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Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...

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Rapid and Refined CD11b Magnetic Isolation of Primary Microglia with Enhanced Purity and Versatility
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CCAAT/enhancer binding protein delta in microglial activation.

Aroa Ejarque-Ortiz1, Núria Gresa-Arribas, Marco Straccia

  • 1Department of Cerebral Ischaemia and Neurodegeneration, IIBB, CSIC, IDIBAPS, Barcelona, Spain.

Journal of Neuroscience Research
|November 13, 2009
PubMed
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CCAAT/enhancer binding protein delta (C/EBP delta) is expressed and upregulated in activated microglia, suggesting its role in neuroinflammation. This study investigates C/EBP delta

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • CCAAT/enhancer binding protein delta (C/EBP delta) regulates genes involved in glial activation.
  • Microglial expression of C/EBP delta is largely unexplored, unlike its known astroglial presence.

Purpose of the Study:

  • To investigate the expression and regulation of C/EBP delta in microglia.
  • To determine the role of C/EBP delta in microglial activation and inflammatory gene expression.

Main Methods:

  • Utilized murine primary microglial cultures and BV2 microglial cell lines.
  • Analyzed C/EBP delta expression via mRNA and protein levels following lipopolysaccharide (LPS) stimulation.
  • Investigated the involvement of Toll-like receptors (TLRs) and extracellular signal-regulated kinase (ERK) pathways.

Main Results:

  • Demonstrated C/EBP delta expression and upregulation in activated microglia and astrocytes by LPS.
  • Identified time- and concentration-dependent effects of LPS on C/EBP delta.
  • Showed that TLR agonists mimic LPS-induced upregulation, while ERK inhibition prevents it.
  • Confirmed C/EBP delta binding to the cyclooxygenase-2 promoter in activated microglia.

Conclusions:

  • C/EBP delta is expressed in microglia and significantly upregulated during activation.
  • C/EBP delta plays a role in regulating proinflammatory gene expression in activated microglia, potentially via TLR and ERK pathways.