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PKR Senses Nuclear and Mitochondrial Signals by Interacting with Endogenous Double-Stranded RNAs
Kim, Yoosik,Park, Joha,Kim, Sujin,Kim, MinA,Kang, Myeong-Gyun,Kwak, Chulhwan,Kang, Minjeong,Kim, Baekgyu,Rhee, Hyun-Woo,Kim, V. Narry Elsevier 2018 Molecular cell Vol.71 No.6
<P><B>Summary</B></P> <P>Protein kinase RNA-activated (PKR) induces immune response by sensing viral double-stranded RNAs (dsRNAs). However, growing evidence suggests that PKR can also be activated by endogenously expressed dsRNAs. Here, we capture these dsRNAs by formaldehyde-mediated crosslinking and immunoprecipitation sequencing and find that various noncoding RNAs interact with PKR. Surprisingly, the majority of the PKR-interacting RNA repertoire is occupied by mitochondrial RNAs (mtRNAs). MtRNAs can form intermolecular dsRNAs owing to bidirectional transcription of the mitochondrial genome and regulate PKR and eIF2α phosphorylation to control cell signaling and translation. Moreover, PKR activation by mtRNAs is counteracted by PKR phosphatases, disruption of which causes apoptosis from PKR overactivation even in uninfected cells. Our work unveils dynamic regulation of PKR even without infection and establishes PKR as a sensor for nuclear and mitochondrial signaling cues in regulating cellular metabolism.</P> <P><B>Highlights</B></P> <P> <UL> <LI> fCLIP-seq reveals PKR-interacting endogenously expressed dsRNAs </LI> <LI> PKR binds to various noncoding RNAs such as retrotransposons and satellite RNAs </LI> <LI> MtRNAs can form intermolecular dsRNAs and strongly interact with PKR </LI> <LI> MtRNAs can regulate PKR phosphorylation and signaling, especially under stress </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
BaekGyu Kim,Jin Yeong Song,Do Young Kim,Jun Gyu Kim,Jun‑Yeop Lee,Dongwhi Choi,Sang Min Park 한국정밀공학회 2023 International Journal of Precision Engineering and Vol.10 No.6
Transparent triboelectric nanogenerators (TENGs) are promising sustainable energy sources utilizable in optoelectronic devices. Here, we report a highly transparent TENG realized using AgNW-spray-deposition with a surfactant (ASDS). The ASDS process achieved coffee-ring-free AgNW with superior light transmittance of 87.6% and sheet resistance of 12.4 Ω/sq (ΦFOM = 21.5 × 10−3Ω−1), and possessed a high degree of design flexibility on 2D, 3D-curved substrates. The AgNW-spray-deposition with surfactant based transparent TENG (AT-TENG) with hydrophobic characteristics enables to generate electrical signals through solid–solid and solid–liquid contact electrification. As proof-of-concept applications, a self-powered bendable tactile sensor, which exploited biomechanical energy from finger-touch motion, and hybrid energy harvester to concurrently harvest solar and raindrop energy, are demonstrated. The self-powered bendable tactile sensor transformed the finger-touch into electrical energy recognized by the computer, and was utilized as a transparent keypad. The hybrid energy harvester, which is AT-TENG unified with a photovoltaic system, generates electricity from light and falling-droplets. The AT-TENG does not significantly degrade the output performance of photovoltaic system, and their parallel connection enables to achieve the maximum output voltage of 7.0 V. AT-TENGs have advantages such as simplicity of fabrication, outstanding transparency, and superior electrical performance, and have potential for future applications in wearable electronics and smart-home systems.
LIN28A Is a Suppressor of ER-Associated Translation in Embryonic Stem Cells
Cho, Jun,Chang, Hyeshik,Kwon, S. Chul,Kim, Baekgyu,Kim, Yoosik,Choe, Junho,Ha, Minju,Kim, Yoon Ki,Kim, V. Narry Elsevier 2012 Cell Vol.151 No.4
<P><B>Summary</B></P> <P>LIN28 plays a critical role in developmental transition, glucose metabolism, and tumorigenesis. At the molecular level, LIN28 is known to repress maturation of let-7 microRNAs and enhance translation of certain mRNAs. In this study, we obtain a genome-wide view of the molecular function of LIN28A in mouse embryonic stem cells by carrying out RNA crosslinking-immunoprecipitation-sequencing (CLIP-seq) and ribosome footprinting. We find that, in addition to let-7 precursors, LIN28A binds to a large number of spliced mRNAs. LIN28A recognizes AAGNNG, AAGNG, and less frequently UGUG, which are located in the terminal loop of a small hairpin. LIN28A is localized to the periendoplasmic reticulum (ER) area and inhibits translation of mRNAs that are destined for the ER, reducing the synthesis of transmembrane proteins, ER or Golgi lumen proteins, and secretory proteins. Our study suggests a selective regulatory mechanism for ER-associated translation and reveals an unexpected role of LIN28A as a global suppressor of genes in the secretory pathway.</P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P> <P><B>Highlights</B></P> <P>► CLIP-seq and ribosome footprinting reveal numerous spliced mRNAs as LIN28A targets ► Let-7 is the only effective miRNA target of LIN28A in embryonic stem cells ► LIN28A binds to AAGNNG, AAGNG, and UGUG in the loop of a small hairpin ► LIN28A is localized in peri-ER area and suppresses ER-associated translation</P>
