Inhibition of PACAP activity by a receptor antagonist results in changes in cell cycle and apoptotic proteins in chick neuroblasts.
J Mol Neurosci
; 27(1): 107-23, 2005.
Article
en En
| MEDLINE
| ID: mdl-16055950
ABSTRACT
We showed previously that early chick neuroblasts stop proliferating and undergo apoptosis when deprived of endogenous pituitary adenylate cyclase-activating polypeptide (PACAP). To identify proteins involved in these processes, we blocked the primary PACAP receptor and determined protein changes using isotope-coded affinity tag (ICAT) analysis. Cell cycle exit was characterized by a decrease in proteins regulating ribosome biogenesis and protein translation. Apoptosis was linked directly to a tumor suppressor that increases apoptosome activity and indirectly to reduced mitochondrial activity. ICAT analysis, combined with flow cytometric analysis, suggested that some cells were differentiating, rather than undergoing apoptosis. In summary, we have confirmed that withdrawal of PACAP from early chick neuroblasts causes cell cycle exit and apoptosis, and identified proteins involved in proliferation, exit, apoptosis, and possibly differentiation.
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Colección:
01-internacional
Asunto principal:
Neuropéptidos
/
Ciclo Celular
/
Apoptosis
/
Receptores de Superficie Celular
/
Neurotransmisores
/
Factores de Crecimiento Nervioso
/
Neuronas
Tipo de estudio:
Prognostic_studies
Límite:
Animals
Idioma:
En
Revista:
J Mol Neurosci
Asunto de la revista:
BIOLOGIA MOLECULAR
/
NEUROLOGIA
Año:
2005
Tipo del documento:
Article
País de afiliación:
Canadá