Nerve growth factor (NGF) induces neuronal differentiation in neuroblastoma cells transfected with the NGF receptor cDNA

1990 ◽  
Vol 10 (9) ◽  
pp. 5015-5020
Author(s):  
H Matsushima ◽  
E Bogenmann
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Neuroblastoma Cell Line ◽  
Term Treatment ◽  
Short Term Treatment ◽  
Nerve Growth ◽  
Ngf Receptor ◽  
Long Term Treatment

Human nerve growth factor (NGF) receptor (NGFR) cDNA was transfected into a neuroblastoma cell line (HTLA 230) which does not express a functional NGF-NGFR signal transduction cascade. Short-term treatment of stably transfected cells (98-3) expressing membrane-bound NGF receptor molecules resulted in a cell cycle-dependent, transient expression of the c-fos gene upon treatment with NGF, suggesting the presence of functional high-affinity NGFR. Extensive outgrowth of neurites and cessation of DNA synthesis occurred in transfectants grown on an extracellular matrix after long-term treatment with NGF, suggesting terminal differentiation. Our data support the idea that introduction of a constitutively expressed NGFR cDNA into cells with neuronal background results in the assembly of a functional NGF-NGFR signal cascade in a permissive extracellular environment.

scholarly journals Nerve growth factor (NGF) induces neuronal differentiation in neuroblastoma cells transfected with the NGF receptor cDNA.

1990 ◽  
Vol 10 (9) ◽  
pp. 5015-5020 ◽  
Author(s):  
H Matsushima ◽  
E Bogenmann
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Neuroblastoma Cell ◽  
Neuroblastoma Cells ◽  
Neuroblastoma Cell Line ◽  
Term Treatment ◽  
Short Term Treatment ◽  
Nerve Growth ◽  
Ngf Receptor ◽  
Long Term Treatment

Human nerve growth factor (NGF) receptor (NGFR) cDNA was transfected into a neuroblastoma cell line (HTLA 230) which does not express a functional NGF-NGFR signal transduction cascade. Short-term treatment of stably transfected cells (98-3) expressing membrane-bound NGF receptor molecules resulted in a cell cycle-dependent, transient expression of the c-fos gene upon treatment with NGF, suggesting the presence of functional high-affinity NGFR. Extensive outgrowth of neurites and cessation of DNA synthesis occurred in transfectants grown on an extracellular matrix after long-term treatment with NGF, suggesting terminal differentiation. Our data support the idea that introduction of a constitutively expressed NGFR cDNA into cells with neuronal background results in the assembly of a functional NGF-NGFR signal cascade in a permissive extracellular environment.

Short- and long-term mechanisms of tau regulation in PC12 cells

1995 ◽  
Vol 108 (8) ◽  
pp. 2857-2864 ◽  
Author(s):  
E. Sadot ◽  
J. Barg ◽  
D. Rasouly ◽  
P. Lazarovici ◽  
I. Ginzburg
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Tau Protein ◽  
Immunoblot Analysis ◽  
Term Treatment ◽  
Mrna Levels ◽  
Short Term Treatment ◽  
Nerve Growth ◽  
Protein Levels

Induction by nerve growth factor of neurite outgrowth in PC12 cells is transcription-dependent and is associated with the accumulation of tau protein. It was recently shown that short-term treatment with staurosporine, a protein kinase alkaloid inhibitor, induced an elevation of tau protein levels and outgrowth of stable neurites. In this study, we analyzed the mechanism(s) by which nerve growth factor and staurosporine exert their effects on tau levels. We demonstrate that nerve growth factor affects tau mRNA stability, thus contributing to the observed increase in tau mRNA levels. On the other hand, tau mRNA levels were not affected by the treatment with staurosporine. We also demonstrate that the phosphorylation of tau protein was reduced after treatment of PC12 cells with nerve growth factor or staurosporine, as shown by immunoblot analysis using specific antibodies and alkaline phosphatase treatment. Thus, regulation of tau levels by nerve growth factor appears to be mediated by transcriptional, post-transcriptional and posttranslational steps, whereas the effect of staurosporine on tau levels may be attributed to its effect on the state of phosphorylation of the protein.

