Evidence map›Paper›PMID 17915024›Full record

ArticleBMC immunology2007

Mycobacterium tuberculosis 6-kDa early secreted antigenic target (ESAT-6) protein downregulates lipopolysaccharide induced c-myc expression by modulating the extracellular signal regulated kinases 1/2.

Niladri Ganguly, Pham H Giang, Sandip K Basu, Fayaz Ahmad Mir, Imran Siddiqui, Pawan Sharma

Open access · goldAbstract read
In one paragraph

Article in BMC immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

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  17. Role of pore-forming toxins in bacterial infectious diseases.Microbiology and molecular biology reviews : MMBR · 2013
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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

6 authors at 3 institutions in 3 countries.

Niladri GangulyImmunology Group, International Centre for Genetic Engineering and Biotechnology Aruna Asaf Ali Marg, New Delhi-110067, India. toniladri@gmail.com
Pham H Giang
Sandip K Basu
Fayaz Ahmad Mir
Imran Siddiqui
Pawan Sharma
International Centre for Genetic Engineering and Biotechnology · INInternational Centre for Genetic Engineering and Biotechnology · ITMax Planck Institute for Infection Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMycobacterium tuberculosis (Mtb) causes death of 2-3 million people every year. The persistence of the pathogenic mycobacteria inside the macrophage occurs through modulation of host cell signaling which allows them, unlike the other non-pathogenic species, to survive inside the host. The secretory proteins of M. tuberculosis have gained attention in recent years both as vaccine candidates and diagnostic tools; they target the immune system and trigger a putatively protective response; however, they may also be involved in the clinical symptoms of the disease.

resultsOur studies showed that RD-1-encoded secretory protein ESAT-6 is involved in modulation of the mitogen-activated protein (MAP) kinase-signaling pathway inside the macrophage. ESAT-6 induced phosphorylation of extracellular signal-regulated kinases 1/2 (ERK1/2) in the cytoplasm but not in the nucleus, which normally is the case for MAP kinases. ESAT-6 also antagonized LPS-induced ERK1/2 phosphorylation in the nucleus. Stimulation of cells by ESAT-6 along with sodium orthovanadate (a tyrosine phosphatase inhibitor) restored phosphorylation of ERK1/2 in the nucleus, suggesting active dephosphorylation of ERK1/2 by some putative phosphatase(s) in the nucleus. Further, ESAT-6 was found to down regulate the expression of LPS-inducible gene c-myc in an ERK1/2-dependent manner.

conclusionThis study showed the effect of secretory proteins of M. tuberculosis in the modulation of macrophage signaling pathways particularly ERK1/2 MAP kinase pathway. This modulation appears to be achieved by limiting the ERK1/2 activation in the nucleus which ultimately affects the macrophage gene expression. This could be a mechanism by which secretory proteins of Mtb might modulate gene expression inside the macrophages.

Indexed as

Immediate-Early ProteinsAnimalsAntigens, BacterialBacterial ProteinsCalcium-Calmodulin-Dependent Protein KinasesCell LineDown-RegulationExtracellular Signal-Regulated MAP KinasesGene ExpressionLipopolysaccharidesMacrophagesMiceMitogen-Activated Protein KinasesMycobacterium tuberculosisp38 Mitogen-Activated Protein KinasesPhosphorylationAntigens, BacterialBacterial ProteinsCalcium-Calmodulin-Dependent Protein KinasesESAT-6 protein, Mycobacterium tuberculosisExtracellular Signal-Regulated MAP KinasesImmediate-Early ProteinsLipopolysaccharidesMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProtein Tyrosine PhosphatasesProto-Oncogene Proteins c-mycRecombinant Fusion Proteins

Identifiers

PMID17915024
PMCPMC2082026
OpenAlexW2101139369

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.