• The KIPS Transactions:PartC
• /
• v.8C no.6
• /
• pp.821-830
• /
• 2001

H.323 proposes to use Mobile IP and H.323 ad hoc conference signaling to provide Handoff function to a mobile terminal. But H.323 ad hoc conference signaling has a drawback. It requires an H.323 endpoint to do a complex conference signaling which makes inter-operability between H.323 endpoints difficult and takes the longer signaling time. In this paper, we propose an Handoff signaling using H.323 rerouting(Third party initiated Pause and Rerouting). H.323 rerouting signaling only requires an H.323 endpoint to do H.323 basic signaling in reestablishing media channel, and makes inter-operability more easier and provides the faster Handoff. To do this, our H.323 GK has derived H.245 control channel using tunneling for all H.323 calls including the fast connect calls which enable endpoints communicate each other if they don\`t have H.245 control channel. In order to evaluate the performance of the proposed signaling, we have conducted an experiment that compares a call transfer signaling using H.323 rerouting with ad hoc conference signaling in inter-operability and signaling delay. The results of our experiment shows that the call transfer signaling can inter-operate with four H.323 endpoints among five H.323 endpoints of other vendors and reduces the signaling delay average 1.4 sec.

• The Journal of Korean Institute of Communications and Information Sciences
• /
• v.29 no.3A
• /
• pp.248-256
• /
• 2004

Woerner had suggested an asynchronous trellis-coded DS/CDMA system based on a multi-sequence signaling, biorthogonal sequence, which is superior to single sequence signaling, such as M-ary PSK, due to their better cross-correlation properties. This paper analyzes and compares system performance between OPSM, a recently-presented multi-sequence signaling scheme, and biorthogonal sequence signaling. Interuser interference moments of the two schemes are derived and compared which verifies that OPSM, having smaller signature sequences per symbol than biorthogonal signaling, reduces cross-correlation. Numerical results compare the power and spectral efficiency of asynchronous trellis-coded DS/CDMA systems based on multi-sequence signaling.

• Bulletin of the Korean Chemical Society
• /
• v.34 no.4
• /
• pp.1269-1271
• /
• 2013

• BMB Reports
• /
• v.38 no.3
• /
• pp.281-289
• /
• 2005

Tumor necrosis factor (TNF) signaling is mediated via two distinct receptors, TNFR2 and TNFR1, which shows partially overlapping signaling mechanisms and biological roles. In the present study, TNFR2 and TNFR1 signal transduction mechanisms involved in activation of $NF{\kappa}B$ and CMV promoter-enhancer were compared with respect to their susceptibility towards inhibitors of intracellular signaling. For this, we used SW480 cells, where we have shown that TNF-signaling can occur independently through each of the two receptors. The TNFR1 response was inhibited by D609, bromophenacyl bromide (BPB), nordihydroguararetic acid (NDGA), and by sodium salicylate, while TNFR2-mediated activation of $NF{\kappa}B$ and CMV promoter-enhancer was resistant to these compounds. The signaling mechanisms known to be affected by these inhibitors include phospholipases as well as redox- and pH-sensitive intracellular components. Our results imply that TNFR2 signaling involved in $NF{\kappa}B$ activation proceeds independently of these inhibitor-sensitive signaling components, indicating distinct signaling pathways not shared with TNFR1.

• BMB Reports
• /
• v.41 no.12
• /
• pp.833-839
• /
• 2008

Angiogenesis in tumors is driven by multiple growth factors that activate receptor tyrosine kinases. An important driving force of angiogenesis in solid tumors is signaling through vascular endothelial growth factor (VEGF) and its receptors (VEGFRs). Angiogenesis inhibitors that target this signaling pathway are now in widespread use for the treatment of cancer. However, when used alone, inhibitors of VEGF/VEGFR signaling do not destroy all blood vessels in tumors and do not slow the growth of most human cancers. VEGF/VEGFR signaling inhibitors are, therefore, used in combination with chemotherapeutic agents or radiation therapy. Additional targets for inhibiting angiogenesis would be useful for more efficacious treatment of cancer. One promising target is the signaling pathway of hepatocyte growth factor (HGF) and its receptor (HGFR, also known as c-Met), which plays important roles in angiogenesis and tumor growth. Inhibitors of this signaling pathway have been shown to inhibit angiogenesis in multiple in vitro and in vivo models. The HGF/c-Met signaling pathway is now recognized as a promising target in cancer by inhibiting angiogenesis, tumor growth, invasion, and metastasis.

• Journal of Microbiology and Biotechnology
• /
• v.31 no.6
• /
• pp.765-774
• /
• 2021

Although research on the osteal signaling pathway has progressed, understanding of gut microbial-dependent signaling pathways for metabolic and immune bone homeostasis remains elusive. In recent years, the study of gut microbiota has shed light on our understanding of bone homeostasis. Here, we review microbiota-mediated gut-bone crosstalk via bone morphogenetic protein/SMADs, Wnt and OPG/receptor activator of nuclear factor-kappa B ligand signaling pathways in direct (translocation) and indirect (metabolite) manners. The mechanisms underlying gut microbiota involvement in these signaling pathways are relevant in immune responses, secretion of hormones, fate of osteoblasts and osteoclasts and absorption of calcium. Collectively, we propose a signaling network for maintaining a dynamic homeostasis between the skeletal system and the gut ecosystem. Additionally, the role of gut microbial improvement by dietary intervention in osteal signaling pathways has also been elucidated. This review provides unique resources from the gut microbial perspective for the discovery of new strategies for further improving treatment of bone diseases by increasing the abundance of targeted gut microbiota.

