Evidence map›Paper›PMID 20845110›Full record

ReviewCurrent topics in microbiology and immunology2011

NF-κB as a target for oncogenic viruses.

Shao-Cong Sun, Ethel Cesarman

Abstract readReview
In one paragraph

Review in Current topics in microbiology and immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Insight into the Epigenetics of Kaposi's Sarcoma-Associated Herpesvirus.International journal of molecular sciences · 2023
    Review
  6. Exploration and analysis of differentially expressed genes in Epstein-Barr virus negative and positive plasmablastic lymphoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Transcriptomic Profiling ofFrontiers in oncology · 2021
    Article
  16. Review
  17. Article
  18. Viral Oncology: Molecular Biology and Pathogenesis.Journal of clinical medicine · 2017
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Shao-Cong SunDepartment of Immunology, The University of Texas MD Anderson Cancer Center, USA. ssun@mdanderson.org
Ethel Cesarman
Cornell University · USThe University of Texas MD Anderson Cancer Center · US

Funding

TpI2 Kinase in Macrophage Activation by MicrobesR01AI057555 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2004 to 2021
$6.7M
Molecular Studies of Noncanonical NF-kb SignalingR01GM084459 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2008 to 2021
$4.4M
Signaling Functions of the Tumor Suppressor CYLDR01AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2006 to 2014
$3.6M
Modeling KSHV latency in vivoR01CA103646 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CESARMAN, ETHEL · 2004 to 2016
$3.5M
Regulation of T-cell function and autoimmune inflammation by deubiquitinases.R37AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2015 to 2021
$2.8M
Survival Signals in AIDS LymphomasR01CA068939 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CESARMAN, ETHEL · 2001 to 2010
$2.6M
KAPOSIS SARCOMA ASSOCIATED VIRUS IN AIDS/LYMPHOMASR29CA068939 · NCI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CESARMAN, ETHEL · 1995 to 1999
–
NCI NIH HHS CA068939NCI NIH HHS CA103646NCI NIH HHS R01 CA068939NCI NIH HHS R01 CA103646NCI NIH HHS R29 CA068939NIAID NIH HHS AI057555NIAID NIH HHS AI064639NIAID NIH HHS R01 AI057555NIAID NIH HHS R01 AI064639NIAID NIH HHS R37 AI064639NIGMS NIH HHS GM084459NIGMS NIH HHS R01 GM084459
6 · The paper itself

Abstract

NF-κB is a pivotal transcription factor that controls cell survival and proliferation in diverse physiological processes. The activity of NF-κB is tightly controlled through its cytoplasmic sequestration by specific inhibitors, IκBs. Various cellular stimuli induce the activation of an IκB kinase, which phosphorylates IκBs and triggers their proteasomal degradation, causing nuclear translocation of activated NF-κB. Under normal conditions, the activation of NF-κB occurs transiently, thus ensuring rapid but temporary induction of target genes. Deregulated NF-κB activation contributes to the development of various diseases, including cancers and immunological disorders. Accumulated studies demonstrate that the NF-κB signaling pathway is a target of several human oncogenic viruses, including the human T cell leukemia virus type 1, the Kaposi sarcoma-associated herpesvirus, and the Epstein-Bar virus. These viruses encode specific oncoproteins that target different signaling components of the NF-κB pathway, leading to persistent activation of NF-κB. This chapter will discuss the molecular mechanisms by which NF-κB is activated by the viral oncoproteins.

Indexed as

AnimalsHerpesvirus 4, HumanHerpesvirus 8, HumanHumansHuman T-lymphotropic virus 1NF-kappa BOncogene Proteins, ViralSignal TransductionNF-kappa BOncogene Proteins, Viral

Identifiers

PMID20845110
PMCPMC3855473
OpenAlexW1720810364

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.