Evidence map›Paper›PMID 31618170›Full record

ArticleProtein and peptide letters2019

NMAAP1 Maintains M1 Phenotype in Macrophages Through Binding to IP3R and Activating Calcium-related Signaling Pathways.

Qihui Liu, Pei Zhu, Shanshan Liu, Mengyan Tang, Yuanxin Wang, Yuan Tian, Zheng Jin, Dong Li, Dongmei Yan

Open access · hybridAbstract read
In one paragraph

Article in Protein and peptide letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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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

9 authors at 2 institutions in 1 country.

Qihui LiuDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Pei ZhuDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Shanshan LiuDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Mengyan TangDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Yuanxin WangDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Yuan TianDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Zheng JinDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Dong LiDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Dongmei YanDepartment of Immunology, College of basic Medical sciences, Jilin University, Changchun, China.
Jilin University · CNJilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNMAAP1 plays a role in regulating macrophage differentiation to the M1 type and exerting antitumoral functions. It is not clear what role and mechanism NMAAP1 does play in the reversal of macrophages from M1 to M2.

methodsWe detected the typing of macrophages with high or low expression of NMAAP1 by QPCR and ELISA, and detected the colocalization of NMAAP1 and endogenous IP3R by laser confocal microscopy, and detected the protein expression in cells by Western-blotting.

resultsOur study found that knockdown NMAAP1 in RAW264.7 cells induced macrophage polarization to the M2 type and up-regulation of NMAAP1 in RAW264.7 cells maintain M1 Phenotype even in the presence of IL-4, a stronger inducer of the M2 type. Additionally, Coimmunoprecipitation revealed a protein-protein interaction between NMAAP1 and IP3R and then activates key molecules in the PKC-dependent Raf/MEK/ERK and Ca2+/CaM/CaMKII signaling pathways. Activation of PKC (Thr638/641), ERK1/2 (Thr202/Tyr204) and CaMKII (Thr286) is involved in the regulation of cell differentiation.

conclusionNMAAP1 interacts with IP3R, which in turn activates the PKC-dependent Raf/MEK/ERK and Ca2+/CaM/CaMKII signaling pathways. These results provide a new explanation of the mechanism underlying M1 differentiation.

Indexed as

Signal TransductionAnimalsCalciumCell DifferentiationCytokinesGene Expression RegulationHumansInositol 1,4,5-Trisphosphate ReceptorsMacrophagesMembrane ProteinsMicePhenotypeProtein BindingRAW 264.7 CellsRNA, Small InterferingUp-RegulationCalciumCytokinesInositol 1,4,5-Trisphosphate ReceptorsMembrane ProteinsNMAAP1 protein, mouseRNA, Small InterferingIP3RM1macrophageNMAAP1polarization.Signaling Pathway

Identifiers

PMID31618170
PMCPMC7040510
OpenAlexW2978423667

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Registered trials

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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.