Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Monogenic Diabetes and Integrated Stress Response Genes Display Altered Gene Expression in Type 1 Diabetes.

Diabetes - 1 Aug 2021

Hiller Helmut, Beachy Dawn E, Lebowitz Joseph J, Engler Stefanie, Mason Justin R, Miller Douglas R, Kusmarteva Irina, Jacobsen Laura M, Posgai Amanda L, Khoshbouei Habibeh, Oram Richard A, Schatz Desmond A, Hattersley Andrew T, Bodenmiller Bernd, Atkinson Mark A, Nick Harry S, Wasserfall Clive H

Abstract excerpt

Type 1 diabetes (T1D) has a multifactorial autoimmune etiology, involving environmental prompts and polygenic predisposition. We hypothesized that pancreata from individuals with and at risk for T1D would exhibit dysregulated expression of genes associated with monogenic forms of diabetes caused by nonredundant single-gene mutations. Using a "monogenetic transcriptomic strategy," we measured the expression of...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autoantibodies
Share to Diabetes Mellitus, Type 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation

Share to Mutation

Share to Pancreas

Share to Transcriptome

Source

Open in PubMed Open full text

Identifiers

PMID: 34035041
DOI: 10.2337/db21-0070
PMCID: PMC8385619

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Monogenic Diabetes and Integrated Stress Response Genes Display Altered Gene Expression in Type 1 Diabetes.PMID 34035041Read ↗

Single-cell gene expression and chromatin accessibility profiling of human pancreatic islets at basal and stimulatory conditions nominates mechanisms of type 1 diabetes genetic riskSemantic proximity Read ↗

Identification of unique cell type responses in pancreatic islets to stressSemantic proximity Read ↗

Multiomics single-cell analysis of human pancreatic islets reveals novel cellular states in health and type 1 diabetesSemantic proximity Read ↗

An Islet-Targeted Genome-Wide Association Scan Identifies Novel Genes Implicated in Cytokine-Mediated Islet Stress in Type 2 DiabetesSemantic proximity Read ↗

Increased Inflammation as well as Decreased Endoplasmic Reticulum Stress and Translation Differentiate Pancreatic Islets of Pre-symptomatic Stage 1 Type 1 Diabetes and Non-diabetic CasesSemantic proximity Read ↗

Increased inflammation as well as decreased endoplasmic reticulum stress and translation differentiate pancreatic islets from donors with pre-symptomatic stage 1 type 1 diabetes and non-diabetic donorsSemantic proximity Read ↗

Multi-omic human pancreatic islet endoplasmic reticulum and cytokine stress response mapping provides type 2 diabetes genetic insights.Semantic proximity Read ↗

Single-cell multiome and spatial profiling reveals pancreas cell type-specific gene regulatory programs driving type 1 diabetes progressionSemantic proximity Read ↗

An integrative single-cell multi-omics profiling of human pancreatic islets identifies T1D associated genes and regulatory signalsSemantic proximity Read ↗

Comparative Multi-omic Mapping of Human Pancreatic Islet Endoplasmic Reticulum and Cytokine Stress Responses Provides Insights into Type 2 Diabetes GeneticsSemantic proximity Read ↗

β‐Cell gene expression stress signatures in types 1 and 2 diabetesSemantic proximity Read ↗

An integrated map of cell type-specific gene expression in pancreatic isletsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.