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| Autor | Nilanjana Maulik, Motoaki Sato, Brendan D. Price, Dipak K. Das |
| Titel | An essential role of NFUB in tyrosine kinase signaling of p38 MAP kinase regulation of myocardial adaptation to ischemia |
| Zeitschrift | FEBS Letters |
| Herausgeber | Federation of European Biochemical Societies |
| Ausgabe | 429 |
| Jahr | 1998 |
| Seiten | 365-369 |
| URL | http://ac.els-cdn.com/S0014579398006322/1-s2.0-S0014579398006322-main.pdf?_tid=008400e4-9db9-11e3-9cc3-00000aacb35d&acdnat=1393290545_14a06ef9a39816cb741381c18c2b903d |
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| Fußnoten | no |
| Fragmente | 1 |
| [1.] Arc/Fragment 037 11 - Diskussion Zuletzt bearbeitet: 2014-02-26 00:43:54 Hindemith | Arc, Fragment, Gesichtet, Maulik et al 1998, SMWFragment, Schutzlevel sysop, Verschleierung |
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| Untersuchte Arbeit: Seite: 37, Zeilen: 11-16 |
Quelle: Maulik et al 1998 Seite(n): 365, Zeilen: l.col: 33-40 |
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| Tissue such as the myocardium can be adapted to ischemic stress by repeatedly subjecting it to short terms of reversible ischemia, each followed by another short duration of reperfusion108, 109. This phenomenon causes the production of oxidative stress, leading to the induction of gene expression, which is subsequently translated into the development of beneficial proteins responsible for the heart’s defence97.
97. Murphy E, Steenbergen C. Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury. Physiol. Rev. 2008;88:581-609. 108. Maulik N, Yoshida T, Zu YL, Sato M, Banerjee A, Das DK. Ischemic preconditioning triggers tyrosine kinase signaling: a potential role for MAPKAP kinase 2. Am J Physiol. 1998;275:H1857-1864. 109. Maulik N, Yoshida T, Engelman RM, Deaton D, Flack JE, 3rd, Rousou JA, Das DK. Ischemic preconditioning attenuates apoptotic cell death associated with ischemia/reperfusion. Mol Cell Biochem. 1998;186:139-145. |
Mammalian heart can be adapted to ischemia by repeatedly subjecting it to short-term reversible ischemia each followed by another short duration of reperfusion [1,2]. This phenomenon, known as ischemic adaptation, causes the production of oxidative stress leading to the induction of gene expression which is subsequently translated into the development of several stress-related proteins responsible for the heart's defense [3].
[1] Reimer, A., vander Heide, R.S. and Jennings, R.B. (1994) Ann. NY Acad. Sci. 723, 99-115. [2] Banerjee, A., Locke-Winter, C., Rogers, K.B., Mitchell, M.B., Bensard, D.D., Brew, E.C., Cairns, C.B. and Harken, A.H. (1993) Circ. Res. 73, 656-670. [3] Das, D.K., Maulik, N. and Moraru, I.I. (1995) J. Mol. Cell. Cardiol. 27, 181-193. |
The source is not given (the two papers by Maulik et al. given are different to the source here documented). The papers referenced under 97, 108 and 109 do not contain the copied text. |
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