Evidence map›Paper›PMID 32522834›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2020

Cell Type- and Stimulation-Dependent Transcriptional Programs Regulated by Atg16L1 and Its Crohn's Disease Risk Variant T300A.

Mukund Varma, Motohiko Kadoki, Ariel Lefkovith, Kara L Conway, Kevin Gao, Vishnu Mohanan, Betsabeh Khoramian Tusi, Daniel B Graham, Isabel J Latorre, Andrew C Tolonen and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Article
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 2 institutions in 1 country.

Mukund VarmaBroad Institute of MIT and Harvard, Cambridge, MA 02142.ORCID 0000-0002-9254-1247
Motohiko KadokiBroad Institute of MIT and Harvard, Cambridge, MA 02142.ORCID 0000-0002-0124-7406
Ariel LefkovithBroad Institute of MIT and Harvard, Cambridge, MA 02142.
Kara L ConwayCenter for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.ORCID 0000-0001-6313-1348
Kevin GaoCenter for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.ORCID 0000-0001-5855-1006
Vishnu MohananBroad Institute of MIT and Harvard, Cambridge, MA 02142.
Betsabeh Khoramian TusiBroad Institute of MIT and Harvard, Cambridge, MA 02142.ORCID 0000-0001-7072-2162
Daniel B GrahamBroad Institute of MIT and Harvard, Cambridge, MA 02142.
Isabel J LatorreBroad Institute of MIT and Harvard, Cambridge, MA 02142.
Andrew C TolonenBroad Institute of MIT and Harvard, Cambridge, MA 02142.ORCID 0000-0001-5907-4504
Bernard KhorCenter for Computational and Integrative Biology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.ORCID 0000-0003-4689-5092
Aylwin NgBroad Institute of MIT and Harvard, Cambridge, MA 02142; aylwin.ng@gmail.com xavier@molbio.mgh.harvard.edu.
Ramnik J XavierBroad Institute of MIT and Harvard, Cambridge, MA 02142; aylwin.ng@gmail.com xavier@molbio.mgh.harvard.edu.ORCID 0000-0002-5630-5167
Broad Institute · USHarvard University · US

Funding

RP5: Chemical proteomic discovery of small-molecule probes for autophagy proteinsU19AI142784 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI CRAVATT, BENJAMIN F · 2019 to 2023
$36.9M
Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
ATG16L1 T300A: genetics to biologyR01DK097485 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI XAVIER, RAMNIK J · 2013 to 2021
$4.1M
NIAID NIH HHS U19 AI142784NIDDK NIH HHS P30 DK043351NIDDK NIH HHS R01 DK097485
6 · The paper itself

Abstract

Genome-wide association studies have identified common genetic variants impacting human diseases; however, there are indications that the functional consequences of genetic polymorphisms can be distinct depending on cell type-specific contexts, which produce divergent phenotypic outcomes. Thus, the functional impact of genetic variation and the underlying mechanisms of disease risk are modified by cell type-specific effects of genotype on pathological phenotypes. In this study, we extend these concepts to interrogate the interdependence of cell type- and stimulation-specific programs influenced by the core autophagy gene

Indexed as

GenotypeAnimalsAutophagy-Related ProteinsCells, CulturedCrohn DiseaseDendritic CellsGenetic Predisposition to DiseaseHumansMiceMice, Inbred C57BLMice, KnockoutOrgan SpecificityPhenotypePolymorphism, GeneticRiskT-LymphocytesAtg16l1 protein, mouseAutophagy-Related Proteins

Identifiers

PMID32522834
PMCPMC7364322
OpenAlexW3033934322

What OpenQuestion holds

Textmetadata
LicenceTDM
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.