Cell Type- and Stimulation-Dependent Transcriptional Programs Regulated by Atg16L1 and Its Crohn's Disease Risk Variant T300A.
Animals
Autophagy-Related Proteins
/ genetics
Cells, Cultured
Crohn Disease
/ genetics
Dendritic Cells
/ physiology
Genetic Predisposition to Disease
Genotype
Humans
Mice
Mice, Inbred C57BL
Mice, Knockout
Organ Specificity
Phenotype
Polymorphism, Genetic
Risk
T-Lymphocytes
/ physiology
Transcriptional Activation
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
15 07 2020
15 07 2020
Historique:
received:
03
07
2019
accepted:
06
05
2020
pubmed:
12
6
2020
medline:
16
3
2021
entrez:
12
6
2020
Statut:
ppublish
Résumé
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
Identifiants
pubmed: 32522834
pii: jimmunol.1900750
doi: 10.4049/jimmunol.1900750
pmc: PMC7364322
mid: NIHMS1598792
doi:
Substances chimiques
Atg16l1 protein, mouse
0
Autophagy-Related Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
414-424Subventions
Organisme : NIDDK NIH HHS
ID : P30 DK043351
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK097485
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI142784
Pays : United States
Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.
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