Up-regulation of Jun/AP-1 during differentiation of N1E-115 neuroblastoma cells.

نویسندگان

  • R P de Groot
  • W Kruijer
چکیده

Neuroblastoma cell lines isolated from neuroblastoma tumors can be induced to differentiate into neuronal cell types by treatment with chemical agents, such as dimethyl sulfoxide and retinoic acid. The molecular mechanisms underlying this differentiation process, however, are completely obscure. In this paper, we show that neuronal differentiation of mouse N1E-115 neuroblastoma cells by dimethyl sulfoxide is accompanied by a prolonged rise in c-jun, junB, and junD expression and AP-1 activity. Multiple sequence elements in the Jun promoters are involved in this process. Furthermore, we show that c-jun and junD, but not junB, are expressed at high levels in the neuronal cell types obtained after dimethyl sulfoxide treatment. These results suggest an important role for c-jun and junD in neuronal differentiation of N1E-115 cells.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Expressional down-regulation of neuronal-type nitric oxide synthase I by glucocorticoids in N1E-115 neuroblastoma cells.

Neuronal-type nitric oxide synthase (NOS I) is involved in ischemia-induced brain damage, and glucocorticoids have been reported to protect from brain damage. This prompted us to investigate if the activity or expression of NOS I was influenced by glucocorticoids. We used the murine neuroblastoma cell line N1E-115 as our experimental model. Short-term incubation (30 min) of the N1E-115 cells wi...

متن کامل

Phosphatidylinositol 3-kinase, Cdc42, and Rac1 act downstream of Ras in integrin-dependent neurite outgrowth in N1E-115 neuroblastoma cells.

Ras and Rho family GTPases have been ascribed important roles in signalling pathways determining cellular morphology and growth. Here we investigated the roles of the GTPases Ras, Cdc42, Rac1, and Rho and that of phosphatidylinositol 3-kinase (PI 3-kinase) in the pathway leading from serum starvation to neurite outgrowth in N1E-115 neuroblastoma cells. Serum-starved cells grown on a laminin mat...

متن کامل

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na /Ca exchange

Kopper, Kara L., and Joseph S. Adorante. Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na /Ca2 exchange. Am J Physiol Cell Physiol 282: C1000–C1008, 2002; 10.1152/ajpcell.00182.2001.—In fura 2-loaded N1E-115 cells, regulation of intracellular Ca2 concentration ([Ca2 ]i) following a Ca2 load induced by 1 M thapsigargin and 10 M carbonylcyanide p-trifluoromethyox...

متن کامل

Regulation of intracellular calcium in N1E-115 neuroblastoma cells: the role of Na(+)/Ca(2+) exchange.

In fura 2-loaded N1E-115 cells, regulation of intracellular Ca(2+) concentration ([Ca(2+)](i)) following a Ca(2+) load induced by 1 microM thapsigargin and 10 microM carbonylcyanide p-trifluoromethyoxyphenylhydrazone (FCCP) was Na(+) dependent and inhibited by 5 mM Ni(2+). In cells with normal intracellular Na(+) concentration ([Na(+)](i)), removal of bath Na(+), which should result in reversal...

متن کامل

Intracellular Ca2+ concentration in the N1E-115 neuronal cell line and its use for peripheric nerve regeneration.

Entubulation repair of peripheral nerve injuries has a lengthy history. Several experimental and clinical studies have explored the effectiveness of many biodegradable and non-degradable tubes with or without addition of molecules and cells. The main objective of the present study was to develop an economical and also an easy way for culturing a neural cell line which is capable of growing, dif...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research

دوره 2 12  شماره 

صفحات  -

تاریخ انتشار 1991