B6(Cg)-Pik3cgtm1Ehi/Cnrm

Status

Under development - register interest

EMMA IDEM:16090
Citation informationRRID:IMSR_EM:16090 

Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information.

International strain nameB6(Cg)-Pik3cgtm1Ehi/Cnrm
Alternative namePI3KγKD/KD
Strain typeTargeted Mutant Strains : Point mutation
Allele/Transgene symbolPik3cgtm1Ehi
Gene/Transgene symbolPik3cg

Information from provider

ProviderAlessandra Ghigo
Provider affiliationuniversity of Turin
Genetic informationKnock-in mice expressing an inactive Pik3cg (PI3Kγ) holoenzyme (kinase dead, KD) were generated by inserting a point mutation in the Pik3cg gene encoding the p110γ catalytic subunit. The Lys833 was converted into Arg, followed by a neomycin resistance gene (Neor) cassette sandwiched between loxP sequences.
Phenotypic informationHomozygous:
Mice homozygous for the kinase-dead PI3Kγ (PI3KγKD) expressing allele (PI3KγKD/KD mice) did not show any overt phenotype.

Heterozygous:
Mice hemizygous for the kinase-dead PI3Kγ (PI3KγKD) expressing allele (PI3KγKD/KD mice) did not show any overt phenotype.
Breeding historyTo generate knock-in animals carrying a kinase-death form of PI3Kγ, the wild-type PI3Kγ locus was replaced by a chimeric minigene containing a mutated form of the human cDNA, in which the Lys833 was converted into Arg, followed by a Neo-resistance cassette sandwiched between loxP sequences. Two out of four recombinant clones were used to generate germ line-transmitting chimeras. Heterozygous mice were crossed with balancer-cre mice to delete the Neor cassette.
References
  • PI3Kgamma modulates the cardiac response to chronic pressure overload by distinct kinase-dependent and -independent effects.;Patrucco Enrico, Notte Antonella, Barberis Laura, Selvetella Giulio, Maffei Angelo, Brancaccio Mara, Marengo Stefano, Russo Giovanni, Azzolino Ornella, Rybalkin Sergei D, Silengo Lorenzo, Altruda Fiorella, Wetzker Reinhard, Wymann Matthias P, Lembo Giuseppe, Hirsch Emilio, ;2004;Cell;118;375-87; 15294162
  • Phosphoinositide 3-kinase γ protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases.;Ghigo Alessandra, Perino Alessia, Mehel Hind, Zahradníková Alexandra, Morello Fulvio, Leroy Jérôme, Nikolaev Viacheslav O, Damilano Federico, Cimino James, De Luca Elisa, Richter Wito, Westenbroek Ruth, Catterall William A, Zhang Jin, Yan Chen, Conti Marco, Gomez Ana Maria, Vandecasteele Grégoire, Hirsch Emilio, Fischmeister Rodolphe, ;2012;Circulation;126;2073-83; 23008439
Homozygous fertileyes
Homozygous viableyes
Homozygous matings requiredyes
Immunocompromisedno

