Patrick E. MacDonald

This study compares functional, transcriptomic, and proteomic profiles of human primary and stem cell-derived beta cells in high and low insulin production states, revealing differences in resilience and protein machinery.

This study shows that MAFB is essential for maintaining adult human α-cell identity and function, linking its downregulation to impaired glucagon secretion and mitochondrial dysfunction in diabetes.

This study maps spatial and functional states of human pancreatic cells in health and disease using combined single-cell and spatial transcriptomics with calcium imaging.

This study compares immature stem-cell-derived β-cells to primary β-cells using multi-omic single-cell methods, identifying SREBP1 as a target for improving β-cell maturation.

The paper uses supervised machine learning to identify impaired mitochondrial quality control in β cells associated with type 2 diabetes using single-cell RNA sequencing data.

The paper uses computational modeling to identify key parameters controlling glucose-induced excitability diversity in human pancreatic β-cells.

This paper introduces mxDVP, a method combining high-plex imaging and mass spectrometry to profile pancreatic islets, identifying 12 endocrine subtypes and revealing spatial heterogeneity and rare cell states.

This study investigates GlyR dysfunction in T2D and high glucose conditions, finding reduced GlyR currents and gene expression, but no splicing changes, and links GlyR activity to gene regulatory networks.

This study identifies TMEM55A as a regulator of α-cell exocytosis and glucagon secretion through PI5P signaling and F-actin remodeling in response to oxidative stress.

This study investigates islet cell dysfunction in type 1 diabetes by integrating electrophysiological, transcriptomic, and machine learning analyses of human islet cells from T1D donors.

The paper infers post-transcriptional regulatory mechanisms in human islets using cell type-specific eQTLs from single-cell RNA-seq data, linking variants to biological processes in health and disease.

This study shows cisplatin exposure impairs pancreatic islet function in male mice by disrupting insulin secretion and causing DNA damage in beta cells.

The paper examines islet isolation and culture outcomes at the Alberta Diabetes Institute IsletCore, finding islet loss occurs within 24 hours of isolation with no further loss after extended culture.

The paper uses single-cell multiome profiling to identify gene regulatory changes in pancreatic islets linked to diabetes risk factors like age, sex, and genetic variants.

HumanIslets.com provides an open platform for accessing and analyzing human islet data, enabling research on diabetes through integrated molecular and cellular phenotyping.

This study identifies FKBP2 as a proline isomerase involved in proinsulin folding, showing its role in preventing misfolding and apoptosis in β-cells.

The paper integrates single-cell multiomic data with genetics to identify gene regulatory changes in beta cells associated with type 2 diabetes.

A genome-wide CRISPR screen in human pancreatic beta cells identifies 580 genes influencing insulin content, supporting 20 candidate type 2 diabetes effector transcripts.

This study investigates how HNF1A regulates human islet cell function by combining genetic, transcriptomic, and functional assays, revealing its role in maintaining insulin and glucagon secretion.

The paper identifies combinatorial transcription factor expression in human islet cells and shows it correlates with functional maturity and electrophysiological activity.

The paper investigates how genetic variants affect gene expression in human pancreatic islets and identifies candidate genes linked to type 2 diabetes.

This study links transcriptomic heterogeneity in pancreatic islet cells to their physiological function using a combined electrophysiological and single-cell RNA sequencing approach, identifying genes and pathways associated with diabetes-related dysfunction.

This study identifies T2D risk alleles in PAM that impair beta cell function through distinct effects on expression and catalytic activity, revealing a novel mechanism involving Chromogranin A.