IMPC phenotypes (gene matching)
- hyperactivity / IMPC
C57BL/6N-Folh1em2Ph/Ph
| Status | Available to order |
| EMMA ID | EM:10058 |
| Citation information | RRID:IMSR_EM:10058 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/6N-Folh1em2Ph/Ph |
| Alternative name | B6.Folh1em2 (17bp deletion) |
| Strain type | Endonuclease-mediated |
| Allele/Transgene symbol | Folh1em2Ph |
| Gene/Transgene symbol | Folh1 |
Information from provider
| Provider | Jan Konvalinka |
| Provider affiliation | Dept. of Proteases of Human Pathogens, Institute of Organic Chemistry and Biochemie ASCR |
| Genetic information | The mutant mouse strain was prepared using TALEN technology. TALENs were designed to target exon 11 of murine Folh1 gene as follows: the left TALEN possessed the RVD sequence NG NG NN HD NI NI NN HD NG NN NN NN NI NG NN (targeted DNA sequence TTGCAAGCTGGGATG), the right TALEN possessed the RVD sequence HD NI NN NG NI NN NI NI HD HD NI NI NN NI NI (targeted DNA sequence TTCTTGGTTCTACTG). The TALENs were thus targeted to cleave within the chromosomal DNA sequence CAGAAGAATTTGGCC. Tail biopsies of pups derived from injected blastocysts were analysed for the presence of TALEN-mediated deletions within this sequence. The mouse carrying deletion of 17bp generating the frame shift was chosen as a founder mouse. |
| Phenotypic information | Homozygous:Homozygous mice do not show any obvious phenotype.Heterozygous:Heterozygous mice do not show any obvious phenotype. |
| Breeding history | Founder mice were bred to C57BL/6N wild-type partners. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institute of Molecular Genetics, Prague, Czech Republic |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal angiogenesis / MGI
- hippocampal neuron degeneration / MGI
- increased anxiety-related response / MGI
- abnormal sciatic nerve morphology / MGI
- increased systemic arterial blood pressure / MGI
- enhanced coordination / MGI
- abnormal peripheral nervous system regeneration / MGI
- decreased susceptibility to injury / MGI
- behavior/neurological phenotype / MGI
- decreased angiogenesis / MGI
- abnormal vascular endothelial cell morphology / MGI
- decreased cerebral infarction size / MGI
- decreased susceptibility to ischemic brain injury / MGI
- mortality/aging / MGI
- increased food intake / MGI
- decreased astrocyte number / MGI
- enhanced spatial learning / MGI
Literature references
- Parallel Metabolomics and Lipidomics of a PSMA/GCPII Deficient Mouse Model Reveal Alteration of NAAG Levels and Brain Lipid Composition.;Sedlák František, Kvasnička Aleš, Marešová Barbora, Brumarová Radana, Dobešová Dana, Dostálová Kateřina, Šrámková Karolína, Pehr Martin, Šácha Pavel, Friedecký David, Konvalinka Jan, ;2024;ACS chemical neuroscience;15;1342-1355; 38377674