Evidence map›Paper›PMID 37366613›Full record

ArticlemBio2023

SHIP1 modulates antimalarial immunity by bridging the crosstalk between type I IFN signaling and autophagy.

Hongyu Li, Shuai Yang, Ke Zeng, Jiayin Guo, Jian Wu, Huaji Jiang, Yingchao Xie, Zhiqiang Hu, Jiansen Lu, Jianwu Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in mBio, 2023. 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
1.1field-weighted citation impact, top 22% 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, 5 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

13 authors at 6 institutions in 2 countries.

Hongyu LiDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.ORCID 0000-0003-1784-4595
Shuai YangGuangdong Province Key Laboratory of Pharmaceutical Functional Genes, MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University , Guangzhou, Guangdong, China.
Ke ZengDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Jiayin GuoDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Jian WuMalaria Functional Genomics Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, Maryland, USA.
Huaji JiangDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Yingchao XieDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Zhiqiang HuDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Jiansen LuDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Jianwu YangDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.
Xin-Zhuan SuMalaria Functional Genomics Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, Maryland, USA.ORCID 0000-0003-3246-3248
Jun CuiGuangdong Province Key Laboratory of Pharmaceutical Functional Genes, MOE Key Laboratory of Gene Function and Regulation, School of Life Sciences, Sun Yat-sen University , Guangzhou, Guangdong, China.
Xiao YuDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University , Guangzhou, Guangdong, China.ORCID 0000-0003-2491-9110
Southern Medical University · CNNational Institutes of Health · USSun Yat-sen University · CNCell Technology (China) · CNShantou University · CNThird Affiliated Hospital of Southern Medical University · CN

Funding

Malaria Parasite Sexual Development, Drug Resistance, and EvolutionZIAAI000892 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SU, XINZHUAN · 2009 to 2025
$23.3M
Division of Intramural Research, National Institute of Allergy and Infectious Diseases (DIR, NIAID) NAGDSTC | Basic and Applied Basic Research Foundation of Guangdong Province () 2019B1515120033GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province () 2021A1515012140Guangdong Zhujiang Youth Scholar Funding NAMOST | National Natural Science Foundation of China (NSFC) 81801579MOST | National Natural Science Foundation of China (NSFC) 82171741The Star-up Fund for High-level talents of Southern Medical University NA
6 · The paper itself

Abstract

Stringent control of the type I interferon (IFN-I) signaling is critical for host immune defense against infectious diseases, yet the molecular mechanisms that regulate this pathway remain elusive. Here, we show that Src homology 2 containing inositol phosphatase 1 (SHIP1) suppresses IFN-I signaling by promoting IRF3 degradation during malaria infection. Genetic ablation of

Indexed as

AutophagyInterferon Type IMalariaPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPlasmodium yoeliiSignal TransductionAnimalsHumansInterferon Regulatory Factor-3MiceMice, Inbred C57BLMice, KnockoutInpp5d protein, mouseInterferon Regulatory Factor-3Interferon Type IIrf3 protein, mousePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesautophagyIRF3PlasmodiumSHIP1type I interferon

Identifiers

PMID37366613
PMCPMC10470592
OpenAlexW4382182092

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.