Evidence map›Paper›PMID 21189284›Full record

ArticleMolecular and cellular biology2011

Transducin β-like protein 1 recruits nuclear factor κB to the target gene promoter for transcriptional activation.

Sivakumar Ramadoss, Jiong Li, Xiangming Ding, Khalid Al Hezaimi, Cun-Yu Wang

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.4field-weighted citation impact, top 31% 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

22 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Causal Role for Neutrophil Elastase in Thoracic Aortic Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023
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  19. An overview of gene therapy in head and neck cancer.Indian journal of human genetics · 2013
    Review
  20. Article
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

5 authors at 2 institutions in 2 countries.

Sivakumar RamadossLaboratory of Molecular Signaling, Oral Biology and Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1668, USA.
Jiong Li
Xiangming Ding
Khalid Al Hezaimi
Cun-Yu Wang
University of California, Los Angeles · USKing Saud University · SA

Funding

Molecular and Genetic Determinants of Invasion in HNSCCR01DE015964 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2004 to 2019
$6.6M
PS-341-induced Apoptosis in Squamous Cell CarcinomaR37DE013848 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2006 to 2015
$3.5M
NF-kB Signaling in Osteoclastogenesis and Osteolytic Bone MetastasisR01CA132134 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, CUN-YU · 2009 to 2013
$1.6M
Inhibition of Bone Formation by TNF/NF-kappa B SignalingR01DE017684 · NIDCR · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WANG, CUN-YU · 2008 to 2011
$1.4M
TNF-ALPHA-MEDIATED APOPTOSIS IN SQUAMOUS CELL CARCINOMAR01DE013848 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WANG, CUN-YU · 2000 to 2004
$1.4M
NCI NIH HHS CA132134NCI NIH HHS R01 CA132134NIDCR NIH HHS DE015964NIDCR NIH HHS DE13848NIDCR NIH HHS DE17684NIDCR NIH HHS R01 DE013848NIDCR NIH HHS R01 DE015964NIDCR NIH HHS R01 DE017684NIDCR NIH HHS R37 DE013848
6 · The paper itself

Abstract

Nuclear factor κB (NF-κB) signaling controls a wide range of cellular functions such as tumor progression and invasion by inducing gene expression. Upon stimulation, NF-κB is translocated to the nucleus and binds to its target gene promoters to activate transcription by recruiting transcription coactivators. Although significant progress has been made in understanding NF-κB-mediated transactivation, little is known about how NF-κB is recruited to its target gene promoters. Here, we report that transducin β-like protein 1 (TBL1) controls the expression of NF-κB target genes by directly binding with NF-κB and facilitating its recruitment to target gene promoters. Tumor necrosis factor alpha stimulation triggered the formation of an NF-κB and TBL1 complex and subsequent target gene promoter binding. Knockdown of TBL1 impaired the recruitment of NF-κB to its target gene promoters. Interestingly, analysis of the Oncomine database revealed that TBL1 mRNA levels were significantly higher in invasive breast cancer tissues than in breast adenocarcinoma tissue. Consistently, TBL1 knockdown significantly reduced the invasive potential of breast cancer cells by inhibiting NF-κB. Our results reveal a new mechanism for the regulation of NF-κB activation, with important implications for the development of novel strategies for cancer therapy by targeting NF-κB.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptional ActivationTranscription, GeneticAdenocarcinomaBreast NeoplasmsFemaleGene Knockdown TechniquesHumansNeoplasm InvasivenessNF-kappa BPromoter Regions, GeneticTransducinTumor Necrosis Factor-alphaNF-kappa BTBL1X protein, humanTransducinTumor Necrosis Factor-alpha

Identifiers

PMID21189284
PMCPMC3067816
OpenAlexW2115202544

What OpenQuestion holds

Textmetadata
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.