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Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 27, Zeilen: 1-23
Quelle: Franke et al 2003
Seite(n): 8989, Zeilen: li.Sp. 57-58 - re.Sp. 1ff.
[Multiple studies supporting the role of Akt in apoptosis suppression have] connected Akt to cell death regulation either by demonstrating its downregulation following pro-apoptotic insults, or by using gene-transfer experiments that transduce both activated, anti-apoptotic and inactive, pro-apoptotic mutants of Akt.

Taken together, these observations suggest that Akt may play a critical role both in the function of cancer cells and in the pathogenesis of degenerative diseases. By promoting the cell survival of mutated, damaged or transformed cells even under adverse conditions, Akt can promote cancer cell growth by protecting cells from apoptosis, which would otherwise be eliminated by programmed cell death. To experimentally prove the importance of Akt kinases in oncogenic transformation, in a seminal paper, Peter Vogt and colleagues demonstrated that a transformed cellular phenotype could be reverted to normal when using a cell model for PI3K-dependent oncogenesis as long as dominant-negative mutants of Akt were expressed concomitantly [Aoki et al., 1998]. Akt is also likely to play a significant role in degenerative diseases, where excessive or inappropriate cell death occurs possibly because proper trophic factor support is lacking. The relevance of Akt signaling in neurodegenerative disease is supported by studies that examine its activity and function in Alzheimer's disease models in vitro [Hong and Lee, 1997; Weihl et al., 1999]. A role for Akt has also been suggested in other models of human degenerative diseases, including cardiac failure [Matsui et al., 1999] and other cardiovascular diseases where there is increased and chronic loss of cells [Reed and Paternostro, 1999].


Aoki M, Batista O, Bellacosa A, Tsichlis P and Vogt PK. The akt kinase: molecular determinants of oncogenicity. (1998). Proc. Natl. Acad. Sci. USA, 95, 14950–14955.

Hong M and Lee VM. (1997). Insulin and insulin-like growth factor-1 regulate tau phosphorylation in cultured human neuronsJ. Biol. Chem. 272, 19547–19553.

Matsui T, Li L, del Monte F, Fukui Y, Franke TF, Hajjar RJ and Rosenzweig A. (1999). Adenoviral gene transfer of activated phosphatidylinositol 3'-kinase and Akt inhibits apoptosis of hypoxic cardiomyocytes in vitro. Circulation, 100, 2373–2379.

Reed JC and Paternostro G. (1999). Postmitochondrial regulation of apoptosis during heart failure. (Proc. Natl. Acad. Sci. USA, 96, 7614–7616.

Weihl CC, Ghadge GD, Kennedy SG, Hay N, Miller RJ and Roos RP. (1999). Mutant presenilin-1 induces apoptosis and downregulates Akt/PKB. J. Neurosci., 19, 5360–5369.

Multiple studies supporting the role of Akt in apoptosis suppression have connected Akt to cell death regulation either by demonstrating its downregulation following pro-apoptotic insults, or by using gene-transfer experiments that transduce both activated, anti-apoptotic and inactive, pro-apoptotic mutants of Akt.

Taken together, these observations suggest that Akt may play a critical role both in the function of cancer cells and in the pathogenesis of degenerative diseases. By promoting the cell survival of mutated, damaged or transformed cells even under adverse conditions, Akt can promote cancer cell growth by protecting cells from apoptosis, which would otherwise be eliminated by programmed cell death. To experimentally prove the importance of Akt kinases in oncogenic transformation, in a seminal paper, Peter Vogt and colleagues demonstrated that a transformed cellular phenotype could be reverted to normal when using a cell model for PI3K-dependent oncogenesis as long as dominant-negative mutants of Akt were expressed concomitantly (Aoki et al., 1998). Akt is also likely to play a significant role in degenerative diseases, where excessive or inappropriate cell death occurs possibly because proper trophic factor support is lacking. The relevance of Akt signaling in neurodegenerative disease is supported by studies that examine its activity and function in Alzheimer’s disease models in vitro (Hong and Lee, 1997; Weihl et al., 1999). A role for Akt has also been suggested in other models of human degenerative diseases, including cardiac failure (Matsui et al., 1999) and other cardiovascular diseases where there is increased and chronic loss of cells (Reed and Paternostro, 1999).


Aoki M, Batista O, Bellacosa A, Tsichlis P and Vogt PK. (1998). Proc. Natl. Acad. Sci. USA, 95, 14950–14955.

Hong M and Lee VM. (1997). J. Biol. Chem., 272, 19547–19553.

Matsui T, Li L, del Monte F, Fukui Y, Franke TF, Hajjar RJ and Rosenzweig A. (1999). Circulation, 100, 2373–2379.

Reed JC and Paternostro G. (1999). Proc. Natl. Acad. Sci. USA, 96, 7614–7616.

Weihl CC, Ghadge GD, Kennedy SG, Hay N, Miller RJ and Roos RP. (1999). J. Neurosci., 19, 5360–5369.

Anmerkungen

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Sichter
(Graf Isolan), SleepyHollow02

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