Long-term treatment with recombinant nerve growth factor for HIV-associated sensory neuropathy

Neurology ◽  
2001 ◽  
Vol 57 (7) ◽  
pp. 1313-1316 ◽  
Author(s):  
G. Schifitto ◽  
C. Yiannoutsos ◽  
D. M. Simpson ◽  
B. T. Adornato ◽  
E. J. Singer ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Sensory Neuropathy ◽  
Term Treatment ◽  
Nerve Growth ◽  
Long Term Treatment

scholarly journals Expression of beta-nerve growth factor and its receptor in rat seminiferous epithelium: specific function at the onset of meiosis.

1992 ◽  
Vol 117 (3) ◽  
pp. 629-641 ◽  
Author(s):  
M Parvinen ◽  
M Pelto-Huikko ◽  
O Söder ◽  
R Schultz ◽  
A Kaipia ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Sertoli Cells ◽  
Seminiferous Epithelium ◽  
Receptor Protein ◽  
Tyrosine Kinase Receptor ◽  
Specific Expression ◽  
Nerve Growth ◽  
Ngf Receptor

beta-Nerve growth factor (NGF) is expressed in spermatogenic cells and has testosterone-downregulated low-affinity receptors on Sertoli cells suggesting a paracrine role in the regulation of spermatogenesis. An analysis of the stage-specific expression of NGF and its low affinity receptor during the cycle of the seminiferous epithelium in the rat revealed NGF mRNA and protein at all stages of the cycle. Tyrosine kinase receptor (trk) mRNA encoding an essential component of the high-affinity NGF receptor was also present at all stages. In contrast, expression of low affinity NGF receptor mRNA was only found in stages VIIcd and VIII of the cycle, the sites of onset of meiosis. The low-affinity NGF receptor protein was present in the plasma membrane of the apical Sertoli cell processes as well as in the basal plasma membrane of these cells at stages VIIcd to XI. NGF was shown to stimulate in vitro DNA synthesis of seminiferous tubule segments with preleptotene spermatocytes at the onset of meiosis while other segments remained nonresponsive. We conclude that NGF is a meiotic growth factor that acts through Sertoli cells.

CRK protein binds to two guanine nucleotide-releasing proteins for the Ras family and modulates nerve growth factor-induced activation of Ras in PC12 cells

1994 ◽  
Vol 14 (8) ◽  
pp. 5495-5500
Author(s):  
M Matsuda ◽  
Y Hashimoto ◽  
K Muroya ◽  
H Hasegawa ◽  
T Kurata ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Sh2 Domain ◽  
Single Amino Acid ◽  
Guanine Nucleotide ◽  
Nerve Growth ◽  
Tyrosine Residues ◽  
Ngf Receptor ◽  
Ras Family

It has been reported that growth factors activate Ras through a complex of an adaptor type SH2-containing molecule, Grb2, and a Ras guanine nucleotide-releasing protein (GNRP), mSos. We report on the involvement of another adaptor molecule, CRK, in the activation of Ras. Overexpression of wild-type CRK proteins CRK-I and CRK-II enhanced the nerve growth factor (NGF)-induced activation of Ras in PC12 cells, although the basal level of GTP-bound active Ras was not altered. In contrast, mutants with a single amino acid substitution in either the SH2 or SH3 domain of the CRK-I protein inhibited the NGF-induced activation of Ras. Two GNRPs for the Ras family, mSos and C3G, were coimmunoprecipitated with the endogenous Crk proteins in PC12 cells. The association between C3G and the CRK mutants was dependent upon the presence of intact SH3. The SH2 domain of CRK bound to the SHC protein phosphorylated on tyrosine residues by NGF stimulation. The results demonstrate that, in addition to Grb2, CRK participates in signaling from the NGF receptor and that two GNRPs appear to transmit signals from these adaptor molecules to Ras.

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