• Molecules and Cells
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• 제45권8호
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• pp.550-563
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• 2022

Hepatocellular carcinoma (HCC) is an aggressive and incurable cancer. Although understanding of the molecular pathogenesis of HCC has greatly advanced, therapeutic options for the disease remain limited. In this study, we demonstrated that SETD5 expression is positively associated with poor prognosis of HCC and that SETD5 depletion decreased HCC cell proliferation and invasion while inducing cell death. Transcriptome analysis revealed that SETD5 loss downregulated the interferon-mediated inflammatory response in HCC cells. In addition, SETD5 depletion downregulated the expression of a critical glycolysis gene, PKM (pyruvate kinase M1/2), and decreased glycolysis activity in HCC cells. Finally, SETD5 knockdown inhibited tumor growth in xenograft mouse models. These results collectively suggest that SETD5 is involved in the tumorigenic features of HCC cells and that targeting SETD5 may suppress HCC progression.

• ETRI Journal
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• 제26권6호
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• pp.669-672
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• 2004

To improve the operation error caused by the thermal fluctuation of electrons, we propose a novel single-electron pass-transistor logic circuit employing a multiple-tunnel junction (MTJ) scheme and modulate a parameters of an MTJ single-electron tunneling device (SETD) such as the number of tunnel junctions, tunnel resistance, and voltage gain. The operation of a 3-MTJ inverter circuit is simulated at 15 K with parameters $C_g=C_T=C_{clk}=1\;aF,\;R_T=5\;M{\Omega},\;V_{clk}=40\;mV$, and $V_{in}=20\;mV$. Using the SETD/MOSFET hybrid circuit, the charge state output of the proposed MTJ-SETD logic is successfully translated to the voltage state logic.

• Molecules and Cells
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• 제45권10호
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• pp.761-761
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• 2022

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• 제29권2호
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• pp.62-72
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• 2018

Objectives: The molecular mechanisms underlying attention-deficit hyperactivity disorder (ADHD) remain unclear. Therefore, this study aimed to identify the genetic susceptibility loci for ADHD in Korean children with ADHD. We performed a case-control and a family-based genome-wide association study (GWAS), as well as genome-wide quantitative trait locus (QTL) analyses, for two symptom traits. Methods: A total of 135 subjects (71 cases and 64 controls), for the case-control analysis, and 54 subjects (27 probands and 27 unaffected siblings), for the family-based analysis, were included. Results: The genome-wide QTL analysis identified four single nucleotide polymorphisms (SNPs) (rs7684645 near APELA, rs12538843 near YAE1D1 and POU6F2, rs11074258 near MCTP2, and rs34396552 near CIDEA) that were significantly associated with the number of inattention symptoms in ADHD. These SNPs showed possible association with ADHD in the family-based GWAS, and with hyperactivity-impulsivity in genome-wide QTL analyses. Moreover, association signals in the family-based QTL analysis for the number of inattention symptoms were clustered near genes IL10, IL19, SCL5A9, and SKINTL. Conclusion: We have identified four QTLs with genome-wide significance and several promising candidates that could potentially be associated with ADHD (CXCR4, UPF1, SETD5, NALCN-AS1, ERC1, SOX2-OT, FGFR2, ANO4, and TBL1XR1). Further replication studies with larger sample sizes are needed.