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条件性敲除鼠

基因敲入鼠

品系背景 基因名称 基因ID 应用说明
C57/BL6 AGK 69923 T cell specific knockout reduces CD8+ T cell proliferation and antitumor immune responses.
C57/BL6 AldhIa2    
C57/BL6 Atg7 74244 Mutation of this gene causes impairment of constitutive and starvation-induced autophagy resulting in defective protein degradation. Homozygous null mice die within 1 day of birth and have decreased body weight. 
C57BL/6 Bcl6 12053 Homozygous null mutants develop myocarditis and pulmonary vasculitis, show impaired germinal center formation in the spleen, and display T helper 2 cell hyperimmune responsiveness. 
C57BL/6 Bmal1 11865 Homozygous mutation of this gene results in abnormal light/dark cycle activity and decreases overall activity levels. Mice homozygous for another knock-out allele exhibit loss of circadian rhythm in locomotor activity, dyslipidemia, ectopic fat formationand altered energy homeostasis.
C57/BL6 Cbfb  12400 Homozygous null mutant embryos exhibit massive CNS hemorrhaging, impaired definitive hematopoiesis, and death around E12.5. Homozygotes for a hypoplastic mutation are born at normal ratios but die soon after birth. Delayed skeletal development leaves bones poorly ossified and hypoplastic at birth. 
C57BL/6 Col1    
C57BL/6 Col2a1 12824 Mutations in this locus affect cartilage development. Homozygotes die perinatally with anomalies such as shortened limbs without epiphiseal growth plates, cleft palate and persistence of notochord. Heterozygotes are dwarfed with reduced cartilage matrix. 
C57/BL6 Cop1 26374 Mice homozygous for a conditional allele activated in prostate epithelial cells exhibit prostate gland hyperplasia and prostate intraepithelial neoplasia due to increased cell proliferation
SD 大鼠 drd2 13489 Homozygous null mice show Parkinson's disease like symptoms, including akinetic and bradykinetic behavior. Mice lacking only the long isoform are hypoactive and exhibit increased sterotypic behavior in response to dopamine agonists
C57/BL6 ELF4 56501 Mice homozygous for disruptions in this gene have hematopoietic cells with impaired proliferative properties. Lymphocyte development and function is altered, particularly with respect to NK cells and NK-T cells. 
C57BL/6 Erk2 26413 Homozygous mutant embryos implant in the uterus, but die shortly thereafter failing to form extraembryonic tissues.
C57/BL6 FTO 26383 Mice homozygous for an ENU-induced or targeted knock-out allele exhibit decreased body weight, adipose tissue, and body fat and increased metabolism, serum lipids, and serum glucagon that may be gender and diet dependent. 
C57/BL6 Gca 227960 Mice homozygous for disruptions in this gene are essentially normal. However they do demonstrate an increased resistance to endotoxic shock. 
C57/BL6 GOLGA7 57437  
C57/BL6 GPR183 321019 Homozygous inactivation of this gene leads to altered B cell migration during immune activation. Mice homozygous for a null allele exhibit decreased plasmacytoid and myeloid dendritic cell number, and increased type I interferon responses upon TLR ligand challenge or viral infection. 
C57BL/6 Gpr54 114229 Homozygous null mutations result in male and female infertility associated with abnormal sexual maturation and hypogonadotropic hypogonadism.
C57/BL6 GPR65 14744 Homozygous mutant mice have thymocytes and splenocytes that are insensitive to pH-dependent cAMP production. 
C57/BL6 GPR68 238377 Mice homozygous for a null allele exhibit decreased osteoclastogenesis, abnormal pH-sensitive osteoclast survival, and background sensitive alterations in brown adipose tissue, monocytes, and macrophages. Mice homozygous for a different allele exhibit attenuated glucose-stimulated insulin secretion. 
C57/BL6 GPR84 80910 Mice homozygous for a knock-out allele exhibit reduced IL4 production in response to CD3 crosslinking. 
C57/BL6 GPT2 108682 Mice homozygous for a knock-out allele exhibit hypoactivity, reduced postnatal brain growth, various metabolic defects in pathways involving amino acid metabolism, the TCA cycle and neuroprotective mechanisms, and premature death. 
