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

Aging and defective lymphoid cell activation.

F D Coffman1, S Cohen

  • 1Department of Pathology, Hahnemann University, Philadelphia, Pennsylvannia 19102-1192.

Experimental Gerontology
|January 1, 1989
PubMed
Summary

Age-related immune cell dysfunction involves impaired DNA replication initiation due to nuclear unresponsiveness to ADR. Neoplastic cells, however, resist an ADR inhibitor, suggesting a link between proliferation control and cancer.

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

p53/56(lyn) antisense shifts the 1,25-dihydroxyvitamin D3-induced G1/S block in HL60 cells to S phase.

Journal of cellular physiology·2000
Same author

Differentiation-related mechanisms which suppress DNA replication.

Experimental cell research·1999
Same author

Protein phosphorylation associated with epipodophyllotoxin-induced apoptosis of lymphoid cells: role of a serine/threonine protein kinase.

Clinical immunology and immunopathology·1998
Same author

Retinoblastoma protein-overexpressing HL60 cells resistant to 1,25-dihydroxyvitamin D3 display increased CDK2 and CDK6 activity and shortened G1 phase.

Oncogene·1998
Same author

Regulation of DNA replication initiation in mammalian lymphocyte systems.

Indian journal of biochemistry & biophysics·1997
Same author

Modulation of topoisomerase activities by tumor necrosis factor.

Cellular immunology·1995

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Lymphocyte proliferation is vital for immune response.
  • Age-related immune deficiencies correlate with increased disease severity and mortality.
  • Defects in T-cell activation signaling, IL-2 production, and IL-2 response mechanisms contribute to impaired immune function in aging.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying age-related lymphocyte proliferation defects.
  • To explore the role of the intracellular factor ADR (Activation of DNA Replication) in lymphocyte nuclear response.
  • To examine the function of an ADR inhibitor in quiescent and neoplastic cells.

Main Methods:

  • Analysis of lymphocyte activation and proliferation.
  • Investigation of nuclear response to ADR in aged and young cells.
  • Study of an ADR inhibitor's effect on quiescent, activated, and neoplastic cell nuclei.

Main Results:

  • Aged lymphocytes exhibit nuclear unresponsiveness to ADR, despite normal ADR production, suggesting defects in ADR binding or downstream signaling.
  • A cytoplasmic ADR inhibitor suppresses ADR-induced DNA synthesis in quiescent and activated cell nuclei.
  • Neoplastic cell nuclei are resistant to the ADR inhibitor, correlating with uncontrolled proliferation.

Conclusions:

  • Nuclear unresponsiveness to ADR is a key factor in age-related lymphocyte proliferation deficits.
  • The ADR inhibitor's differential effect on neoplastic cells suggests its potential role in regulating cell growth.
  • Understanding ADR signaling may provide insights into both cellular quiescence and uncontrolled proliferation in cancer.

Related Experiment Videos