Evidence map›Paper›PMID 17652167›Full record

ArticlePhysiological genomics2007

Identification of genomic targets downstream of p38 mitogen-activated protein kinase pathway mediating tumor necrosis factor-alpha signaling.

Cindy Zer, George Sachs, Jai Moo Shin

Open access · greenAbstract read
In one paragraph

Article in Physiological genomics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 41 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Cindy ZerDepartment of Physiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA.
George Sachs
Jai Moo Shin
VA Greater Los Angeles Healthcare System · US

Funding

Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
THE GASTRIC ACID PUMP AS A TARGET FOR ULCER TREATMENTR01DK058333 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SACHS, GEORGE · 2000 to 2009
$2.6M
GASTRIC ENTEROCHROMAFFIN-LIKE CELL IN ULCER DISEASER01DK046917 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SACHS, GEORGE · 1994 to 2005
$798k
The Gastric Acid Pump as a Target for Ulcer TreatmentR56DK058333 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SACHS, GEORGE · 2010 to 2010
$229k
SIMIAN RETROVIRUSES--NOVEL GENE DELIVERY VECTORSR21DK053462 · NIDDK · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI MACHIDA, CURTIS A · 1998 to 1999
–
NIDDK NIH HHS DK-41301NIDDK NIH HHS DK-46917NIDDK NIH HHS DK-53462NIDDK NIH HHS DK-58333NIDDK NIH HHS P30 DK041301NIDDK NIH HHS R01 DK046917NIDDK NIH HHS R01 DK058333NIDDK NIH HHS R56 DK058333
6 · The paper itself

Abstract

Inhibition of p38 MAPK suppresses the expression of proinflammatory cytokines such as TNF-alpha and IL-1 beta in macrophages and fibroblast-like synoviocytes (FLS). However, there have been no genomewide studies on the gene targets of p38 MAPK signaling in synoviocytes. Microarray technology was applied to generate a comprehensive analysis of all genes regulated by the p38 MAPK signaling pathway in FLS. Gene expression levels were measured with Agilent oligonucleotide microarrays. Four independent sets of mRNA modulated by TNF-alpha and vehicle were used to measure the change of gene expression due to TNF-alpha, and three experiments were done to ascertain the effect of SB-203580, a p38 MAPK inhibitor, on TNF-alpha-induced genes. Microarray data were validated by RT-quantitative polymerase chain reaction. One hundred forty-one significantly expressed genes were more than twofold upregulated by TNF-alpha. Thirty percent of these genes were downregulated by the p38 inhibitor SB-203580, whereas 67% of these genes were not significantly changed. The SB-203580-inhibited genes include proinflammatory cytokines such as interleukins and chemokines, proteases including matrix metallopeptidases, metabolism-related genes such as cyclooxygenases and phosphodiesterase, genes involved in signal transduction, and genes encoding for transcription factors, receptors, and transporters. Approximately one-third of the TNF-alpha-induced genes in FLS are regulated by the p38 MAPK signal pathway, showing that p38 MAPK is a possible target for suppressing proinflammatory gene expressions in rheumatoid arthritis.

Indexed as

AnimalsCells, CulturedChemokine CXCL2Chemokines, CXCChemotaxis, LeukocyteFibroblastsGene Expression ProfilingGene Expression RegulationImidazolesJNK Mitogen-Activated Protein KinasesMaleNeutrophilsOligonucleotide Array Sequence Analysisp38 Mitogen-Activated Protein KinasesPyridinesRatsChemokine CXCL2Chemokines, CXCCxcl2 protein, ratCxcl3 protein, ratImidazolesJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPyridinesRNA, MessengerSB 203580Tumor Necrosis Factor-alpha

Identifiers

PMID17652167
PMCPMC2880477
OpenAlexW2117366861

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.