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

Gene induction by interferons: functional complementation between trans-acting factors induced by alpha interferon

S K Bandyopadhyay1, D V Kalvakolanu, G C Sen

  • 1Department of Molecular Biology, Cleveland Clinic Foundation, Ohio 44195-5069.

Molecular and Cellular Biology
|October 1, 1990
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

trans-4,4'-Dihydroxystilbene (DHS) protects PC12 cells from oxidative damage but induces reactive oxygen species-mediated apoptosis in SHSY-5Y cell line.

Indian journal of experimental biology·2018
Same author

Association of Oxidative Stress and Obesity with Insulin Resistance in Type 2 Diabetes Mellitus.

Mymensingh medical journal : MMJ·2016
Same author

Peste des petits ruminants vaccine and vaccination in India: sharing experience with disease endemic countries.

Virusdisease·2015
Same author

GRIM-19 mutations fail to inhibit v-Src-induced oncogenesis.

Oncogene·2013
Same author

Role of prostaglandin in the regulation of gastric H(+)-Transporting system.

Indian journal of clinical biochemistry : IJCB·2012
Same author

Targeted therapy via oral administration of attenuated Salmonella expression plasmid-vectored Stat3-shRNA cures orthotopically transplanted mouse HCC.

Cancer gene therapy·2012

HeLaM cells exhibit unique interferon responses. Researchers identified two components, ISGF3 gamma and ISGF3 alpha, crucial for interferon-stimulated gene factor 3 (ISGF3) activation, revealing distinct induction and stability properties.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Virology

Background:

  • HeLaM cells display distinct transcriptional responses to alpha interferon.
  • This unique characteristic extends to induced transcription of chimeric genes containing interferon-stimulated response elements.
  • Understanding the molecular basis of these special requirements in HeLaM cells is essential.

Purpose of the Study:

  • To analyze interferon-stimulated gene factors (ISGF) in HeLaM cells.
  • To elucidate the molecular mechanisms underlying the unique interferon response in HeLaM cells.
  • To characterize the individual components of ISGF3 and their roles in transcriptional regulation.

Main Methods:

  • Gel shift assays were employed to study ISGF3 activation.
  • In vitro reconstitution experiments were performed by mixing cytoplasmic fractions.

Related Experiment Videos

  • The properties of induced ISGF3 gamma and ISGF3 alpha were analyzed independently.

    • Main Results:

    • ISGF3 activation in HeLaM cells is inhibited by 2-aminopurine and requires ongoing protein synthesis, unless pretreated with gamma interferon.
    • Active ISGF3 was reconstituted in vitro by mixing cytoplasmic fractions from gamma interferon-treated and alpha interferon/cycloheximide-treated HeLaM cells.
    • ISGF3 gamma induction requires protein synthesis and is blocked by 2-aminopurine, remaining active for 24 hours in both nuclear and cytoplasmic fractions.
    • ISGF3 alpha activation is independent of protein synthesis, translocates to the nucleus only with ISGF3 gamma, and decays rapidly in the cytoplasm.

    Conclusions:

    • ISGF3 gamma is proposed to be the product of signal 1, while ISGF3 alpha is the product of signal 2.
    • The distinct properties of ISGF3 gamma and ISGF3 alpha explain the unique interferon response characteristics of HeLaM cells.
    • This study provides insights into the complex regulation of interferon-stimulated gene transcription.