| 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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