Evidence map›Paper›PMID 23386607›Full record

ArticleThe Journal of biological chemistry2013

The human antimicrobial peptide LL-37, but not the mouse ortholog, mCRAMP, can stimulate signaling by poly(I:C) through a FPRL1-dependent pathway.

Divyendu Singh, Rongsu Qi, Jarrat L Jordan, Lani San Mateo, C Cheng Kao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

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  19. Identification of U11snRNA as an endogenous agonist of TLR7-mediated immune pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019
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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

5 authors at 2 institutions in 1 country.

Divyendu SinghDepartment of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47405-7005.
Rongsu QiDepartment of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47405-7005.
Jarrat L JordanJanssen Pharmaceutical Companies of Johnson & Johnson, Radnor, Pennsylvania 19087.
Lani San MateoJanssen Pharmaceutical Companies of Johnson & Johnson, Radnor, Pennsylvania 19087.
C Cheng KaoDepartment of Molecular and Cellular Biochemistry, Indiana University, Bloomington, Indiana 47405-7005. Electronic address: ckao@indiana.edu.
Indiana University Bloomington · USJohnson & Johnson (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LL-37 is an antimicrobial peptide produced by human cells that can down-regulate the lipopolysaccharide-induced innate immune responses and up-regulate double-stranded (ds) RNA-induced innate responses through Toll-like receptor 3 (TLR3). The murine LL-37 ortholog, mCRAMP, also inhibited lipopolysaccharide-induced responses, but unlike LL-37, it inhibited viral-induced responses in mouse cells. A fluorescence polarization assay showed that LL-37 was able to bind dsRNA better than mCRAMP. In the human lung epithelial cell line BEAS-2B, LL-37, but not mCRAMP, colocalized with TLR3, and the colocalization was increased in the presence of dsRNA. The presence of poly(I:C) increased the accumulation of LL-37 in Rab5 endosomes. Signaling by cells induced with both LL-37 and poly(I:C) was sensitive to inhibitors that affect clathrin-independent trafficking, whereas signaling by poly(I:C) alone was not, suggesting that the LL-37-poly(I:C) complex trafficked to signaling endosomes by a different mechanism than poly(I:C) alone. siRNA knockdown of known LL-37 receptors identified that FPRL1 was responsible for TLR3 signaling induced by LL-37-poly(I:C). These results show that LL-37 and mCRAMP have different activities in TLR3 signaling and that LL-37 can redirect trafficking of poly(I:C) to effect signaling by TLR3 in early endosomes in a mechanism that involves FPRL1.

Indexed as

Amino Acid SequenceAnimalsAntimicrobial Cationic Peptidesbeta-CyclodextrinsCathelicidinsCell LineEndocytosisEndosomesHumansInterleukin-6LipopolysaccharidesMiceMolecular Sequence DataPoly I-CProtein BindingProtein TransportAntimicrobial Cationic Peptidesbeta-CyclodextrinsCathelicidinsFPR2 protein, humanIL6 protein, humanInterleukin-6Lipopolysaccharidesmethyl-beta-cyclodextrinPoly I-CReceptors, Formyl PeptideReceptors, LipoxinTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID23386607
PMCPMC3605644
OpenAlexW2094490061

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.