ReviewImmunologic research2001
Molecular mechanisms in lymphocyte activation and growth.
Review in Immunologic research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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.
Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Control of the inflammatory response mechanisms mediated by natural and induced regulatory T-cells in HCV-, HTLV-1-, and EBV-associated cancers.Mediators of inflammation · 2014Review
- Intestinal myofibroblasts produce nitric oxide in response to combinatorial cytokine stimulation.Journal of cellular physiology · 2013Article
- Role of accessory proteins of HTLV-1 in viral replication, T cell activation, and cellular gene expression.Frontiers in bioscience : a journal and virtual library · 2004Review
- Interleukin-10 modified dendritic cells induce allo-hyporesponsiveness and prolong small intestine allograft survival.World journal of gastroenterology · 2003Article
- The adenovirus e3 promoter is sensitive to activation signals in human T cells.Journal of virology · 2003Article
- Critical role of human T-lymphotropic virus type 1 accessory proteins in viral replication and pathogenesis.Microbiology and molecular biology reviews : MMBR · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription factor NF-kappaB is biochemically coupled to the T cell antigen receptor (TCR) and activated transiently during an adaptive immune response. The author's laboratory is investigating the signal-dependent regulation of NF-kappaB, its downstream gene targets, and its function in lymphocyte biology. Our studies have revealed novel enzymatic checkpoints in the NF-kappaB signaling pathway and constitutive repressors of NF-kappaB that might be clinically applicable for therapeutic control of the immune system. We have also found that the Tax transforming protein encoded by human T cell leukemia virus type 1 (HTLV1) binds to and persistently activates an inducible protein kinase in the TCR/NF-kappaB axis. This viral/host interaction appears to trigger the inappropriate expression of NF-kappaB and the development of HTLV1-associated disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.