its effects in inflammation-related diseases through a discussion of its recently discovered downstream targets. Regarding to the previous discoveries and new insights in inflammation-associated diseases, suggesting CEBPD could also be a central gene in inflammation. Importantly, the results of this study indicate that the investigation of CEBPD could open a new avenue to help better understand the inflammatory response.

Original languageEnglish
Article number6
JournalJournal of biomedical science
Volume22
Issue number1
DOIs
Publication statusPublished - 2015 Jan 16

Fingerprint

CCAAT-Enhancer-Binding Protein-delta
Inflammation
Genes
CCAAT-Enhancer-Binding Proteins
Biological Phenomena
Cell death
Metabolism
Cell Movement
Cues
Cell Differentiation
Cell Death
Transcription Factors
Growth

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Pharmacology (medical)

Cite this

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Biological roles of CCAAT/enhancer-binding protein delta during inflammation. / Ko, Chiung Yuan; Chang, Wen Chang; Wang, Ju-Ming.

In: Journal of biomedical science, Vol. 22, No. 1, 6, 16.01.2015.

Research output: Contribution to journalReview article

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