Tg(tetO-APPSwInd)885Dbo
Transgene Detail

Summary

• Symbol: Tg(tetO-APPSwInd)885Dbo
• Name: transgene insertion 885, David R Borchelt
• MGI ID: MGI:3639702
• Synonyms: TetAPPswe/ind line 885, Tg(tetO-APP*Swe*Ind)885Dbo
• Transgene: Tg(tetO-APPSwInd)885Dbo Location: unknown
• Alliance: Tg(tetO-APPSwInd)885Dbo page

Transgene origin

• Strain of Origin: (C57BL/6J x C3H/HeJ)F2

Transgene description

• Transgene Type: Transgenic (Humanized sequence, Inducible, Inserted expressed sequence)
• Inducer: doxycycline/tetracycline
• Mutation: Insertion
• Tg(tetO-APPSwInd)885Dbo expresses 1 gene
  Transgene expresses:
  

  Organism

  Expressed Gene

  Homolog in Mouse

  Note

  human

  APP (351)

  App	(MGI:88059)

• Tg(tetO-APPSwInd)885Dbo expression driven by 1 gene
  Transgene expression driven by:
  

  Organism	Driver Gene	Note
  Not Specified	tetO

• Mutation details: The transgene expresses the mutant human amyloid protein precursor APPSwInd, which bears both the Swedish (K670N/M671L) and the Indiana (V717F) mutations, under the control of the tetracycline-responsive element (tetO). When bred to another transgenic mouse expressing reverse tertracyclin-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (fTA) to creat a bitransgenic animal, tissue APPSwInd transgene expression can be regulated with the tetracycline analog, doxycycline. These double transgenic show the highest APPSwInd expression and have the highest doxycycline requirements for suppression of transgene expression. (J:80782, J:109829)

Expression

In Structures Affected by this Mutation:

2 anatomical structure(s)

Find Mice (IMSR)

• Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)
• Carrying this Mutation: Mouse Strains: 2 strains available Cell Lines: 0 lines available

Notes

Founder line 8-85 is the highest expressing line, and is representative of a number of lines made with this construct.

References

• Original: J:109829 Jankowsky JL, et al., Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease. PLoS Med. 2005 Dec;2(12):e355
• All: 9 reference(s)