2011
DOI: 10.1038/onc.2011.458
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Direct promoter induction of p19Arf by Pit-1 explains the dependence receptor RET/Pit-1/p53-induced apoptosis in the pituitary somatotroph cells

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Cited by 21 publications
(52 citation statements)
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“…Recently, in the normal male pituitary gland, the existence of TUNEL-positive cells that coexpress Pit-1 (GH) and p19Arf has been demonstrated [95] (fig. 3d).…”
Section: Apoptosis and Its Equilibria With Stem Cell Recruitment In Tmentioning
confidence: 99%
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“…Recently, in the normal male pituitary gland, the existence of TUNEL-positive cells that coexpress Pit-1 (GH) and p19Arf has been demonstrated [95] (fig. 3d).…”
Section: Apoptosis and Its Equilibria With Stem Cell Recruitment In Tmentioning
confidence: 99%
“…For example, the Ret knockout causes pituitary hyperplasia at birth due to excess somatotroph numbers, while a retrovirus expressing Ret can prevent estrogen-induced hyperplasia [92]. The apoptotic pathway has a survival correlate when the ligand is present: GDNF prevents RET processing, inducing dimerization, tyrosine kinase activation and phosphorylation of intracellular proteins [92,95,96]. One of the activated survival pathways involves Akt, which represses Pit-1 expression to levels insufficient to initiate apoptosis and compatible with life and GH production.…”
Section: Apoptosis and Its Equilibria With Stem Cell Recruitment In Tmentioning
confidence: 99%
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“…When stimulated by GDNF, it behaved as as an oncogene able to activate intracellular signaling and cell survival. Instead, in the absence of GDNF, RET behaved as a tumor suppressor; caspase-mediated RET processing induced Pit-1 expression, that, in turn, caused p19Arf and p53 upregulation and apoptosis [46,49].…”
Section: Ret As a Tumor Suppressormentioning
confidence: 99%