C57/BL6 HS6ST2 50786 Female homozygous or male hemizygous mice for a disruption in this gene display a normal phenotype. 
C57/BL6 IDO1 15930 Mice homozygous for a null allele fail to induce IFN-alpha production by dendritic cells after B7 ligation, and show epididymal inflammation, teratospermia, and elevated caudal epididymal sperm counts along with higher protein and cytokine levels and reduced leukocyte count and proteasome activity. 
C57/BL6 Ighm 16019 Mice homozygous for a knock-out allele exhibit abnormal immune system morphology and physiology. 
C57/BL6 IL17A 16171 Homozygotes for a targeted null mutation exhibit reduced contact, delayed-type and airway hypersensitivity responses and impaired T-dependent antibody production. 
C57/BL6 IL1F10 215274  
C57/BL6 IL1R 16177 Mice homozygous for a knock-out allele exhibit increased susceptibility to bacterial infection, reduced IL1b responsiveness, delayed tooth eruption, decreased susceptibility to experimental autoimmune uveoritinitis, decreased susceptibility to kidney reperfusion injury, and late onset obesity.
C57/BL6 Kat14 228714 Mice homozygous for a null allele exhibit embryonic lethality during organogenesis, decreased size, increased apoptosis, and disrupted cell cycling. Mice heterozygous for one targeted allele exhibit corneal opacity. 
C57BL/6 Kiss1 280287 Homozygote null mice are infertile with abnormal sexual maturation associated with hypogonadotropism 
C57/BL6 klf6 23849 Mice homozygous for a null allele exhibit embryonic lethality during organogenesis, small size, pallor, decreased cellular proliferation and delayed liver development. Mice heterozygous for a null allele exhibit delays in embryonic hematopoeisis. 
C57BL/6 Kras 16653 Mice homozygous for a null allele exhibit embryonic lethality, decreased fetal growth, pericardial edema, anemia, and liver hypoplasia. Mice heterozygous for various knock-in alleles exhibit increased tumorigenesis. 
C57/BL6 L3mbtl3 237339 Mice homozygous for a null mutation die between E17.5 ? 19.5 due to disturbed erythropoiesis which result in anemia. 
FVB L3mbtl3 237339 Mice homozygous for a null mutation die between E17.5 ? 19.5 due to disturbed erythropoiesis which result in anemia. 
FVB  Lgr4 107515 Homozygotes for a knock-out allele show embryonic and perinatal death, open eyelids, and abnormal renal development. One gene trap mutation leads to reduced body weight, sterility, and impaired male reproductive tract development. Another gene trap mutation causes ocular anterior segment anomalies. 
C57/BL6 MBD2 17191 Mice homozygous for disruption sin this gene are grossly normal. Maternal nurturing problems exist however and they are somewhat resistant to dumor development. 
C57/BL6 Mettl14 210529 Mice homozygous for a knock-out allele exhibit embryonic lethality and decreased histone acetylation. Mice homozygous for a conditional allele activated in neuronal stem cells exhibit decreased NSC proliferation and premature differentiation and decreased number of late-born neurons. 
C57/BL6 Mettl3 56335 Mice homozygous for a knock-out allele exhibit embryonic lethality between E3.5 and E8.5 with a deficiency in adopting the epiblast egg cylinder. 
C57BL/6 Mfn1 67414 Mice homozygous for disruptions in this gene die in mid gestation. Structural and functional abnormalities of mitochondria are reported. 
C57BL/6 Mfn2 170731 Mice homozygous for disruptions in this gene die in mid-gestation. Structural and functional abnormalities of mitochondria are reported. 
B6.129 Nlrp3 216799 Mice homozygous for null mutations exhibit attenuated inflammatory responses related to decrease secretion of IL-1beta and IL-18. Mice heterozygous for activating mutations suffer from autoinflammatory attacks that lead to organ failure and death before weaning. 
C57/BL6 Ofd1 237222 Hemizygous conditional deletion of this gene results in embryonic lethality during organogenesis, impaired left-right axis patterning, and malformation of Henson's node cells. Heterozygous conditional deletion of this gene results in neonatal lethality, cystic kidneys, polydactyly, and cleft palate. 
