IMPC phenotypes (gene matching)
C57BL/6J.129-Zfp36tm1.1Geno/H
| Status | Available to order |
| EMMA ID | EM:16233 |
| Citation information | RRID:IMSR_EM:16233 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 name | C57BL/6J.129-Zfp36tm1.1Geno/H |
| Alternative name | Zfp36aa |
| Strain type | Targeted Mutant Strains |
| Allele/Transgene symbol | Zfp36tm1.1Geno |
| Gene/Transgene symbol | Zfp36 |
Information from provider
| Provider | Andy Clark |
| Provider affiliation | Inflammation and Ageing, University of Birmingham |
| Genetic information | Targeted substitution of Ser52 and Ser178 codons of the endogenous Zfp36 gene with alanine codons. For selection of recombined ES stem cells a neomycin cassette was introduced to the Zfp36 intron. After identification of founder mice, the neomycin cassette was excised by crossing to a Cre-expressing strain. There is a residual ~100bp insertion in the intron, comprising the remaining LoxP site and flanking sequences. |
| Phenotypic information | Homozygous:No detectable phenotype under normal breeding conditions. Resistant to experimentally induced inflammatory pathologies (e.g. endotoxemia, polymicrobial sepsis, serum transfer-induced arthritis).Heterozygous:No detectable phenotype under normal breeding conditions. Resistant to experimentally induced inflammatory pathologies (e.g. endotoxemia, polymicrobial sepsis, serum transfer-induced arthritis). |
| Breeding history | The original mutation was created by homologous recombination using 129Sv embryonic stem cells. Founder mice were identified by PCR screening. The strain has been back-crossed against C57BL/6 for approximately 15 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 |
Disease and phenotype information
MGI phenotypes (gene matching)
- increased leukocyte cell number / MGI
- increased neutrophil cell number / MGI
- increased monocyte cell number / MGI
- extramedullary hematopoiesis / MGI
- increased granulocyte number / MGI
- alopecia / MGI
- enlarged spleen / MGI
- spleen hyperplasia / MGI
- enlarged lymph nodes / MGI
- dermatitis / MGI
- decreased body weight / MGI
- abnormal vasodilation / MGI
- postnatal growth retardation / MGI
- thymus hypoplasia / MGI
- conjunctivitis / MGI
- heart inflammation / MGI
- liver inflammation / MGI
- vascular inflammation / MGI
- decreased inflammatory response / MGI
- premature death / MGI
- abnormal thymus cortex morphology / MGI
- abnormal thymus medulla morphology / MGI
- abnormal macrophage physiology / MGI
- decreased systemic arterial blood pressure / MGI
- arthritis / MGI
- decreased susceptibility to induced arthritis / MGI
- oxidative stress / MGI
- abnormal nitric oxide homeostasis / MGI
- decreased susceptibility to experimental autoimmune encephalomyelitis / MGI
- decreased lymphocyte cell number / MGI
- abnormal renal glomerulus morphology / MGI
- homeostasis/metabolism phenotype / MGI
- thrombocytosis / MGI
- increased cellular sensitivity to oxidative stress / MGI
- absent subcutaneous adipose tissue / MGI
Literature references
- Dominant Suppression of Inflammation via Targeted Mutation of the mRNA Destabilizing Protein Tristetraprolin.;Ross Ewan A, Smallie Tim, Ding Qize, O'Neil John D, Cunliffe Helen E, Tang Tina, Rosner Dalya R, Klevernic Iva, Morrice Nicholas A, Monaco Claudia, Cunningham Adam F, Buckley Christopher D, Saklatvala Jeremy, Dean Jonathan L, Clark Andrew R, ;2015;Journal of immunology (Baltimore, Md. : 1950);195;265-76; 26002976