Biology subjects

Mun, S.

Publications and source records attributed to Mun, S..

6 recordsLinked to original sources

bioRxiv2026

Skin-Related Effects of Corynebacterium amycolatum SB-1 Ferment Filtrate and Functional Characterization of Ellagic Acid

Previous research has established a link between the genus Corynebacterium in the skin microbiota and skin health; however, studies investigating the specific effects of Corynebacterium-derived substances on skin cells remain limited. In this study, we isolated eight strains of Corynebacterium from the facial skin of female participant. To investigate the potential skin improvement effects of these isolates, three cultured skin cell lines (Hs68, HaCaT, and B16-F10) were treated with the supernatants of each strain. We then evaluated and compared the gene expression levels (ELN, COL1A1, IL-1{beta}, and HAS3) alongside their inhibitory effects on melanin biosynthesis. Corynebacterium amycolatum SB-1 was selected as the final candidate for subsequent analysis, primarily based on its rapid growth rate and high cell yield. Using LC-TOF/MS, we screened the postbiotic candidates from the SB-1 strain and identified ellagic acid as a known polyphenolic antioxidant with potent anti-melanogenic effects beneficial for skin improvement. To validate the effects of ellagic acid on skin cells, we assessed FLG gene expression and its inhibition of melanin biosynthesis. Additionally, RNA sequencing was performed to elucidate the underlying molecular mechanisms, revealing that ellagic acid is significantly involved in inhibiting melanogenesis and promoting collagen synthesis. Taken together, our results highlight ellagic acid derived from strain SB-1 as a highly effective bioactive compound for improving skin health, specifically targeting hyperpigmentation and skin aging.

genomics↗

bioRxiv2026

TACE reprograms RANKL-mediated differentiation of macrophages by activating the non-canonical pathway of IRF3

Inflammation is associated with an influx of inflammatory macrophages and increased activation and differentiation of osteoclasts. Receptor activator of NF-kB ligand (RANKL) is a key driver for osteoclast differentiation. However, the pathogenic mechanisms augmenting RANKL-induced osteoclast differentiation in inflammatory conditions are not fully elucidated. Here, we show that TNF- converting enzyme (TACE) plays a critical role in pathological bone erosion and enhances osteoclast differentiation in inflammatory conditions. Myeloid cell-specific TACE deletion in a murine arthritis model attenuates joint inflammation and bone destruction. TACE deficiency suppresses distal RANKL signaling in macrophages by increasing IRF3 activation, while enhancing proximal RANKL signaling, leading to the suppression of osteoclast differentiation. Mechanistically, IRF3 activation limits macrophage reprogramming by suppressing NFATc1 and HB-EGF in response to RANKL through a non-canonical pathway. HB-EGF, a TACE substrate, activates EGFR signaling and promotes osteoclastogenesis by inhibiting IRF3 activation. TACE regulates the reciprocal inhibition of the IRF3-HBEGF axis. Our study highlights a role for TACE as a rheostat, balancing both pro- and anti-osteoclastogenic signals.

cell biology↗

bioRxiv2024

Cellular dsRNA interactome reveals the regulatory map of exogenous RNA sensing

RNA-binding proteins (RBPs) provide a critical post-transcriptional regulatory layer in determining RNA fate. Currently, UV crosslinking followed by oligo-dT pull-down is the golden standard in identifying the RBP repertoire, but such method is ineffective in capturing RBPs that recognize double-stranded RNAs (dsRNAs). Here, we utilize anti-dsRNA antibody immunoprecipitation followed by quantitative mass spectrometry to comprehensively identify RBPs bound to cellular dsRNAs without any external stimulus. Notably, our dsRNA interactome contains proteins involved in sensing N6-methyladenosine RNAs and stress granule components. We further perform targeted CRISPR-Cas9 knockout functional screening and discover proteins that can regulate the interferon (IFN) response during exogenous RNA sensing. Interestingly, depleting dsRBPs mostly attenuate the IFN response, and they act as antiviral factors during human {beta}-coronavirus HCoV-OC43 infection. Our dsRNA interactome capture provides an unbiased and comprehensive characterization of putative dsRBPs and will facilitate our understanding of dsRNA sensing in both physiological and pathological contexts.

molecular biology↗

bioRxiv2023

A Glance into the Density of Transcriptomic Activity, Embodied by the HOX Genes, in Neonatal and Aging Dermal Cells