C57BL/6 P2Y1 18441 Mice homozygous for either one of two independently generated knock-out alleles exhibit decreased platelet aggregation, increased bleeding time, and resistance to induced thromboembolism. 
C57BL/6 p53 22059 Mutations in this locus affect cell-cycle regulation and apoptosis. Null homozygotes show high, early-onset tumor incidence; some have persistent hyaloid vasculature and cataracts. Truncated or temperature-sensitive alleles cause early aging phenotypes.
C57/BL6 PDIA3 14827 Mice homozygous for a knock-out allele die by E13.5 with minor changes in ER calcium capacity and unfolded protein response in mouse embryonic fibroblasts. Mice homozygous for a gene trap allele die prior to birth while heterozygous mice exhibit abnormalbone volume bone morphology. 
C57BL/6 Pstk 214580  
C57/BL6 Rac3 170758 Homozygous null mice display decreased stride length and impaired thermal nociception, but have improved motor learning and retention of motor behaviors and normal brain morphology.
C57/BL6 Rcan1 54720 Unstressed homozygous mutant mice show no overt phenotype other than a slight reduction in heart size and an impaired T helper 1 response. Stress-induced cardiac hypertrophy, however, is attenuated in mutant mice. 
C57/BL6 Rcn2 26611 Mice homozygous for a null allele exhibit lowered basal blood pressure and attenuated angiotensin II-induced hypertension. 
C57/BL6 Rnf123 84585  
C57/BL6 Sec62 69276  
C57/BL6 SFMBT2 353282  
C57/BL6 SHMT2 108037 Mice homozygous for a knock-out allele exhibit lethlity after E13.5, decreased size, anemia and reduced MEF cellular respiration and proliferation. 
C57/BL6 SLC30A9 109108  
C57BL/6 Sps1 109079 Mice homozygous for a knock-out allele exhibit embryonic growth retardation and complete lethality by E14.5 with failure of the amnion to separate from the yolk sac. Mice homozygous for a conditional allele activated in the liver exhibit reduced liver iron and manganese levels.
C57BL/6 Sps2 20768  
C57/BL6 STX17 67727  
C57/BL6 Sumo2 170930 Mice homozygous for a null allele display severe embryonic growth retardation and die at approximately embryonic day E10.5. 
C57/BL6 TMEM173 72512 Mice homozygous for a knock-out allele exhibit increased susceptibility to viral infection and abnormal innate immunity. Mice homozygous for an ENU-induced allele exhibit altered response to bacterial and viral infection.
C57/BL6 Tnfaip3 21929 Homozygous null mice display runting, severe multi-organ inflammation, hypersensitivity to lipopolysaccharide and TNF, and premature death. Older mice homozygous for point mutations that disrupt deubiquitinating activity develop splenomegaly and show an increased number of myeloid cells. 
C57/BL6 traf4 22032 Homozygotes for targeted null mutations show respiratory problems, various skeletal defects, spina bifida and partial lethality around embryonic day 14. Homozygotes for an ENU-induced mutation exhibit postnatal lethality and hypopigmentation.
C57BL/6 Trek1 16526 Homozygous null mice display increased sensitivity to pharmacologically induced seizures and ischemia.
C57/BL6 TRIM45 229644  
C57BL/6 Twik1    
C57BL/6 Uhrf1 18140 Mice homozygous for disruption of this marker die early in gestation showing growth retardation and various malformations.
C57BL/6 Uhrf2 109113 Homozygous KO causes deregulated expression of neuron-related genes, reduced DNA methylation in the brain and impaired contextual conditioning and spatial memory. 
C57/BL6 Uox 22262 Homozygous null mutants exhibit marked hyperuricemia and urate nephropathy. Most mutants die prior to four weeks of age. Homozygotes for a large paracentric inversion disrupting this same gene exhibit a similar phenotype
C57/BL6 Wtap 60532 Mice homozygous for a mutation display lethality during embryogenesis with abnormalities appearing during gastrulation. 
C57BL/6 β-catenin    
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