Tg(Rip1-Akt*)#Perm
Transgene Detail
|
|
| Symbol: |
Tg(Rip1-Akt*)#Perm |
| Name: |
transgene insertion, M Permutt |
| MGI ID: |
MGI:5318863 |
| Synonyms: |
AktdnRIP, RIP-kdAkt |
| Transgene: |
Tg(Rip1-Akt*)#Perm Location: unknown
|
| Alliance: |
Tg(Rip1-Akt*)#Perm page
|
|
| Strain of Origin: |
C57BL/6 x CBA
|
|
| Transgene Type: |
|
Transgenic (Dominant negative, Inserted expressed sequence) |
| Mutation: |
|
Insertion
|
| |
|
Mutation details: This transgene expresses a kinase dead form of Akt1, with mutation at the ATP binding site that has been shown to act in a dominant negative manner, from the rat insulin 1 promoter. Immunofluorescence staining of pancreatic sections with anti-HA and anti-insulin antibodies showed that the majority of pancreatic beta cells (approximately 80 percent) expressed the transgene. Four transgenic founders were obtained and two lines were studied further, but no line numbers were given.
(J:93417)
|
|
|
| Mouse strains and cell lines
available from the International Mouse Strain Resource
(IMSR) |
| Carrying this Mutation: |
Mouse Strains: 0 strains available
Cell Lines: 0 lines available
|
|
| Original: |
J:93417 Bernal-Mizrachi E, et al., Defective insulin secretion and increased susceptibility to experimental diabetes are induced by reduced Akt activity in pancreatic islet beta cells. J Clin Invest. 2004 Nov;114(7):928-36 |
| All: |
2 reference(s) |
|
Analysis Tools
