B6.Cg-Tg(Cebpb-rtTA2S*S2)1Bjd Tg(tetO-Saa2)Psim/H
Status | Available to order |
EMMA ID | EM:13347 |
International strain name | B6.Cg-Tg(Cebpb-rtTA2S*S2)1Bjd Tg(tetO-Saa2)Psim/H |
Alternative name | B6.Cg-Tg(tetO-Saa2)Psim Tg(Cebpb-rtTA2S*S2)1Bjd |
Strain type | Transgenic Strains |
Allele/Transgene symbol | Tg(Cebpb-rtTA2S*S2)1Bjd, Tg(tetO-Saa2)Psim |
Gene/Transgene symbol | Tg(Cebpb-rtTA2S*S2)1Bjd, Tg(tetO-Saa2)Psim |
Information from provider
Provider | Paul Simons |
Provider affiliation | UCL |
Additional owner | TET Systems GmbH & Co. KG Im Neuenheimer Feld 582 D-69120 Heidelberg, Germany Tel. +49 6221 5 88 04 00 Fax +49 6221 5 88 04 04 info@tet-systems.com |
Genetic information | Transgenic mice with doxycycline-inducible expression of amyloidogenic mouse serum amyloid A (SAA) protein. Double transgenic for mouse SAA2 gene under the control of a tet-responsive promoter, and a reverse tet-transactivator gene driven by the rat Cebpb (CEBP-β) promoter. The two transgenes were introduced separately by pronuclear microinjection. |
Phenotypic information | Homozygous:None in the absence of doxycycline treatment. Expression of SAA may be induced by administration of doxycycline. Serum concentrations of SAA up to ~10 mg/ml elicited by treatment with doxycycline (2 mg/ml in drinking water). Long-term induction leads to AA amyloidosis, with AA amyloid deposited in spleen, liver, heart and kidneys. Amyloid deposition may be accelerated by i.v. injection of ex vivo AA amyloid into doxycycline-induced mice. NB: mice are brown in colour despite having been backcrossed onto C57BL/6J (associated with tet transactivator integration). Heterozygous:None in the absence of doxycycline treatment. Expression of SAA may be induced by administration of doxycycline. Serum concentrations of SAA up to ~5 mg/ml elicited by treatment with doxycycline (2 mg/ml in drinking water). Long-term induction leads to AA amyloidosis, with AA amyloid deposited in spleen, liver, heart and kidneys. Amyloid deposition may be accelerated by i.v. injection of ex vivo AA amyloid into doxycycline-induced mice. |
Breeding history | SAA transgenic line generated by microinjection into (C57BL/6 X CBA)F2 embryos and backcrossing with C57BL/6 mice. Crossed with B6.Cg-Tg(Cebpb-rtTA2S*S2)1Bjd/Cnrm (EMMA strain ID EM:00404) to generate double transgenics, then backcrossed 10 generations with C57BL/6 before breeding both transgenes to homozygosity. Maintained homozygous >10 generations. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Literature references
- Amyloid persistence in decellularized liver: biochemical and histopathological characterization.;Mazza Giuseppe, Simons J Paul, Al-Shawi Raya, Ellmerich Stephan, Urbani Luca, Giorgetti Sofia, Taylor Graham W, Gilbertson Janet A, Hall Andrew R, Al-Akkad Walid, Dhar Dipok, Hawkins Philip N, De Coppi Paolo, Pinzani Massimo, Bellotti Vittorio, Mangione P Patrizia, ;2016;Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis;23;1-7; 26646718
- Pathogenetic mechanisms of amyloid A amyloidosis.;Simons J Paul, Al-Shawi Raya, Ellmerich Stephan, Speck Ivana, Aslam Samrina, Hutchinson Winston L, Mangione Palma P, Disterer Petra, Gilbertson Janet A, Hunt Toby, Millar David J, Minogue Shane, Bodin Karl, Pepys Mark B, Hawkins Philip N, ;2013;Proceedings of the National Academy of Sciences of the United States of America;110;16115-20; 23959890
- Monitoring systemic amyloidosis using MRI measurements of the extracellular volume fraction.;Campbell-Washburn Adrienne E, Price Anthony N, Ellmerich Stephan, Simons J Paul, Al-Shawi Raya, Kalber Tammy L, Ghatrora Rupinder, Hawkins Philip N, Moon James C, Ordidge Roger J, Pepys Mark B, Lythgoe Mark F, ;2013;Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis;20;93-8; 23621497
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