Browsing by Author "Chen, Chia-Yen"

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Functional Characterization of Glycine N-Methyltransferase and Its Interactive Protein DEPDC6/DEPTOR in Hepatocellular Carcinoma
(2012-02-01)
Yen, Chia-Hung
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Lu, Yao-Cheng
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Li, Chung-Hsien
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Lee, Cheng-Ming
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Chen, Chia-Yen
Glycine N-methyltransferase (GNMT) is a tumor suppressor for hepatocellular carcinoma (HCC). High rates of Gnmt knockout mice developed HCC. Epigenetic alteration and dysregulation of several pathways including wingless-type MMTV integration site (Wnt), mitogen-activated protein kinase (MAPK) and Janus kinase and signal transducer and activator of transcription (JAK-STAT) are associated with HCC development in Gnmt knockout mice. We hypothesized that GNMT may regulate signal transduction through interacting with other proteins directly. In this report, we identified a mammalian target of rapamycin (mTOR) inhibitor (DEP domain containing MTOR-interacting protein (DEPDC6/DEPTOR)) as a GNMT-binding protein by using yeast two-hybrid screening. Fluorescence resonance energy transfer assay demonstrated that the C-terminal half of GNMT interact with the PSD-95/DIg1/ZO-1 (PDZ) domain of DEPDC6/DEPTOR. Immunohistochemical staining showed that 27.5% (14/51) of HCC patients had higher expression levels of DEPDC6/DEPTOR in the tumorous tissues than in tumor-adjacent tissues, especially among HCC patients with hepatitis B viral infection (odds ratio 10.3, 95% confidence interval (CI) 1.05-11.3) or patients with poor prognosis (death hazard ratio 4.51, 95% CI 1.60-12.7). In terms of molecular mechanism, knockdown of DEPDC6/DEPTOR expression in HuH-7 cells caused S6K and 4E-BP activation, but suppressed Akt. Overexpression of DEPDC6/DEPTOR activated Akt and increased survival of HCC cells. Overexpression of GNMT caused activation of mTOR/raptor downstream signaling and delayed G2/M cell cycle progression, which altogether resulted in cellular senescence. Furthermore, GNMT reduced proliferation of HuH-7 cells and sensitized them to rapamycin treatment both in vitro and in vivo. In conclusion, GNMT regulates HOC growth in part through interacting with DEPDC6/DEPTOR and modulating mTOR/raptor signaling pathway. Both GNMT and DEPDC6/DEPTOR are potential targets for developing therapeutics for HCC. Online address: http://www.molmed.org doi: 10.2119/molmed.2011.00331
Functional Characterization of Glycine N-Methyltransferase and Its Interactive Protein DEPDC6/DEPTOR in Hepatocellular Carcinoma (vol 18, pg 286, 2012)
(2012-03-01)
Yen, Chia-Hung
;
Lu, Yao-Cheng
;
Li, Chung-Hsien
;
Lee, Cheng-Ming
;
Chen, Chia-Yen
Topology-aware handoff scheme for surveillance patrol robot
(2013-08-01)
Tseng, Chien-Chao
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Lin, Chia-Liang
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Shih, Bih-Yaw
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Chen, Chia-Yen
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Chen, Chen-Yuan
With the advances in wireless communication technology and artificial intelligence, robots are gradually being introduced as a part of our life. Similarly to most mobile devices, mobile robots suffer from handoff latency. This paper proposes TASPR, a Topology-Aware Surveillance Patrol Robot, which can integrate the robotic status and topology information to assist handoff between access points (APs). TASPR uses Topology-Aware Hand-Off Scheme (TAHOS) to find the most promising AP from a list of candidate APs. When TASPR decides to initiate a handoff procedure, it analyzes moving direction, received signal strength and topology information to filter out unnecessary scannings. Thus, TAHOS has less handoff latency compared to conventional handoff procedure and neighbor graph algorithm (NGA).
WiFi assisted NAT traversal scheme for surveillance patrol robot
(2014-04-01)
Tseng, Chien-Chao
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Lin, Chia-Liang
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Shih, Bih-Yaw
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Chen, Chia-Yen
;
Chen, Chen-Yuan
With the advances in wireless communication technology and artificial intelligence, robots are gradually being introduced as part of our life. Previous research proposed a SIP-enabled Surveillance Patrol Robot (SSPR), which tracks a moving object actively and informs the householder of such security alarm. However, the underlying signaling protocol for communication and data streams suffer from the network address translation (NAT) traversal problem as most peer-to-peer (P2P) applications. NAT is a commonly adopted technique to share one public IPv4 address among several hosts located behind a NAT device for alleviating the exhaustion of IPv4 address. NAT devices typically block session requests originating from outside, prevent the establishment of peer-to-peer (P2P) sessions and cause NAT traversal problem. This study proposes WANTS, a WiFi Assisted NAT Traversal Scheme for SSPR. When SSPR is activated, it retrieves the topology information from a server to choose the candidate access point (AP) for handoff. Then SSPR uses the collected network context information to assist its NAT traversal procedure after handoff. Experimental results confirm that WANTS reduces not only connectivity check delay but also protocol messages as compared to the Interactivity Connectivity Establishment (ICE), which is the most acknowledged approach to creating a session across NATs.