2001
DOI: 10.1074/jbc.m008552200
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Abstract: Survival factors suppress apoptosis by activating the serine/threonine kinase Akt. To investigate the molecular mechanism underlying activated Akt's ability to protect neurons from hypoxia or nitric oxide (NO) toxicity, we focused on the apoptosis-related functions of p53 and caspases. We eliminated p53 by employing p53-deficient neurons and increased p53 by infection with recombinant adenovirus capable of transducing p53 expression, and we now show that p53 is implicated in the apoptosis induced by hypoxia or… Show more

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Cited by 218 publications
(153 citation statements)
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References 39 publications
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“…The smaller degree of neuroprotection was not the result of a smaller Interestingly, cell survival did not correlate with the magnitude of activation of Akt and ERK. This was somewhat surprising in that the two kinases are thought to play key roles in mediating growth factor-induced neuroprotection (Tamatani et al, 1998;Brunet et al, 1999;Hetman et al, 1999;Matsuzaki et al, 1999;Yamaguchi et al, 2001;Zheng and Quirion, 2004). In our studies, BDNF, IGF-1, and FGF-2 were found to be all approximately equally effective at activating Akt.…”
Section: Discussionmentioning
confidence: 53%
See 1 more Smart Citation
“…The smaller degree of neuroprotection was not the result of a smaller Interestingly, cell survival did not correlate with the magnitude of activation of Akt and ERK. This was somewhat surprising in that the two kinases are thought to play key roles in mediating growth factor-induced neuroprotection (Tamatani et al, 1998;Brunet et al, 1999;Hetman et al, 1999;Matsuzaki et al, 1999;Yamaguchi et al, 2001;Zheng and Quirion, 2004). In our studies, BDNF, IGF-1, and FGF-2 were found to be all approximately equally effective at activating Akt.…”
Section: Discussionmentioning
confidence: 53%
“…In addition to examining enhancement of cell survival, we have compared the coupling of receptors for these growth factors to activation of Akt (protein kinase B) and the Extracellular-regulated kinase (ERK) mitogen-activated protein (MAP) kinases. These kinases are thought to be key components in mediating growth factorinduced neuroprotection (Tamatani et al, 1998;Brunet et al, 1999;Hetman et al, 1999;Matsuzaki et al, 1999;Yamaguchi et al, 2001;Zheng and Quirion, 2004). We found significant differences in the neuroprotective efficacy of IGF-1, FGF-2, and BDNF and the pattern of receptor coupling to ERK and Akt.…”
Section: Introductionmentioning
confidence: 48%
“…48,49,57 In support of this theory, a number of somatic oncogenic mutations of the PIK3CA gene, which encodes the p110-a catalytic subunit, have recently been Figure 3 A new pathway for the p53 life or death switch. p53 might determine cell fate through the transcriptional regulation of netrin-1 and UNC5B under physiological conditions.…”
Section: Life or Death: Another Pathway For The P53 Switchmentioning
confidence: 99%
“…However, PI3K-AKT was previously shown to block p53-dependent apoptosis. 48,49 It is therefore possible that this pathway might be involved in the phenomenon (Figure 2). Further investigation of these potential pathways will be necessary to clarify the mechanism of netrin-1 antiapoptotic signaling.…”
Section: P53 and Netrin-1mentioning
confidence: 99%
“…Maximal activity of Akt is achieved through phosphorylation by phosphoinositide-dependent kinase 1 at Ser 473 to confer protection against genomic DNA degradation [38,246,249] and membrane PS exposure [38,42,104]. During a number of injury paradigms, such as toxic insults involving excitotoxicity [106], free radical exposure [45,42,148], hypoxia [38], or trauma [162], Akt is phosphorylated leading to increased activity and protection against PCD induction (Fig.…”
Section: Expression Of Akt Occurs Throughout Mammalian Tissues But Imentioning
confidence: 99%