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MARK signaling

Nanork, P., Wongsiri, S. and Oldroyd, B. P. (2007). Preservation and loss of the honey bee (Apis) egg-marking signal across evolutionary time. Behav. Ecol. Sociobiol., 61, 1509-1514. [Pg.279]

Anderson DH. Role of lipids in the MARK signaling pathway. Prog. Lipid Res. 2006 45(2) 102-119. [Pg.453]

Figure 4.11 MS3 spectra produced from collision induced of the OTA daughter ion at m/z 358 (left) and of the ZAN daughter ion at m/z 303 (right). The marked signals of OTA (m/z 239 and 341) and ZAN (m/z 163, 189 and 207) are used for quantitative analysis. (Spectra acquired in positive ion mode collision energy applied to the parent ion 80% of maximum value MS3 experiments of daughter ions at 100% of maximum collision energy). (Adapted from Flamini et al., 2007, RCM), 21 (22), 3737-3742... Figure 4.11 MS3 spectra produced from collision induced of the OTA daughter ion at m/z 358 (left) and of the ZAN daughter ion at m/z 303 (right). The marked signals of OTA (m/z 239 and 341) and ZAN (m/z 163, 189 and 207) are used for quantitative analysis. (Spectra acquired in positive ion mode collision energy applied to the parent ion 80% of maximum value MS3 experiments of daughter ions at 100% of maximum collision energy). (Adapted from Flamini et al., 2007, RCM), 21 (22), 3737-3742...
Exposure of normal human epidermal keratinocy tes (NHEKs) to UVB radiation induces intracellular release of hydrogen peroxide (oxidative stress) and phosphorylation of MARK cell signaling pathways. Pretreatment of NHEK with EGCG inhibits UVB-induced hydrogen peroxide production and its mediated phosphorylation of MARK signaling pathways. It has been demonstrated that tea polyphenols inhibit PKC, MARK, and AP-1 activities in NIH 3T3 cells. °... [Pg.167]

Ryu, B., Li, Y., Qian, Z. J., Kim, M. M., and Kim, S. K. (2009). Differentiation of human osteosarcoma cells by isolated phlorotannins is subtly linked to COX-2, iNOS, MMPs, and MARK signaling Implication for chronic articular disease. Chem. Biol. Interact. 179, 192-201. [Pg.110]

FIGURE 13.7 Schematic model of the cross talk between Wnt signaling and MARK signaling pathways. [Pg.188]

Kelleher, R. J., 3rd, Govindaiajan, A.,Jung, H. Y., Kang, H., and Tonegawa, S. (2004) Translational control by MARK signaling in long-term synaptic plasticity and memory. CeU, 116, 467-479... [Pg.8]

Body control awareness Marking signaling of danger zones 0.22 0.25 0.22 0.23... [Pg.706]

Sen A, O Malley K, Wang Z, Raj GV, Defranco DB, Hammes SR. 2010. Paxillin regulates androgen- and epidermal growth factor-induced MARK signaling and cell proliferation in prostate cancer cells. J Biol Chem 285(37) 28787-28795. [Pg.547]

Yacoub A, McKinstry R, Hinman D et al. (2003) Epidermal growth factor and ionizing radiation up-regulate the DNA repair genes XRCCl and ERCCl in DU145 and LNCaP prostate carcinoma through MARK signaling. Radiat Res 159 439-452... [Pg.219]

Li X, Du JR, Yu Y, Bai B (2010) Tanshinone IIA inhibits smooth muscle proliferation and intimal hyperplasia in the rat carotid balloon-injured model through inhibition of MARK signaling pathway. Zheng XY 129 273... [Pg.3579]

Mazzucchelli, C. BrambiUa, R. (2000). Ras-related and MARK signalling in neuronal plasticity and memory formation. Cellular and Molecular Life Sciences, 57, 604—611. [Pg.295]

Figure 3 The role of MARK signaling pathways in mitochondria-dependent apoptosis antioxidant enzymes, the Bcl-2 protein family, and the influence of flavonoids and isoflavonoids. MARK, mitogen-activated protein kinase. Figure 3 The role of MARK signaling pathways in mitochondria-dependent apoptosis antioxidant enzymes, the Bcl-2 protein family, and the influence of flavonoids and isoflavonoids. MARK, mitogen-activated protein kinase.
Figure 5 The potential sites of action of flavonoids in the prevention of cell damage. Oxidative stress results in the oxidation of lipids, proteins, and deoxyribonucleic acid (DNA), which is in turn sensed by signaling pathways, such as the MARK signaling cascade and mitochondria. These events interlink to cause induction of apoptosis/necrosis in response to the initial oxidative insult. Flavonoids may act by direct scavenging of the oxidizing species or intermediate, by direct protein interactions with signaling molecules, or by interaction with mitochondria. MARK, mitogen-activated protein kinase. Figure 5 The potential sites of action of flavonoids in the prevention of cell damage. Oxidative stress results in the oxidation of lipids, proteins, and deoxyribonucleic acid (DNA), which is in turn sensed by signaling pathways, such as the MARK signaling cascade and mitochondria. These events interlink to cause induction of apoptosis/necrosis in response to the initial oxidative insult. Flavonoids may act by direct scavenging of the oxidizing species or intermediate, by direct protein interactions with signaling molecules, or by interaction with mitochondria. MARK, mitogen-activated protein kinase.
FIGURE 1 ft ft p38 mitogen activated kinase (MARK) signaling model. p38 MARK signaling response to ceii stress and microbiai infection. [Pg.236]

FIGURE 14.15 A real spectrum, showing the Stark effect on benzonitrile, C HjCN. The + and signs mark signals that are splitting due to the electric field. Source Reprinted with permission from The American Chemical Society. [Pg.490]


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