Benjamin L. Parker

GenomeProt integrates genomics, transcriptomics, and proteomics to characterise proteoforms, discovering novel proteins and variant-containing peptides in human brain and melanoma samples.

The paper identifies SCAF4-CPA and KHDRBS1/SAM68 as key regulators of RNAPII termination under CDK12 inactivation, showing termination dynamics influence elongation rate and response to inhibition.

This study quantifies global PPI changes in skeletal muscle insulin resistance using PCP-MS and qXL-MS, revealing dysregulated interactions with chaperones and PDIA6.

This study shows that Rac1 deficiency in muscle reduces mitochondrial function and fatty acid metabolism, leading to muscle wasting and highlights potential therapeutic targets for age-related muscle decline.

The paper presents a proteomic dataset from rat cardiomyocytes treated with doxorubicin, identifying proteins regulated in young hearts and highlighting sex differences in cardiotoxicity.

This study identifies prenylation as a regulator of cardiomyocyte proliferation through multiple targets, suggesting its potential for cardiac regeneration.

The paper identifies new gene products and transcript isoforms in macrophage differentiation and activation, revealing how alternative promoters influence innate immune functions.

The paper uses long-read sequencing to identify novel RNA isoforms in neuropsychiatric risk genes, revealing previously undetected exons and isoforms that may contribute to disease mechanisms.

The paper quantifies UFMylation sites in mouse tissues and ALS patient biopsies, finding increased myosin UFMylation in ALS.

The paper shows DPPA2/4 in NSCLC create a unique chromatin state by uncoupling PRC complex recruitment from activity, promoting tumourigenesis.

The paper evaluates the clinical validity of heterozygous ALPK3 loss-of-function variants as a cause of hypertrophic cardiomyopathy, finding strong gene-disease association with reduced penetrance.

The paper identifies a selective JNK inhibitor that blocks metastasis in triple-negative breast cancer by targeting metabolic pathways.

eNODAL is a clustering method for nutriomics data that integrates experimental design with unsupervised learning to identify interpretable clusters of omics features affected by drug-diet interactions.

ThunderBolt provides an interactive web platform for analyzing large proteomics datasets through guided exploration, preprocessing, and statistical analysis.

The paper develops SnapKin, a deep learning ensemble model for kinase-substrate prediction from phosphoproteomics data, achieving the best performance in this task.

This study identifies mitochondrial fusion and beta-oxidation as key drivers of muscle wasting in a Drosophila cancer cachexia model and shows interventions can mitigate muscle loss.

The paper investigates how Bmal1 rescue and time-restricted feeding affect liver and muscle proteomes in mice, finding BMAL1 has a greater impact than feeding cycles.

The paper identifies three genetic loci influencing mitochondrial proteins and heart hypertrophy in mice using proteomics and association mapping.

The paper maps N-glycoproteome changes during neutrophil granulopoiesis, showing granule-specific glycosylation and remodelling driven by protein expression shifts.

The paper identifies UFMylation as a negative regulator of skeletal muscle function through proteome-wide systems genetics in mice and validates it in a disease model.

CoffeeProt is an open-source tool that integrates proteomics, genetics, and phenotypic data to identify functionally relevant genetic associations in mouse and human populations.

This paper standardizes a proteotype analysis workflow across multiple international sites to enable distributed, reproducible proteomic data generation for precision medicine.