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Membrane androgen receptor activation triggers pro-apoptotic responses in vitro and in vivo and blocks migration in colon cancer

von S. G.

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[1.] Shg/Fragment 026 20 - Diskussion
Zuletzt bearbeitet: 2014-11-01 21:23:33 Singulus
Fragment, Franke et al 2003, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Shg

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 26, Zeilen: 20-31
Quelle: Franke et al 2003
Seite(n): 8989, Zeilen: li.Sp. 40-57
1.3.3. Apoptosis responses by AKT pathway

Akt is a good candidate for mediating PI3K-dependent cell-survival responses. An important function of activated PI3K in cells is the inhibition of programmed cell death [Yao and Cooper, 1995]. The first evidence to show that Akt acts as an anti-apoptotic signaling molecule was observed in cerebellar granule neurons after trophic factor withdrawal [Dudek et al., 1997], and in fibroblasts after forced expression of c-Myc [Kauffmann-Zeh et al., 1997]. Subsequent work in many laboratories has established the principle role of Akt in the regulation of cell survival in several cell types, consistent with its ubiquitous expression pattern. Akt has been implicated as an anti-apoptotic in many different cell death paradigms, including withdrawal of extracellular signaling factors, oxidative and osmotic stress, irradiation and treatment of cells with chemotherapeutic drugs and ischemic shock [Franke et al., 1997; Downward, 1998].


Downward J. (1998) Mechanisms and consequences of activation of protein kinase B/Akt. Curr Opin Cell Biol. 10:262-267.

Dudek H, Datta SR, Franke TF, Birnbaum MJ, Yao R, Cooper GM, Segal RA, Kaplan DR and Greenberg ME. (1997). Regulation of neuronal survival by the serine-threonine protein kinase Akt. Science, 275, 661–665.

Franke TF, Kaplan DR and Cantley LC. (1997). PI3K: downstream AKTion blocks apoptosis. Cell, 88, 435–437.

Kauffmann-Zeh A, Rodriguez-Viciana P, Ulrich E, Gilbert C, Coffer P, Downward J and Evan G. (1997). Suppression of c-Myc-induced apoptosis by Ras signalling through PI(3)K and PKB.(1997). Nature, 385, 544–548.

Yao R and Cooper GM. (1995) Requirement for phosphatidylinositol-3 kinase in the prevention of apoptosis by nerve growth factor.Science, 267, 2003–2006.

Apoptosis suppression by Akt

An important function of activated PI3K in cells is the inhibition of programmed cell death (Yao and Cooper, 1995), and Akt is a good candidate for mediating these PI3K-dependent cell-survival responses. The initial evidence to show that Akt acts as an anti-apoptotic signaling molecule was observed in cerebellar granule neurons after trophic factor withdrawal (Dudek et al., 1997), and in fibroblasts after forced expression of c-Myc (Kauffmann-Zeh et al., 1997). Subsequent work in many laboratories has established the principle role of Akt in the regulation of cell survival in several cell types, consistent with its ubiquitous expression pattern. Akt has been implicated as an anti-apoptotic in many different cell death paradigms, including withdrawal of extracellular signaling factors, oxidative and osmotic stress, irradiation and treatment of cells with chemotherapeutic drugs and ischemic shock (Franke et al., 1997a; Downward, 1998).


Downward J. (1998). Curr. Opin. Cell Biol., 10, 262–267.

Dudek H, Datta SR, Franke TF, Birnbaum MJ, Yao R, Cooper GM, Segal RA, Kaplan DR and Greenberg ME. (1997). Science, 275, 661–665.

Franke TF, Kaplan DR and Cantley LC. (1997a). Cell, 88, 435–437.

Kauffmann-Zeh A, Rodriguez-Viciana P, Ulrich E, Gilbert C, Coffer P, Downward J and Evan G. (1997). Nature, 385, 544–548.

Yao R and Cooper GM. (1995). Science, 267, 2003–2006.

Anmerkungen

Ohne Hinweis auf eine Übernahme.

Sichter
(Graf Isolan), SleepyHollow02


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