A5100435068- DNA Repair Mechanisms
- MicroRNA in disease regulation
- Epigenetics and DNA Methylation
- Cancer-related Molecular Pathways
- RNA Interference and Gene Delivery
- Cancer-related gene regulation
- Legionella and Acanthamoeba research
- Ubiquitin and proteasome pathways
- RNA Research and Splicing
- Microtubule and mitosis dynamics
- Mitochondrial Function and Pathology
- PARP inhibition in cancer therapy
- Genomics and Chromatin Dynamics
- RNA and protein synthesis mechanisms
- Wnt/β-catenin signaling in development and cancer
- Cell death mechanisms and regulation
- Nuclear Structure and Function
- Genetic factors in colorectal cancer
- CRISPR and Genetic Engineering
- Cancer Research and Treatments
- Carcinogens and Genotoxicity Assessment
- Autophagy in Disease and Therapy
- Metal-Catalyzed Oxygenation Mechanisms
- interferon and immune responses
- Polyomavirus and related diseases
Chosun University
2014-2025
Boston University
2013-2024
VA Boston Healthcare System
2013-2024
Gyeonggi Research Institute
2021
Hallym University
2018
Korea Yakult (South Korea)
2014
Samsung Medical Center
2009
Sungkyunkwan University
2009
Edith Nourse Rogers Memorial Veterans Hospital
2008
Geriatric Research Education and Clinical Center
2008
Homologous recombination (HR) is critical for error-free repair of DNA double-strand breaks. Chromatin loading RAD51, a key protein that mediates the recombination, crucial step in execution HR repair. Here, we present evidence SUMOylation RAD51 recruitment to chromatin and We found topoisomerase 1-binding arginine/serine-rich (TOPORS) induces at lysine residues 57 70 response damaging agents. The was facilitated by an ATM-induced phosphorylation TOPORS threonine 515 upon damage. Knockdown...
Abstract Wnt signaling is essential for cell growth and tumor formation abnormally activated in colorectal cancer (CRC), contributing to progression; however, the specific role regulatory mechanisms involved development remain unclear. Here, we show that Ephexin1, a guanine nucleotide exchange factor, significantly overexpressed CRC correlated with increased Wnt/β-catenin pathway activity. Through comprehensive analysis, including RNA sequencing data from TCGA functional assays, observed...
Transforming growth factor (TGF)-β1 is well established as a critical IgA isotype switching and Smad molecules have been reported to act transducers transcriptional factors in the expression of TGF-β1-targeted genes. We examined involvement proteins TGF-β1-induced expression. First, we found that TGF-β1 significantly increases endogenous germ-line (GL) α transcripts by LPS-stimulated CH12.LX.4933 (μ+) B lymphoma cells. To investigate its signaling mechanisms, cell line was transfected with...
MSH6, a key component of the MSH2–MSH6 complex, plays fundamental role in repair mismatched DNA bases. Herein, we report that MSH6 is novel Ku70-interacting protein identified by yeast two-hybrid screening. Ku70 and Ku86 are two regulatory subunits DNA-dependent kinase, which an essential double-strand breaks (DSBs) through non-homologous end-joining (NEHJ) pathway. We found association with enhanced response to treatment radiomimetic drug neocarzinostatin (NCS) or ionizing radiation (IR),...
MDC1 is critical component of the DNA damage response (DDR) machinery and orchestrates ensuring assembly DDR protein at sites, therefore loss results in genomic instability tumorigenicity. However, molecular mechanisms controlling expression are currently unknown. Here, we show that miR-22 inhibits translation via direct binding to its 3' untranslated region, leading impaired repair instability. We demonstrated activated Akt1 senescence hinder function by upregulating endogenous miR-22....
Chromatin remodeling is tightly controlled under physiological conditions. Alterations in chromatin structure are involved the pathogenesis of neuronal systems. We found that monoallelic deletion CREB binding protein (CBP) results induction ERG-associated with SET domain (ESET) and increases trimethylation histone H3 (K9) condensation pericentromeric heterochromatin neurons. Nested mutational analysis ESET promoter further demonstrated Ets-2 transcription factor regulates transcriptional...
53BP1 (p53-binding protein 1) is a conserved nuclear that phosphorylated in response to DNA damage and rapidly recruited the site of double strand breaks, demonstrating its role early events repair damaged DNA. In this study, we used yeast two-hybrid system identify proteins interact with 53BP1. Identification characterization interactions may help further elucidate function regulation We identified phosphatase 5 (PP5), serine/threonine has been implicated multiple cellular function, as...
