The PC12 pheochromocytoma cell line responds to nerve growth factor (NGF) by exiting from the cell cycle and differentiating to induce extending neurites. Cyclin D1 is an important regulator of G1/S phase cell cycle progression, and it is known to play a role in myocyte differentiation in cultured cells. Herein, NGF induced cyclin D1 promoter, mRNA, and protein expression via the p21 RAS pathway. Antisense- or small interfering RNA to cyclin D1 abolished NGF-mediated neurite outgrowth, demonstrating the essential role of cyclin D1 in NGF-mediated differentiation. Expression vectors encoding mutants of the Ras/mitogen-activated protein kinase pathway, and chemical inhibitors, demonstrated NGF induction of cyclin D1 involved cooperative interactions of extracellular signal-regulated kinase, p38, and phosphatidylinositol 3-kinase pathways downstream of p21 RAS . NGF induced the cyclin D1 promoter via Sp1, nuclear factor-κB, and cAMP-response element/activated transcription factor sites. NGF induction via Sp1 involved the formation of a Sp1/p50/p107 complex. Cyclin D1 induction by NGF governs differentiation and neurite outgrowth in PC12 cells. © 2008 by The American Society for Cell Biology.

Nerve growth factor regulation of cyclin D1 in PC12 cells through a p21 RAS extracellular signal-regulated kinase pathway requires cooperative interactions between Sp1 and nuclear factor-κB / Marampon, Francesco; Casimiro, Mathew C.; Fu, Maofu; Powell, Michael J.; Popov, Vladimir M.; Lindsay, Jaime; Zani, Bianca M.; Ciccarelli, Carmela; Watanabe, Genichi; Lee, Richard J.; Pestell, Richard G.. - In: MOLECULAR BIOLOGY OF THE CELL. - ISSN 1059-1524. - 19:6(2008), pp. 2566-2578. [10.1091/mbc.E06-12-1110]

Nerve growth factor regulation of cyclin D1 in PC12 cells through a p21 RAS extracellular signal-regulated kinase pathway requires cooperative interactions between Sp1 and nuclear factor-κB

Marampon, Francesco;Zani, Bianca M.;
2008

Abstract

The PC12 pheochromocytoma cell line responds to nerve growth factor (NGF) by exiting from the cell cycle and differentiating to induce extending neurites. Cyclin D1 is an important regulator of G1/S phase cell cycle progression, and it is known to play a role in myocyte differentiation in cultured cells. Herein, NGF induced cyclin D1 promoter, mRNA, and protein expression via the p21 RAS pathway. Antisense- or small interfering RNA to cyclin D1 abolished NGF-mediated neurite outgrowth, demonstrating the essential role of cyclin D1 in NGF-mediated differentiation. Expression vectors encoding mutants of the Ras/mitogen-activated protein kinase pathway, and chemical inhibitors, demonstrated NGF induction of cyclin D1 involved cooperative interactions of extracellular signal-regulated kinase, p38, and phosphatidylinositol 3-kinase pathways downstream of p21 RAS . NGF induced the cyclin D1 promoter via Sp1, nuclear factor-κB, and cAMP-response element/activated transcription factor sites. NGF induction via Sp1 involved the formation of a Sp1/p50/p107 complex. Cyclin D1 induction by NGF governs differentiation and neurite outgrowth in PC12 cells. © 2008 by The American Society for Cell Biology.
2008
Animals; base sequence; cell cycle; cell proliferation; Cyclin D1; extracellular signal-regulated MAP Kinases; humans; MAP Kinase signaling system; mice; NF-kappa B; NF-kappa B p50 Subunit; nerve growth factor; neurites; PC12 cells; Phosphatidylinositol 3-Kinases; promoter regions; genetic; protein binding; proto-oncogene proteins p21(ras); RNA messenger; RNA small interfering; rats; retinoblastoma-like protein p107; Sp1 transcription factor; transcription genetic; p38 mitogen-activated protein Kinases; molecular biology; cell biology
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Nerve growth factor regulation of cyclin D1 in PC12 cells through a p21 RAS extracellular signal-regulated kinase pathway requires cooperative interactions between Sp1 and nuclear factor-κB / Marampon, Francesco; Casimiro, Mathew C.; Fu, Maofu; Powell, Michael J.; Popov, Vladimir M.; Lindsay, Jaime; Zani, Bianca M.; Ciccarelli, Carmela; Watanabe, Genichi; Lee, Richard J.; Pestell, Richard G.. - In: MOLECULAR BIOLOGY OF THE CELL. - ISSN 1059-1524. - 19:6(2008), pp. 2566-2578. [10.1091/mbc.E06-12-1110]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1259181
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