Skin is an organ having a crucial role in the protection of muscle, bone, and internal organs and undergoing continuous self-renewal and aged. The growing interest in the prevention of skin aging and rejuvenation has sparked a surge of industrial and research studies focusing on the biological and transcriptional changes that occur during skin development and aging. In this study, we aimed to identify transcriptional differences between two main types of human skin cells: the HDFs and the HEK isolated from 30 neonatal and 30 adults (old) skin. Through differentially expressed gene (DEG) profiling using DEseq2, 604 up-, and 769 down-regulated genes were identified in the old group. The functional classification analysis using Metascape Gene Ontology and Reactome pathway was performed. We report the systematic transcriptomic changes in key biological markers involved in skin formation and maintenance and a unique difference in HOX gene families which are important for developing embryonic formation and regulating numerous biological processes. Among the 39 human HOX genes, 10 genes (HOXA10, 11, 13, HOXB13, HOXC11, and HOXD9-13) were significantly down-regulated, and 25 genes HOXA2-7, HOXB1-9, HOXC4-6 and 8-9, and HOXD1,3,4 and 8) were up-regulated, especially in the old HDFs. We have successfully established a correlation between HOX genes and the process of skin aging, thereby proposing HOX genes as a novel marker for assessing skin aging. Our findings provide compelling evidence supporting the involvement of HOX genes in this biological phenomenon such as skin aging.

genomics↗

bioRxiv2019

Human Reference Genome and a High Contiguity Ethnic Genome AK1

Studies have shown that the current human reference genome (GRCh38) might miss information for some populations, but \"exactly what we miss\" is still elusive due to the lower contiguity of non-reference genomes. We juxtaposed the GRCh38 with high contiguity genome assemblies, AK1, to show that [~]1.8% ([~]53.4 Mbp) of AK1 sequences missed in GRCh38 with [~]0.76% ([~]22.2 Mbp) of ectopic chromosomes. The unique AK1 sequences harbored [~]1,390 putative coding elements. We found that [~]5.3Mb ([~]0.2%) of the AK1 sequences aligned and recovered the \"unmapped\" reads of fourteen individuals (5 East-Asians, 4 Europeans, and 5 Africans) as a reference. The regions that \"unmapped\" reads aligned included 110 common (shared between [≥]2 individuals) and 38 globally ([≥]7 individuals) missing regions with 25 candidate coding elements. We verified that many of the common missing regions exist in multiple populations and chimpanzees DNA. Our study illuminates not only the discovery of missing information but the use of highly precise ethnic genomes in understanding human genetics.

genomics↗

bioRxiv2016

Contribution of mobile elements to the uniqueness of human genome with more than 15,000 human-specific insertions

Mobile elements (MEs) collectively constituted to at least 51% of the human genome. Due to their past incremental accumulation and ongoing DNA transposition of members from certain subfamilies, MEs serve as a significant source for both inter- and intra-species genetic diversity during primate and human evolution. Since MEs can exert direct impact on gene function via a plethora of mechanism, it is believed that the ME-derived genetic diversity has contributed to the phenotypic differences between human and non-human primates, as well as among human populations and individuals. To define the specific contribution of MEs in making Human sapiens as a biologically unique species, we aim to compile a complete list of MEs that are only uniquely present in the human genome, i.e., human-specific MEs (HS-MEs).\n\nBy making use of the most recent reference genome sequences for human and many other primates and a unbiased more robust and integrative multi-way comparative genomic approach, we identified a total of 15,463 HS-MEs. This list of HS-MEs represents a 120% increase from prior studies with over 8,000 being newly identified as HS-MEs. Collectively, these ~15,000 HS-MEs have contributed to a total of 15 million base pair (Mbp) sequence increase through insertion, generation of target site duplications, and transductions, as well as a 0.5 Mbp sequence loss via insertion- mediated deletions, leading to a net total of 14.5 Mbp genome size increase. Other new observations made with these HS-MEs include: 1) identification of several additional ME subfamilies with significant transposition activities not visible with prior smaller datasets (e.g. L1HS, L1PA2, and HERV-K); 2) A clear similarity of the retrotransposition mechanism among L1, Alus, and SVAs that is distinct from HERVs based on the pre- integration site sequence motifs; 3) Y-chromosome as a strikingly hot target for HS-MEs, particularly for LTRs, which showed an insertion rate 15 times higher than the genome average; 4) among the ME types, SVAs seem to show a very strong bias in inserting into existing SVAs. Among the HS-MEs, more than 8,000 elements were integrated into the vicinity of ~4900 unique genes, in regions including CDS, untranslated exon regions, promoters, and introns of protein coding genes, as well as promoters and exons of non- coding RNAs. In seven cases, MEs participate in protein coding. Furthermore, 1,213 HS-MEs contributed to a total of 3,124 experimentally identified binding sites for 146 of the 161 transcriptional factors in association with 622 genes. All these data suggest that these HS-MEs, despite being very young, already showed sufficient sign for their participation in gene function via regulation of transcription, splicing, and protein coding, with more potential for future participation.\n\nIn conclusion, our results demonstrate that the amount of MEs uniquely occurred in the human genome is much higher than previously known, and we predict that the same is true regarding their impact on human genome evolution and function. The comprehensive list of HS-MEs provides an important reference resource for studying the impact of DNA transposition in human genome evolution and gene function.

evolutionary biology↗