SCIRP Mobile Website
Paper Submission

Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.

 

Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
   
Paper Publishing WeChat
Book Publishing WeChat
(or Email:book@scirp.org)

Article citations

More>>

Sergeant, N., Delacourte, A. and Buée, L. (2005) Tau Protein as a Differential Biomarker of Tauopathies. Biochimica et Biophysica Acta (BBA), Molecular Basis of Disease, 1739, 179-197. http://dx.doi.org/10.1016/j.bbadis.2004.06.020

has been cited by the following article:

  • TITLE: Nerve Growth Factor Enhances Tau Isoform Expression and Transcription in IMR32 Cells

    AUTHORS: Cheryl L. Cragg, Bettina E. Kalisch

    KEYWORDS: Nerve Growth Factor (NGF), Tau, Signal Transduction, Transcription, Nitric Oxide (NO), IMR32 Cells, PC12 Cells

    JOURNAL NAME: Neuroscience and Medicine, Vol.5 No.2, April 30, 2014

    ABSTRACT: The present study characterized the nerve growth factor (NGF)-mediated regulation of tau protein expression and transcription in IMR32 human neuroblastoma cells. Treatment of IMR32 cells with 50 ng/mL NGF resulted in increased levels of specific tau protein isoforms. A 550 bp fragment of the tau promoter was cloned and treatment of transfected IMR32 and PC12 cells with NGF also resulted in increased promoter activation, suggesting that the NGF-mediated increase in tau isoforms is regulated, at least in part, at the level of transcription. Pretreatment with the MAP kinase inhibitor U0126 or the PKC inhibitor bisindolylmaleimide 1 (BIS-1) attenuated the NGF-mediated increase in tau transcription, indicating that the NGF-mediated activation of the MAP kinase and PKC signaling pathways modulate tau transcription. Pre-treatment of cells with the Akt inhibitor, LY294002 or with NOS inhibitors Nω-nitro-L-arginine methylester (L-NAME) or s-methylisothiourea (S-MIU) had no effect on the NGF-mediated increase in tau promoter activation, suggesting that NO and the NGF-Akt signaling pathway do not modulate tau transcription. Taken together, these data demonstrate that NGF increases the levels of multiple human tau isoforms in IMR32 cells which may result, at least in part, from NGF-mediated PKC and MAP kinase-induced tau transcription.