Evidence map›Paper›PMID 33006758›Full record

ArticleClinical and experimental immunology2021

Inactivation of TMEM106A promotes lipopolysaccharide-induced inflammation via the MAPK and NF-κB signaling pathways in macrophages.

X Zhang, T Feng, X Zhou, P M Sullivan, F Hu, Y Lou, J Yu, J Feng, H Liu, Y Chen

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

17 citing papers in PubMed, 20 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

10 authors at 3 institutions in 2 countries.

X ZhangDepartment of Immunology, Peking University School of Basic Medical Sciences, Beijing, China.
T FengWeill Institute for Cell and Molecular Biology, Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA.
X ZhouWeill Institute for Cell and Molecular Biology, Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA.
P M SullivanWeill Institute for Cell and Molecular Biology, Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA.
F HuWeill Institute for Cell and Molecular Biology, Department of Molecular Biology and Genetics, Cornell University, Ithaca, NY, USA.
Y LouMedical and Healthy Analytical Center, Peking University, Beijing, China.
J YuDepartment of Immunology, Peking University School of Basic Medical Sciences, Beijing, China.
J FengDepartment of Immunology, Peking University School of Basic Medical Sciences, Beijing, China.
H LiuDepartment of Geriatrics, Peking University Third Hospital, Beijing, China.
Y ChenDepartment of Immunology, Peking University School of Basic Medical Sciences, Beijing, China.ORCID 0000-0002-1324-603X
Peking University · CNCornell University · USCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pattern recognition receptors, such as Toll-like receptors (TLRs), play an important role in the host defense against invading microbial pathogens. Their activation must be precisely regulated, as inappropriate activation or overactivation of TLR signaling pathways may result in inflammatory disorders, such as septic shock or autoimmune diseases. TMEM106A is a type II transmembrane protein constitutively expressed in macrophages. Our current study demonstrated that TMEM106A levels were increased in macrophages upon lipopolysaccharide (LPS) stimulation, as well as in the peripheral monocytes of patients with sepsis. Tmem106a knockout mice were more sensitive to lipopolysaccharide (LPS)-induced septic shock than wild-type mice. Further experiments indicated that Tmem106a ablation enhanced the expression of CD80, CD86 and major histocompatibility complex (MHC)-II in mouse macrophages upon LPS stimulation, accompanied with up-regulation of tumor necrosis factor (TNF)-α, interleukin (IL)-6, interferon (IFN)-β and inducible nitric oxide synthase (iNOS), indicating the activation of macrophages and polarization towards the M1 inflammatory phenotype. Moreover, elevated mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) signaling were found to be involved in the LPS-induced inflammatory response in Tmem106a

Indexed as

AnimalsExtracellular Signal-Regulated MAP KinasesInflammationLipopolysaccharidesMacrophages, PeritonealMAP Kinase Signaling SystemMiceMice, KnockoutNF-kappa BTumor Suppressor ProteinsExtracellular Signal-Regulated MAP KinasesLipopolysaccharidesNF-kappa BTumor Suppressor ProteinsinflammationlipopolysaccharidemacrophageTMEM106A

Identifiers

PMID33006758
PMCPMC7744488
OpenAlexW3090510463

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.