Gas1 Is Induced during and Participates in Excitotoxic Neuronal Death

Mellström, Britt; Ceña, Valentı́n; Lamas, Marta; Perales, Carlos; González, Carmen; Naranjo, José R.

doi:10.1006/mcne.2001.1092

Cited by 39 publications

(51 citation statements)

References 68 publications

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“…Lrig1, a transmembrane protein containing leucine-rich repeats and Ig-like domains, interacts with Ret thereby inhibiting its recruitment to lipid rafts, the binding to the GDNF-GFRa1 complex, receptor autophosphorylation, and MAPK activation in response to GDNF (Ledda et al, 2008). Growth Arrest Specific 1 (Gas1) is a molecule involved in cell cycle arrest and widely expressed during development, but also induced during, and participating in, excitotoxic neuronal death (Mellstrom et al, 2002). Interestingly, Gas1 shows high structural similarity to the GFRa (Cabrera et al, 2006;Schueler-Furman et al, 2006).…”

Section: Negative Regulation Of Gdnf Expressionmentioning

confidence: 99%

Driving GDNF expression: The green and the red traffic lights

Saavedra

Baltazar

Duarte

2008

Progress in Neurobiology

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Section: Negative Regulation Of Gdnf Expressionmentioning

confidence: 99%

Driving GDNF expression: The green and the red traffic lights

Saavedra

Baltazar

Duarte

2008

Progress in Neurobiology

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“…A recent article shows that Gas1 has an opposite effect on neuronal cells promoting their apoptosis after excitotoxic insults. 46 In vivo, studies on Gas1-null animals showed that it is required for growth of granule and glial cells and for the complete development of the cerebellum. 23 Overexpression of Gas1 leads to growth arrest in embryonic limb cells and promotes interdigital cell death.…”

Section: Gas1 and Apoptosismentioning

confidence: 99%

Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis

Spagnuolo

Corada

Orsenigo

et al. 2004

Blood

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“…8 Recently, several reports have shown that Gas1 is involved in programmed cell death (apoptosis) in different types of cells. 7,9,10 Furthermore, we have shown that the targeted overexpression of gas1 induces apoptosis in retrovirally tranduced C6 cells and inhibits tumor growth in vivo.…”

Section: Introductionmentioning

confidence: 99%

Targeted-simultaneous expression of Gas1 and p53 using a bicistronic adenoviral vector in gliomas

et al. 2007

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The targeted expression of transgenes is one of the principal goals of gene therapy, and it is particularly relevant for the treatment of brain tumors. In this study, we examined the effect of the overexpression of human gas1 (growth arrest specific 1) and human p53 cDNAs, both under the transcriptional control of a promoter of the human glial fibrillary acidic protein (gfa2), employing adenoviral expression vectors, in glioma cells. We showed that the targeted overexpression of gas1 and p53 (AdSGas1 and AdSp53, respectively) in rat glioma cells (C6) reduced the number of viable cells and induced apoptosis. Moreover, the adenovirally targeted expression of these genes also reduced tumor growth in vivo. Unexpectedly, there was no additive effect when both gas1 and p53 were simultaneously expressed in the same cells using a bicistronic adenoviral vector. We suggest that Gas1 does not act in combination with p53 in the C6 and U373 glioma cell lines, inducing apoptosis and cell cycle arrest. Our results indicate that the targeted expression of tumor suppressor genes (gas1 and p53) regulated by the gfa2 promoter, together with adenoviral vectors may provide an interesting approach for adjuvant selective glioma gene therapy.

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Gas1 Is Induced during and Participates in Excitotoxic Neuronal Death

Cited by 39 publications

References 68 publications

Driving GDNF expression: The green and the red traffic lights

Driving GDNF expression: The green and the red traffic lights

Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis

Targeted-simultaneous expression of Gas1 and p53 using a bicistronic adenoviral vector in gliomas

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