Evidence map›Paper›PMID 28169274›Full record

ArticleNature communications2017

Armc5 deletion causes developmental defects and compromises T-cell immune responses.

Yan Hu, Linjiang Lao, Jianning Mao, Wei Jin, Hongyu Luo, Tania Charpentier, Shijie Qi, Junzheng Peng, Bing Hu, Mieczyslaw Martin Marcinkiewicz and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 62 citations in OpenAlex.

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  7. A Rare De Novo Mutation in theInternational journal of molecular sciences · 2024
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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

12 authors at 4 institutions in 3 countries.

Yan HuCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Linjiang LaoCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Jianning MaoCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Wei JinCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Hongyu LuoCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Tania CharpentierInstitut national de la recherche scientifique-Institut Armand-Frappier (INRS-IAF), 531 Boul. des Prairies, Laval, Québec, Canada H7V 1B7.
Shijie QiCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Junzheng PengCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Bing HuAnatomic Pathology, AmeriPath Central Florida, 4225 Fowler Ave. Tampa, Orlando, Florida 33617, USA.
Mieczyslaw Martin MarcinkiewiczCytochem Inc., 6465 Av Durocher, Outremont, Montréal, Québec, Canada H2V 3Z1.
Alain LamarreInstitut national de la recherche scientifique-Institut Armand-Frappier (INRS-IAF), 531 Boul. des Prairies, Laval, Québec, Canada H7V 1B7.ORCID 0000-0002-7913-871X
Jiangping WuCentre de recherche (CR), Centre hospitalier de l'Université de Montréal (CHUM), 900 Rue Saint Denis, Montréal, Québec, Canada H2X 0A9.
Centre Hospitalier de l’Université de Montréal · CAInstitut National de la Recherche Scientifique · CAFlorida Orthopaedic Institute · USSinochem Group (China) · CN

Funding

CIHR MOP 123389CIHR MOP69089CIHR MOP89797CIHR MOP97829
6 · The paper itself

Abstract

Armadillo repeat containing 5 (ARMC5) is a cytosolic protein with no enzymatic activities. Little is known about its function and mechanisms of action, except that gene mutations are associated with risks of primary macronodular adrenal gland hyperplasia. Here we map Armc5 expression by in situ hybridization, and generate Armc5 knockout mice, which are small in body size. Armc5 knockout mice have compromised T-cell proliferation and differentiation into Th1 and Th17 cells, increased T-cell apoptosis, reduced severity of experimental autoimmune encephalitis, and defective immune responses to lymphocytic choriomeningitis virus infection. These mice also develop adrenal gland hyperplasia in old age. Yeast 2-hybrid assays identify 16 ARMC5-binding partners. Together these data indicate that ARMC5 is crucial in fetal development, T-cell function and adrenal gland growth homeostasis, and that the functions of ARMC5 probably depend on interaction with multiple signalling pathways.

Indexed as

Adrenal GlandsAnimalsArmadillo Domain ProteinsCell DifferentiationCell LineCell ProliferationEncephalomyelitis, Autoimmune, ExperimentalFemaleFetal DevelopmentGerm-Line MutationHumansHyperplasiaImmunity, CellularMaleMiceMice, Inbred C57BLArmadillo Domain ProteinsArmc5 protein, mouseMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID28169274
PMCPMC5309699
OpenAlexW2586245389

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.