Information from EMMA

Archiving centreCNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy

Disease and phenotype information

IMPC phenotypes (gene matching)
  • decreased circulating potassium level / IMPC
MGI phenotypes (gene matching)
  • increased leukocyte cell number / MGI
  • increased neutrophil cell number / MGI
  • increased monocyte cell number / MGI
  • decreased neutrophil cell number / MGI
  • abnormal myocardial fiber morphology / MGI
  • decreased thymocyte number / MGI
  • skin lesions / MGI
  • weight loss / MGI
  • abnormal immune cell physiology / MGI
  • thymus hypoplasia / MGI
  • abnormal T cell activation / MGI
  • abnormal inflammatory response / MGI
  • decreased inflammatory response / MGI
  • abnormal definitive hematopoiesis / MGI
  • abnormal T cell differentiation / MGI
  • increased susceptibility to bacterial infection / MGI
  • increased susceptibility to viral infection / MGI
  • abnormal leukocyte physiology / MGI
  • abnormal T cell physiology / MGI
  • abnormal macrophage physiology / MGI
  • decreased immunoglobulin level / MGI
  • abnormal neutrophil physiology / MGI
  • abnormal blood coagulation / MGI
  • decreased circulating alanine transaminase level / MGI
  • decreased susceptibility to induced arthritis / MGI
  • impaired macrophage chemotaxis / MGI
  • decreased macrophage cell number / MGI
  • abnormal cardiac muscle relaxation / MGI
  • abnormal CD8-positive, alpha-beta T cell physiology / MGI
  • decreased platelet calcium level / MGI
  • increased eosinophil cell number / MGI
  • abnormal response to infection / MGI
  • decreased cytotoxic T cell cytolysis / MGI
  • decreased T cell proliferation / MGI
  • abnormal heart ventricle morphology / MGI
  • immune system phenotype / MGI
  • abnormal platelet physiology / MGI
  • abnormal T-helper 2 physiology / MGI
  • increased cardiac muscle contractility / MGI
  • abnormal NK cell differentiation / MGI
  • decreased CD4-positive, alpha beta T cell number / MGI
  • decreased CD8-positive, alpha-beta T cell number / MGI
  • increased tumor necrosis factor secretion / MGI
  • decreased interferon-gamma secretion / MGI
  • increased interleukin-1 beta secretion / MGI
  • decreased interleukin-2 secretion / MGI
  • increased interleukin-6 secretion / MGI
  • impaired neutrophil recruitment / MGI
  • impaired neutrophil chemotaxis / MGI
  • decreased platelet aggregation / MGI
  • increased sensitivity to induced morbidity/mortality / MGI

Literature references

  • PI3Kgamma modulates the cardiac response to chronic pressure overload by distinct kinase-dependent and -independent effects.;Patrucco Enrico, Notte Antonella, Barberis Laura, Selvetella Giulio, Maffei Angelo, Brancaccio Mara, Marengo Stefano, Russo Giovanni, Azzolino Ornella, Rybalkin Sergei D, Silengo Lorenzo, Altruda Fiorella, Wetzker Reinhard, Wymann Matthias P, Lembo Giuseppe, Hirsch Emilio, ;2004;Cell;118;375-87; 15294162
  • Phosphoinositide 3-kinase γ protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases.;Ghigo Alessandra, Perino Alessia, Mehel Hind, Zahradníková Alexandra, Morello Fulvio, Leroy Jérôme, Nikolaev Viacheslav O, Damilano Federico, Cimino James, De Luca Elisa, Richter Wito, Westenbroek Ruth, Catterall William A, Zhang Jin, Yan Chen, Conti Marco, Gomez Ana Maria, Vandecasteele Grégoire, Hirsch Emilio, Fischmeister Rodolphe, ;2012;Circulation;126;2073-83; 23008439

Information on how we integrate external resources can be found here

Register interest

Availabilities

Requesting frozen sperm or embryos is generally advisable wherever possible, in order to minimise the shipment of live mice.

Due to the dynamic nature of our processes strain availability may change at short notice. The local repository manager will advise you in these circumstances.

* In addition users have to cover all the shipping costs (including the cost for returning dry-shippers, where applicable).

More details on pricing and delivery times

Practical information

Example health report
(Current health report will be provided later)

Material Transfer Agreement (MTA)
For this strain no provider MTA is needed. Distribution is based on the EMMA conditions only.

EMMA conditions
Legally binding conditions for the transfer

Right strain for your research?

The information provided on this page is, to the best of EMMA’s knowledge, based on data supplied by the original provider. End users are responsible for reviewing these details and for validating the strain and its suitability for their experimental use.​
Not found what you were looking for? Search here for other strains available from EMMA.


Search
INFRAFRONTIER® and European Mouse Mutant Archive - EMMA® are registered trademarks at the European Union Intellectual Property Office (EUIPO).