Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Multiple Ets factors and interferon regulatory factor-4 modulate CD68 expression in a cell type-specific manner.

Dawn O'Reilly1, Carmel M Quinn, Tariq El-Shanawany

  • 1Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, United Kingdom.

The Journal of Biological Chemistry
|April 5, 2003
PubMed
Summary

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Sebetralstat for breakthrough attacks in patients with hereditary angioedema receiving long-term prophylaxis in KONFIDENT-S.

The journal of allergy and clinical immunology. Global·2026
Same author

Macrophages in embryonic development.

Nature reviews. Immunology·2026
Same author

Clinicopathologic and molecular predictors of survival in BRCA-deficient tubo-ovarian high-grade serous carcinoma.

Nature communications·2026
Same author

Class A scavenger receptor MARCO negatively regulates Ace expression and aldosterone production.

eLife·2025
Same author

National Audit of Long-Term Real-World Outcomes of Berotralstat Use in UK Patients With Hereditary Angioedema.

Allergy·2025
Same author

Beyond <i>BRCA</i> deficiency: Clinical and molecular predictors of survival in patients with <i>BRCA</i>-deficient tubo-ovarian high-grade serous carcinoma.

medRxiv : the preprint server for health sciences·2025

CD68 expression in macrophages requires Ets transcription factors Elf-1 and PU.1. Interferon regulatory factors (IRFs) like IRF-4 and IRF-8 repress CD68 in myeloid cells, while PU.1/IRF-4 interactions down-regulate it in B lymphocytes.

Area of Science:

  • Immunology
  • Molecular Biology
  • Gene Regulation

Background:

  • CD68 is a transmembrane glycoprotein crucial for mononuclear phagocyte lineage cells, including macrophages.
  • Understanding CD68 gene regulation is vital for comprehending macrophage function and immune responses.

Purpose of the Study:

  • To elucidate the transcriptional mechanisms controlling CD68 gene expression in myeloid and lymphoid cells.
  • To identify the specific transcription factors and their interactions regulating the CD68 promoter.

Main Methods:

  • Deletion analysis of the CD68 5'-flanking region.
  • Site-directed mutagenesis to disrupt Ets binding sites.
  • Electrophoretic mobility shift assays (EMSA) to assess transcription factor binding.
  • Chromatin immunoprecipitation (ChIP) assays to confirm in vivo factor association.

Related Experiment Videos

Main Results:

  • The proximal -150 bp of the CD68 promoter shows high activity in macrophages, dependent on Ets factors.
  • PU.1 and Elf-1 bind to the CD68 promoter, with Elf-1 enhancing activity and PU.1 being essential.
  • PU.1 forms repressive heterocomplexes with IRF-4 and IRF-8 in macrophages, down-regulating CD68 promoter activity.
  • IRF-4 and IRF-8 do not bind the CD68 promoter in macrophages but IRF-4 binds in B lymphocytes.

Conclusions:

  • CD68 expression in myeloid cells is regulated by the Ets transcription factors Elf-1 and PU.1.
  • Repression of CD68 in lymphoid cells involves combinatorial interactions between PU.1 and IRF-4.
  • Differential regulation of CD68 by transcription factors contributes to cell-type-specific functions.