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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


Fußnoten    no
Fragmente    2

Fragmente der Quelle:
[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

Untersuchte Arbeit:
Seite: 37, Zeilen: 11-16
Quelle: Maulik et al 1998
Seite(n): 365, Zeilen: l.col: 33-40
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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