Biology subjects

Mun, H.

Publications and source records attributed to Mun, H..

3 recordsLinked to original sources

bioRxiv2026

ProCAST: A Bioinformatics Suite for Mass Spectrometry-Based Protein Corona Proteomics Analysis

When nanoparticles are exposed to biological fluids, they spontaneously adsorb proteins, forming a protein corona that defines their biological identity and dictates cellular uptake, biodistribution, and toxicity. Characterizing protein coronas includes using proteomics approaches (e.g., LC-MS/MS) to identify proteins and generate vast lists of adsorbed proteins, often visualized via complex heatmaps. While heatmaps display data they do not offer heuristic guide, leaving the driving mechanisms of adsorption unknown. Moreover, interpretation of protein corona proteomics data remains limited by fragmented workflows, inconsistent preprocessing, and visual outputs that are often descriptive rather than readily interpretable. These conventional methods identify adsorbed proteins but fail to explain why specific proteins are selected or how they influence the particles biological fate. Here, we developed ProCAST (Protein Corona Analysis and Statistical Tool), an R-based framework for protein corona proteomics that integrates proteomics data, nanoparticle metadata, protein annotations, and multi-level visualization within a single analytical workflow. ProCAST facilitates abundant protein clustering based on sample conditions, sequence descriptors, property or protein correlations, and gene ontology-based functional visualization. It also distinguishes abundant proteins from frequent proteins, providing distinct layers of information from the same dataset. ProCAST was used to re-analyze previously published PAMAM G4 dendrimer-FBS datasets, demonstrating that ProCAST reproduces descriptor-level visualizations and offers new insights through clearer comparisons of functional patterns and hypothesis generation from dominant corona proteins. By organizing results as complementary views of the same dataset, ProCAST facilitates the shift of protein corona analysis from descriptive outputs toward structured, comparative, and experimentally testable interpretations.

bioinformatics↗

bioRxiv2025

Neat1 alleviates ischemic injury in skeletal muscles

Peripheral artery disease (PAD) has historically been regarded as an age-related vascular disorder; however, recent attention has shifted toward the myopathic components of the disease. Conventional interventions, such as revascularization, have had limited success in reversing muscle pathology or preventing adverse outcomes like amputation. Hypoxia-inducible factors (HIFs) are key regulators of cellular responses to ischemia, including the promotion of angiogenesis and glycolysis. While pharmacological stabilization of HIF proteins represents a promising therapeutic strategy, its efficacy is diminished in aged muscles due to their intrinsically low basal HIF expression. We hypothesized that long noncoding RNAs (lncRNAs) might enhance the hypoxic response in aged muscle through post-transcriptional regulation of HIF expression. Our study identified a long noncoding RNA Neat1, as a critical mediator of the hypoxia-induced stress response, including upregulation of Hif1. In a murine hindlimb ischemia model, Neat1 knockout mice exhibited extensive necrosis following femoral artery ligation, whereas Neat1 overexpression conferred protection against ischemic injury. Mechanistically, we found that Neat1 regulates the stability of Hif1a mRNA, as Hif1a transcript levels were significantly reduced in Neat1-deficient muscle cells. Importantly, aged muscles displayed a blunted hypoxic response due to diminished Hif1a expression--an effect that was reversed through Neat1 overexpression, resulting in improved resistance to ischemic damage. In summary, our findings highlight Neat1 as a novel regulator of muscle adaptation to hypoxia in aging. Enhancing Neat1 expression may represent a promising therapeutic strategy for improving ischemic outcomes in patients with peripheral artery disease.

cell biology↗

bioRxiv2023

Mature microRNA-binding protein QKI promotes microRNA-mediated gene silencing

Although Argonaute (AGO) proteins have been the focus of microRNA (miRNA) studies, we observed AGO-free mature miRNAs directly interacting with RNA-binding proteins, implying the sophisticated nature of fine-tuning gene regulation by miRNAs. To investigate microRNA-binding proteins (miRBPs) globally, we analyzed PAR-CLIP data sets to identify RBP quaking (QKI) as a novel miRBP for let-7b. Potential existence of AGO-free miRNAs were further verified in genetically engineered AGO-depleted human and mouse cells. We have shown that QKI serves as an auxiliary factor empowering AGO2/let-7b-mediated gene silencing. Depletion of QKI decreases interaction of AGO2 with let-7b and target mRNA, consequently controlling target mRNA decay. QKI, however, also suppresses the dissociation of let-7b from AGO2, and slows assembly of AGO2/miRNA/target mRNA complexes at the single-molecule level. We also revealed that QKI suppresses cMYC expression at post-transcriptional level, and decreases proliferation and migration of HeLa cells, demonstrating that QKI is a tumor suppressor gene by in part augmenting let-7b activity. Our data show that QKI is a new type of RBP implicated in the versatile regulation of miRNA-mediated gene silencing.

biochemistry↗