( Hae Won Yoo ),( Jae Woo Park ),( Jeong-ju Yoo ),( Sang-gyune Kim ),( Young Seok Kim ),( Young Chang ),( Soung Won Jeong ),( Jae Young Jang ),( Sae Hwan Lee ),( Hong Soo Kim ),( Baekgyu Jun ),( Young 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: METAVIR staging classifies structural deformation caused by hepatic fibrosis semi-quantitatively. However, there could be disagreement of fibrosis staging by METAVIR among pathologists. Quantification of fibrosis using computer-assisted image analysis can offer relative objective information for liver fibrosis. We measured hepatic fibrosis quantitatively using collagen proportionate area (CPA) and assessed its impact on predicting the development of liver decompensation (which was defined as the presence of ascites, variceal bleeding and hepatic encephalopathy). Methods: During January 2010 to June 2018, we assessed 582 patients who got liver biopsy and computer assisted image analysis (ZEN 2.3 lite software by ZEISS) were available. Clinical and laboratory data were collected at baseline and at the time of the last follow-up or progression to liver decompensation (LD). Forty-two patients with acute hepatitis who had no underlying chronic liver disease were excluded. Results: The mean age was 45.3±13.7 years, and most common etiology of liver disease was chronic hepatitis B (28.6%) and followed by fatty liver disease (26.9%). Median follow-up duration was 37 months during which 28 out of 540 patients experienced LD. Mean analyzed dimension of collagen was 5653362±2423925 μm2 and included portal tract was 8.9±3.9. Mean CPA was 8.91±7.10%. A positive correlation between CPA and liver fibrosis stage was observed (r=0.553, P<0.001) (Figure 1). Albumin at baseline (HR: 0.257, 95% CI: 0.094- 0.701, P=0.008), CPA (HR: 1.107 per 1% increase, 95% CI: 1.059-1.157, P<0.001), presence of diabetes mellitus (HR: 4.315, 95% CI: 1.063-17.510, P=0.041), and presence of alcoholic hepatitis (reference : chronic hepatitis B) (HR : 5.811, CI : 1.351-24.987, P=0.018) were independent predictors of liver decompensation on multivariate Cox-regression analysis. The concordance indices of CPA and METAVIR stage for progression to LD were 0.803±0.044 and 0.758±0.041, respectively, without significant difference. When dividing patients with calculating cut-point with maximally selected rank difference, higher CPA (≥16.6%) predicts LD better than lower CPA (Logrank test: P<0.001) (Figure 2). Conclusions: The CPA correlates very well with the METAVIR stage of liver fibrosis and also is an independent predictor of clinical outcomes in liver disease. It is expected to be useful quantitative determination of liver fibrosis and prognosis.
Choi Baekgyu,Kang Chang Kyung,Park Seongwan,Lee Dohoon,Lee Andrew J.,Ko Yuji,Kang Suk-Jo,Kang Kyuho,Kim Sun,Koh Youngil,Jung Inkyung 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Clonal hematopoiesis of indeterminate potential (CHIP), a common aging-related process that predisposes individuals to various inflammatory responses, has been reported to be associated with COVID-19 severity. However, the immunological signature and the exact gene expression program by which the presence of CHIP exerts its clinical impact on COVID-19 remain to be elucidated. In this study, we generated a single-cell transcriptome landscape of severe COVID-19 according to the presence of CHIP using peripheral blood mononuclear cells. Patients with CHIP exhibited a potent IFN-γ response in exacerbating inflammation, particularly in classical monocytes, compared to patients without CHIP. To dissect the regulatory mechanism of CHIP (+)-specific IFN-γ response gene expression in severe COVID-19, we identified DNMT3A CHIP mutation-dependent differentially methylated regions (DMRs) and annotated their putative target genes based on long-range chromatin interactions. We revealed that CHIP mutant-driven hypo-DMRs at poised cis-regulatory elements appear to facilitate the CHIP (+)-specific IFN-γ-mediated inflammatory immune response. Our results highlight that the presence of CHIP may increase the susceptibility to hyperinflammation through the reorganization of chromatin architecture, establishing a novel subgroup of severe COVID-19 patients.
Impact of Sleep Disorder as a Risk Factor for Dementia in Men and Women
( Hye Jin Jee ),( Wonseok Shin ),( Ho Joong Jung ),( Baekgyu Kim ),( Bo Kyung Lee ),( Yi-sook Jung ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.1
Sleep is an essential physiological process, especially for proper brain function through the formation of new pathways and processing information and cognition. Therefore, when sleep is insufficient, this can result in pathophysiologic conditions. Sleep deficiency is a risk factor for various conditions, including dementia, diabetes, and obesity. Recent studies have shown that there are differences in the prevalence of sleep disorders between genders. Insomnia, the most common type of sleep disorder, has been reported to have a higher incidence in females than in males. However, sex/gender differences in other sleep disorder subtypes are not thoroughly understood. Currently, increasing evidence suggests that gender issues should be considered important when prescribing medicine. Therefore, an investigation of the gender-dependent differences in sleep disorders is required. In this review, we first describe sex/gender differences not only in the prevalence of sleep disorders by category but in the efficacy of sleep medications. In addition, we summarize sex/gender differences in the impact of sleep disorders on incident dementia. This may help understand gender-dependent pathogenesis of sleep disorders and develop therapeutic strategies in men and women.