Abstract Genistein, a phyto-estrogen, can potentially replace endogenous estrogens in postmenopausal women, but the underlying molecular mechanisms remain incompletely understood. To obtain insight into effect of genistein on bone differentiation, RNA sequencing (RNA-seq) analysis was used to detect differentially expressed genes (DEGs) genistein-treated vs. untreated MC3T3-E1 mouse osteoblastic cells. Osteoblastic cell differentiation monitored by measuring osteoblast factors (ALP...
MDC1 plays a critical role in the DNA damage response (DDR) by interacting directly with several factors including γ-H2AX. However, mechanism which is recruited to damaged sites remains elusive. Here, we show that interacts helix-loop-helix (HLH)-containing protein called inhibitor of DNA-binding 3 (ID3). In double-strand breaks (DSBs) genome, ATM phosphorylates ID3 at serine 65 within HLH motif, and this modification allows direct interaction MDC1. Moreover, depletion results impaired...
Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) required for in NIH3T3 cells. treatment resulted activation ERK, and U0126, inhibitors MEK/ERK signaling pathway, prevented Moreover, was associated with cytochrome C release, which could be MEK inhibitors. Taken together, our findings suggest ERK...
Abstract The Hsp70-binding protein 1 (HspBP1) belongs to a family of co-chaperones that regulate Hsp70 activity and whose biological significance is not well understood. In the present study, we show when HspBP1 either knocked down or overexpressed in BRCA1-proficient breast cancer cells, there were profound changes tumorigenesis, including anchorage-independent cell growth vitro tumor formation xenograft models. However, did affect tumorigenic properties BRCA1-deficient cells. mechanisms...
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDiscovery of a novel class orally active, non-peptide angiotensin II antagonistsB. De, M. Winn, T. Zydowsky, D. J. Kerkman, F. DeBernardis, Lee, S. Buckner, R. Warner, Brune, and Cite this: Med. Chem. 1992, 35, 20, 3714–3717Publication Date (Print):October 1, 1992Publication History Published online1 May 2002Published inissue 1 October 1992https://pubs.acs.org/doi/10.1021/jm00098a018https://doi.org/10.1021/jm00098a018research-articleACS...
An AU-rich element (ARE) in the 3′-untranslated region (UTR) of bcl-2 mRNA has previously been shown to be responsible for destabilizing during apoptosis through increasing AUF1 binding. In present study, we investigated effect upstream ARE on stability using serial deletion constructs 3′-UTR bcl-2. Deletion 30 nucleotides mostly consisting CA repeats, located ARE, resulted stabilization abundance, absence or presence ARE. The specificity repeats terms was proven by substituting with other...
DNA double-strand breaks (DSBs) are one of the most lethal types damage due to fact that unrepaired or mis-repaired DSBs lead genomic instability chromosomal aberrations, thereby causing cell death tumorigenesis. The classical non-homologous end-joining pathway (c-NHEJ) is major repair mechanism for rejoining DSBs, and catalytic subunit DNA-dependent protein kinase (DNA-PKcs) a critical factor in this pathway; however, regulation DNA-PKcs expression remains unknown. In study, we demonstrate...
Abstract Human CtIP maintains genomic integrity primarily by promoting 5′ DNA end resection, an initial step of the homologous recombination (HR). A few mechanisms have been suggested as to how recruitment damage sites is controlled, but it likely that we do not yet full understanding process. Here, provide evidence and functioning are controlled SIAH2 E3 ubiquitin ligase. We found interacts ubiquitinates at its N-terminal lysine residues. Mutating key residues impaired DSBs stalled...
53BP1 is an important genome stability regulator, which protects cells against double-strand breaks. Following DNA damage, rapidly recruited to sites of breakage, along with other damage response proteins, including γ-H2AX, MDC1, and BRCA1. The recruitment requires a tandem Tudor fold associates methylated histones H3 H4. It has already been determined that the majority proteins are phosphorylated by ATM and/or ATR after then break sites. also at several sites, like but this phosphorylation...
Bis (Bag-3, CAIR), a Bcl-2-interacting protein, promotes the anti-apoptotic activity of Bcl-2 and increased levels have been observed in several disease models. The involvement some Bcl-2-binding proteins differentiation has recently reported. However, relevance to cellular remains unknown. findings herein show that expression is up-regulated during HL-60 cells. To investigate effect on differentiation, we established Bis-overexpressing cells (HL-60-bis). HL-60-bis low nuclear: cytoplasmic...