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Shin, Gu-Choul,Kang, Hong Seok,Lee, Ah Ram,Kim, Kyun-Hwan Informa UK (TaylorFrancis) 2016 Autophagy Vol.12 No.12
<P>Death receptors of TNFSF10/TRAIL (tumor necrosis factor superfamily member 10) contribute to immune surveillance against virus-infected or transformed cells by promoting apoptosis. Many viruses evade antiviral immunity by modulating TNFSF10 receptor signaling, leading to persistent infection. Here, we report that hepatitis B virus (HBV) X protein (HBx) restricts TNFSF10 receptor signaling via macroautophagy/autophagy-mediated degradation of TNFRSF10B/DR5, a TNFSF10 death receptor, and thus permits survival of virus-infected cells. We demonstrate that the expression of the TNFRSF10B protein is dramatically reduced both in liver tissues of chronic hepatitis B patients and in cell lines transfected with HBV or HBx. HBx-mediated downregulation of TNFRSF10B is caused by the lysosomal, but not proteasomal, degradation pathway. Immunoblotting analysis of LC3B and SQSTM1, and microscopy analysis of tandem-fluorescence-tagged LC3B revealed that HBx promotes complete autophagy. Inhibition of autophagy with a pharmacological inhibitor and LC3B knockdown revealed that HBx-induced autophagy is crucial for TNFRSF10B degradation. Immunoprecipitation and GST affinity isolation assays showed that HBx directly interacts with TNFRSF10B and recruits it to phagophores, the precursors to autophagosomes. We confirmed that autophagy activation is related to the downregulation of the TNFRSF10B protein in liver tissues of chronic hepatitis B patients. Inhibition of autophagy enhanced the susceptibility of HBx-infected hepatocytes to TNFSF10. These results identify the dual function of HBx in TNFRSF10B degradation: HBx plays a role as an autophagy receptor-like molecule, which promotes the association of TNFRSF10B with LC3B; HBx is also an autophagy inducer. Our data suggest a molecular mechanism for HBV evasion from TNFSF10-mediated antiviral immunity, which may contribute to chronic HBV infection.</P>
PRKCSH contributes to TNFSF resistance by extending IGF1R half-life and activation in lung cancer
Shin Gu-Choul,Lee Hyeong Min,Kim Nayeon,Seo Sang-Uk,Kim Kwang Pyo,Kim Kyun-Hwan 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Tumor necrosis factor superfamily (TNFSF) resistance contributes to the development and progression of tumors and resistance to various cancer therapies. Tumor-intrinsic alterations involved in the adaptation to the TNFSF response remain largely unknown. Here, we demonstrate that protein kinase C substrate 80K-H (PRKCSH) abundance in lung cancers boosts oncogenic IGF1R activation, leading to TNFSF resistance. PRKCSH abundance is correlated with IGF1R upregulation in lung cancer tissues. Specifically, PRKCSH interacts with IGF1R and extends its half-life. The PRKCSH-IGF1R axis in tumor cells impairs caspase-8 activation, increases Mcl-1 expression, and inhibits caspase-9, leading to an imbalance between cell death and survival. PRKCSH deficiency augmented the antitumor effects of natural killer (NK) cells, representative TNFSF effector cells, in a tumor xenograft IL-2Rg-deficient NOD/SCID (NIG) mouse model. Our data suggest that PRKCSH plays a critical role in TNFSF resistance and may be a potential target to improve the efficacy of NK cell-based cancer therapy.
Shin, Gu-Choul,Na, Byoung-Kuk,Lee, Joo-Yeon,Ahn, Jung-Bae,Park, Jong-Won,Lee, Jin-Soo,Kim, Jee-Hee,Kim, Woo-Joo,Kang, Chun The Korean Society for Microbiology 2003 Journal of Bacteriology and Virology Vol.33 No.4
Although Korean influenza virus isolates have been genetically associated with the vaccine strains of the corresponding year, influenza B viruses have prevailed almost every year in Korea during the past decades. We have 'analyzed the genetic characteristics and evolutionary patterns of the haemagglutinin (HA) 1 domains of influenza B viruses isolated during 1988-1999 using direct RT-PCR and sequencing. Phylogenetic analysis of influenza B viruses isolated in Korea indicated that antigenically and genetically distinguishable strains of the lineage II and lineage III variants had been cocirculated. Variants prevailed in early 1990s are represented in 1996/97 and 1998/99 and some different variants have been co circulated geographically and prevailed concurrently in Korea. All HA1s of Korean isolates have amino acid substitutions mainly in the region between position 124 and 310, which was previously proposed an immunodominant region. Insertion-deletion patterns of the HA gene revealed that Korean influenza B viruses were evolved from Lee40 with different manner between lineage II and III viruses. Lineage III viruses were also divided into two groups as conserved group and inserted group, in relation to Lee40. But lineage II viruses had evolved with directional pattern. Antigenic index proposed that influenza B isolates prevailed since 1996/97 seasons might had emerged from the antigenic variants of a Seo1697-like virus and that new variants might appear from the lineage II viruses resulting in persistent prevalence in Korea.
파라인플루엔자 바이러스의 진단 및 형 분석을 위한 Multiplex Reverse Transcription Polymerase Chain Reaction의 개발
신구철(Gu-Choul Shin),박찬(Chan Park),이주연(Joo-Yeon Lee),나병국(Byoung-Kuk Na),박종원(Jong-Won Park),강춘(Chun Kang),김지희(Jee-Hee Kim),김우주(Woo-Joo Kim),송철용(Chul-Yong Song) 대한미생물학회 2001 Journal of Bacteriology and Virology Vol.31 No.2