Upstream Signal (upstream + signal)

Distribution by Scientific Domains


Selected Abstracts


A novel coding method with remodulation format used in a WDM-PON to enhance extinction ratio

MICROWAVE AND OPTICAL TECHNOLOGY LETTERS, Issue 12 2009
Bo Huang
Abstract We report a new approach to eliminate the extinction ratio (ER) limitation in a wavelength division multiplexed passive optical network using RZ-ASK/DPSK remodulation format corresponding to downstream/upstream signals, respectively. A novel precoding method can improve the ER tolerance from 6 to 13 dB for a 40-Gb/s RZ-ASK downstream and 622-Mb/s DPSK upstream experimental transmission with <1 dB penalty. Rayleigh and stimulated Brillouin backscattering effects are simulated and analyzed in the deployment of a bidirectional 40G Ethernet PON probably using in practical application. © 2009 Wiley Periodicals, Inc. Microwave Opt Technol Lett 51: 2994,2997, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.24750 [source]


Potential attenuation of p38 signaling by DDB2 as a factor in acquired TNF resistance

INTERNATIONAL JOURNAL OF CANCER, Issue 3 2005
Chun-Ling Sun
Abstract Our previous study demonstrated that DDB2, a DNA repair protein, attenuates cell surface membrane-associated death signal induced by UV or FasAb; DDB2 is overexpressed in cisplatin-selected cells. However, the molecular mechanism underlying the protective role of DDB2 along the apoptotic pathway remains unknown. Our study identified the cross-resistance of the cisplatin-selected cells to tumor necrosis factor-, (TNF-,). Since knock-down of the DDB2 level rendered cells (HR18) sensitive to the treatment, the cell sensitivity to TNF-, appears inversely proportional to the cellular level of DDB2. Treatment of HeLa cells with TNF-, transiently induced activation of p38MAPK signal, but this induction was significantly reduced in the resistant cells. Overexpression of DDB2 attenuated the activation of p38 in cells. TNF-,-induced apoptotic signals, represented by caspase-8 and downstream substrate cleavage, were reduced in resistant cells compared to their sensitive counterparts. Inhibition of p38 signal by SB202190 clearly attenuated TNF-,-induced apoptotic signals. Moreover, overexpression of DDB2 in HR18 cells also attenuated TNF-, induced caspase activation. These results suggest that p38MAPK activation may be a key upstream signal of TNF-,-induced apoptosis and that attenuation of p38 signal by DDB2 overexpression may be responsible for acquired TNF-, resistance. © 2005 Wiley-Liss, Inc. [source]


A Computational Study of Feedback Effects on Signal Dynamics in a Mitogen-Activated Protein Kinase (MAPK) Pathway Model

BIOTECHNOLOGY PROGRESS, Issue 2 2001
Anand R. Asthagiri
Exploiting signaling pathways for the purpose of controlling cell function entails identifying and manipulating the information content of intracellular signals. As in the case of the ubiquitously expressed, eukaryotic mitogen-activated protein kinase (MAPK) signaling pathway, this information content partly resides in the signals' dynamical properties. Here, we utilize a mathematical model to examine mechanisms that govern MAPK pathway dynamics, particularly the role of putative negative feedback mechanisms in generating complete signal adaptation, a term referring to the reset of a signal to prestimulation levels. In addition to yielding adaptation of its direct target, feedback mechanisms implemented in our model also indirectly assist in the adaptation of signaling components downstream of the target under certain conditions. In fact, model predictions identify conditions yielding ultra-desensitization of signals in which complete adaptation of target and downstream signals culminates even while stimulus recognition (i.e., receptor-ligand binding) continues to increase. Moreover, the rate at which signal decays can follow first-order kinetics with respect to signal intensity, so that signal adaptation is achieved in the same amount of time regardless of signal intensity or ligand dose. All of these features are consistent with experimental findings recently obtained for the Chinese hamster ovary (CHO) cell lines (Asthagiri et al., J. Biol. Chem.1999, 274, 27119,27127). Our model further predicts that although downstream effects are independent of whether an enzyme or adaptor protein is targeted by negative feedback, adaptor-targeted feedback can "back-propagate" effects upstream of the target, specifically resulting in increased steady-state upstream signal. Consequently, where these upstream components serve as nodes within a signaling network, feedback can transfer signaling through these nodes into alternate pathways, thereby promoting the sort of signaling cross-talk that is becoming more widely appreciated. [source]


Age-related differences in MAP kinase activity in VSMC in response to glucose or TNF-,

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2003
Muyao Li
Aortic vascular smooth muscle cells (VSMC) were used to study the effect of age on responses to high glucose concentrations or the cytokine, tumor necrosis factor-alpha (TNF-,). Activator protein-1 (AP-1) binding to DNA increased more in VSMC from old versus young rats (P,<,0.02) and was related to increased expression of its components, c-Fos, Fra-1, and JunD. The relationship to upstream signals, i.e., activities of mitogen-activated protein kinases (MAPK), was studied using antibodies to total and phosphorylated forms of extracellular signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK) and p38. High glucose and TNF-, increased ERK phosphorylation more in old (P,<,0.05); whereas only TNF-, induced JNK activation in young (P,<,0.04). PD98059, a MEK inhibitor, attenuated AP-1 activation, lowered c-Fos and Fra-1 protein levels and reduced cell number and cells positive for proliferating cell nuclear antigen in old. We concluded that age differentially influenced activation of signaling pathways in VSMC exposed to high glucose or TNF-,. This may contribute to the increased risk for vascular disease associated with aging and diabetes mellitus (DM). J. Cell. Physiol. 197: 418,425, 2003© 2003 Wiley-Liss, Inc. [source]


Specific cleavage of ribosomal RNA and mRNA during victorin-induced apoptotic cell death in oat

THE PLANT JOURNAL, Issue 6 2006
Trinh X. Hoat
Summary Here we report that rRNA and mRNA are specifically degraded in oat (Avena sativa L.) cells during apoptotic cell death induced by victorin, a host-selective toxin produced by Cochliobolus victoriae. Northern analysis indicated that rRNA species from the cytosol, mitochondria and chloroplasts were all degraded via specific degradation intermediates during victorin-induced apoptotic cell death but, in contrast, they were randomly digested in necrotic cell death induced by 30 mm CuSO4 and heat shock. This indicates that specific rRNA cleavage could be controlled by an intrinsic program. We also observed specific cleavage of mRNA of housekeeping genes such as actin and ubiquitin during victorin-induced cell death. Interestingly, no victorin-induced mRNA degradation was detected with stress-responding genes such as PR-1, PR-10 and GPx throughout the experimental period. The RNA degradation mostly, but not always, occurred in parallel with DNA laddering, but pharmacological studies indicated that these processes are regulated by different signaling pathways with some overlapping upstream signals. [source]