- altered response to myocardial infarction / MGI
- abnormal cardiovascular system physiology / MGI
- premature death / MGI
- disorganized myocardium / MGI
- increased myocardial infarction size / MGI
- increased tumor growth/size / MGI
- renal/urinary system phenotype / MGI
- cardiovascular system phenotype / MGI
- immune system phenotype / MGI
- increased macrophage cell number / MGI
- ventricular fibrillation / MGI
- decreased susceptibility to endotoxin shock / MGI
- decreased sensitivity to induced morbidity/mortality / MGI
- abnormal mitochondrial ATP synthesis coupled electron transport / MGI
- decreased hematocrit / MGI
- hyperglycemia / MGI
- decreased circulating insulin level / MGI
- decreased erythrocyte cell number / MGI
- increased insulin sensitivity / MGI
- impaired glucose tolerance / MGI
- increased physiological sensitivity to xenobiotic / MGI
- increased sensitivity to induced morbidity/mortality / MGI
- abnormal thymus morphology / MGI
- impaired macrophage phagocytosis / MGI
- homeostasis/metabolism phenotype / MGI
B6.129-Tgm2tm1Gml/Cnrm
Status | Available to order |
EMMA ID | EM:02283 |
International strain name | B6.129-Tgm2tm1Gml/Cnrm |
Alternative name | TG2KO |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Tgm2tm1Gml, |
Gene/Transgene symbol | Tgm2 |
Information from provider
Provider | Gerry Melino |
Provider affiliation | University of Tor Vergata |
Genetic information | The targeting vector was constructed by cloning an ~4-kb EcoRV/BamHI fragment containing the sequence from intron 6 to exon 9, into the pPNT vector, 3' of the neomycin resistance gene between the XbaI and BamHI unique sites. An ~2-kb fragment containing intron 3 was generated by genotyping using primers designed on the basis of the sequence of exons 4 and 5. This fragment was cloned into the XhoI site of the pPNT vector 5' of the neomycin resistance gene. This construct deletes 1.2 kb containing part of exon 5, intron 5, exon 6, and a small piece of intron 6 up to the EcoRV site. |
Phenotypic information | Defects in glucose tolerance; defects on phagocytosis-associated crosstalk between macrophages and apoptotic cells; defective function of mitochondrial respiratory complex I. |
Breeding history | Backcrossed for 10 generations. |
References |
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Information from EMMA
Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Disease and phenotype information
MGI allele-associated human disease models
MGI phenotypes (allele matching)
Literature references
- Role of transglutaminase 2 in glucose tolerance: knockout mice studies and a putative mutation in a MODY patient.;Bernassola Francesca, Federici Massimo, Corazzari Marco, Terrinoni Alessandro, Hribal Marta L, De Laurenzi Vincenzo, Ranalli Marco, Massa Ornella, Sesti Giorgio, McLean W H Irwin, Citro Gennaro, Barbetti Fabrizio, Melino Gerry, ;2002;FASEB journal : official publication of the Federation of American Societies for Experimental Biology;16;1371-8; 12205028
- Transglutaminase 2-/- mice reveal a phagocytosis-associated crosstalk between macrophages and apoptotic cells.;Szondy Zsuzsa, Sarang Zsolt, Molnar Peter, Nemeth Tamas, Piacentini Mauro, Mastroberardino Pier Giorgio, Falasca Laura, Aeschlimann Daniel, Kovacs Judit, Kiss Ildiko, Szegezdi Eva, Lakos Gabriella, Rajnavolgyi Eva, Birckbichler Paul J, Melino Gerry, Fesus Laszlo, ;2003;Proceedings of the National Academy of Sciences of the United States of America;100;7812-7; 12810961
- Transglutaminase 2 ablation leads to defective function of mitochondrial respiratory complex I affecting neuronal vulnerability in experimental models of extrapyramidal disorders.;Battaglia Giuseppe, Farrace Maria Grazia, Mastroberardino Pier Giorgio, Viti Irene, Fimia Gian Maria, Van Beeumen Jozef, Devreese Bart, Melino Gennaro, Molinaro Gemma, Busceti Carla Letizia, Biagioni Francesca, Nicoletti Ferdinando, Piacentini Mauro, ;2007;Journal of neurochemistry;100;36-49; 17064362
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