English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Generation of the tamoxifen-inducible DBH-Cre transgenic mouse line DBH-CT

MPS-Authors
/persons/resource/persons208227

Stubbusch,  J.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

/persons/resource/persons208087

Majdazari,  A.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

/persons/resource/persons208191

Schmidt,  M.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

/persons/resource/persons208168

Rohrer,  H.
Developmental Neurobiology Group, Max Planck Institute for Brain Research, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Stubbusch, J., Majdazari, A., Schmidt, M., Schütz, G., Deller, T., & Rohrer, H. (2011). Generation of the tamoxifen-inducible DBH-Cre transgenic mouse line DBH-CT. Genesis, 49(12), 935-941.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002E-1D03-5
Abstract
We generated transgenic mice bearing a tamoxifen-dependent Cre recombinase expressed under the control of the dopamine-beta-hydroxylase promoter. By crossing to the ROSA26 reporter mice we show that tamoxifen-induced Cre recombinase in adult mice specifically activates beta-galactosidase expression in differentiated noradrenergic neurons of the central and peripheral nervous system. Tamoxifen application in adult mice did not induce beta-galactosidase activity in parasympathetic neurons that transiently express DBH during development. Thus, this transgenic mouse line represents a valuable tool to study gene function in mature noradrenergic neurons by conditional inactivation. genesis 49:935941, 2011. (c) 2011 Wiley Periodicals, Inc.