• Proceedings of the Korean Biophysical Society Conference
• /
• 2003.06a
• /
• pp.29-29
• /
• 2003

Compartmentation of intracellular signaling pathways serves as an important mechanism conferring the specificity of G protein-coupled receptor (GPCR) signaling. In the heart, stimulation of $\beta$$_2$-adrenoceptor ($\beta$$_2$-AR), a prototypical GPCR, activates a tightly localized protein kinase A (PKA) signaling, which regulates substrates at cell surface membranes, bypassing cytosolic target proteins (eg, phospholamban). Although a concurrent activation of $\beta$$_2$-AR-coupled $G_{i}$ proteins has been implicated in the functional compartmentation of PKA signaling, the exact mechanism underlying the restriction of the $\beta$$_2$-AR-PKA pathway remains unclear. In the present study, we demonstrate that phosphatidylinositol 3-kinase (PI3K) plays an essential role in confining the $\beta$$_2$-AR-PKA signaling. Inhibition of PI3K with LY294002 or wortmannin enables $\beta$$_2$-AR-PKA signaling to reach intracellular substrates, as manifested by a robust increase in phosphorylation of phospholamban, and markedly enhances the receptor-mediated positive contractile and relaxant responses in cardiac myocytes. These potentiating effects of PI3K inhibitors are not accompanied by an increase in $\beta$$_2$-AR-induced cAMP formation. Blocking $G_{i}$ or $G_{$\square$$\square$}$ signaling with pertussis toxin or $\beta$ARK-ct, a peptide inhibitor of $G_{$\square$$\square$}$, completely prevents the potentiating effects induced by PI3K inhibition, indicating that the pathway responsible for the functional compartmentation of $\beta$$_2$-AR-PKA siglaling sequentially involves $G_{i}$, $G_{$\square$$\square$}$, and PI3K. Thus, PI3K constitutes a key downstream event of $\beta$$_2$-AR- $G_{i}$ signaling, which confines and negates the concurrent $\beta$$_2$-AR/Gs-mediated PKA signaling.gnaling.

• Molecules and Cells
• /
• v.47 no.1
• /
• pp.100004.1-100004.11
• /
• 2024

Insulin is essential for maintaining normoglycemia and is predominantly secreted in response to glucose stimulation by β-cells. Incretin hormones, such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide, also stimulate insulin secretion. However, as obesity and type 2 diabetes worsen, glucose-dependent insulinotropic polypeptide loses its insulinotropic efficacy, whereas GLP-1 receptor (GLP-1R) agonists continue to be effective owing to its signaling switch from Gs to Gq. Herein, we demonstrated that endoplasmic reticulum (ER) stress induced a transition from Gs to Gq in GLP-1R signaling in mouse islets. Intriguingly, chemical chaperones known to alleviate ER stress, such as 4-PBA and TUDCA, enforced GLP-1R's Gq utilization rather than reversing GLP-1R's signaling switch induced by ER stress or obese and diabetic conditions. In addition, the activation of X-box binding protein 1 (XBP1) or activating transcription factor 6 (ATF6), 2 key ER stress-associated signaling (unfolded protein response) factors, promoted Gs utilization in GLP-1R signaling, whereas Gq employment by ER stress was unaffected by XBP1 or ATF6 activation. Our study revealed that ER stress and its associated signaling events alter GLP-1R's signaling, which can be used in type 2 diabetes treatment.

• Proceedings of the KIEE Conference
• /
• 2002.07b
• /
• pp.1220-1222
• /
• 2002

The railway signaling system consists of several vital computerized equipments. Now the project for development of signaling system for the next-generation high-speed train is progressed according to the consortium. The developing signaling system by this project, kTCS(Korean Train Control System), is composed of kTCS-CTC, kTCS-IXL, kTCS-ATC and etc. The KTCS signaling has to be operated as a integrated system by interface between each signaling. To achieve these, communication protocols between each signaling have to be designed and message codes are defined. In this paper the configuration of integrated kTCS system and designed communication protocol is presented.

• BMB Reports
• /
• v.32 no.2
• /
• pp.103-111
• /
• 1999

Hh proteins represent a new signaling paradigm in metazoan development. In species ranging from fruit flies to humans, Hh proteins mediate multiple processes vital to appropriate pattern formation in the developing embryo. Hh proteins undergo an autoprocessing event in which the full-length protein is cleaved into N-terminal and C-terminal domains (Hh-N and Hh-C, respectively), and a cholesterol moiety becomes covalently attached to Hh-N. All known signaling activities of Hh proteins are mediated by Hh-N while both the cleavage and cholesterol transfer reactions are mediated by Hh-C. The cholesterol attached to Hh-N is required to retrict the range of Hh signaling and may be involved in ensuring appropriate reception of the Hh signal in target tissues. Disruptions of Hh signaling pathways lead to severe developmental defects in newborns and cancers in adults. While studies of Hh proteins have yielded a wealth of new insight into the molecular mechanisms of metazoan development, many outstanding questions concerning Hh signaling mechanisms ensure that unraveling the secrets of this molecule will keep scientists well entertained for the foreseeable future.