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全身性敲除鼠

条件性敲除鼠

基因敲入鼠

背景品系 基因名称 基因ID 应用说明
C57BL/6 A20Tnfaip3 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. 
SD 大鼠 Abcb1a 18671 Mutations in this gene result in increased sensitivity to various drugs, including avermectins and vinblastine. Mice with a null allele develop spontanous colitis. 
SD 大鼠 Abcb1b 18669 Mice homozygous for targeted mutations that inactivate the gene are hypersensitive to effects of drugs transported by phosphoglycoproteins.
C57BL/6 Abin1 57783 Mice homozygous for a null allele exhibit perinatal lethality associated with anemia and focal apoptosis in the fetal liver. Mice homozygous for a gene trap allele exhibit partial prenatal lethality and SLE-like inflammatory disease.
C57BL/6 ACE2  70008 Targeted disruption of this locus results in reduced cardiac contractility. Male mice hemizygous for a knock-out allele exhibit increased susceptibility to induced colitis.
C57BL/6 Add3 27360 Mice homozygous for a knock-out allele exhibit normal blood pressure and show no significant alterations in red blood cell or platelet structure and function.
C57BL/6 Ager 11596 Homozygotes for a null allele show increased bone mass and strength, reduced osteoclast number, abnormal blood vessel healing, and altered development of nephropathy and pain perception in induced diabetes. Homozygotes for another null allele show restored diabetes-induced angiogenic responses.
C57BL/6 AGT 11606 Homozygous null mutation of this gene results in small body size and lower body fat, decreased blood pressure and hypotension, kidney abnormalities, polydipsia and polyuria.
SD 大鼠 Agxt  11611 Mice homozygous for a null allele exhibit increased urinary oxalate levels and male mice suffer from bladder stones.
C57BL/6 Aplnr 23796 Mice homozygous for a knock-out allele exhibit early lethality, decreased cardiac contractility, and decreased exercise endurance. Mice for another knock-out allele develop pulmonary venoocclusive disease with heart right ventricle hypertrophy and elevated pulmonary pressures.
C57BL/6 ApoB 238055 Homozygous null mutants usually die by midgestation and longer survivors exhibit exencephaly. Heterozygotes show reduced plasma cholesterol and apolipoprotein levels. Single isoform B100 and B48 null mutants are viable.
C57BL/6 App 11820 Mice homozygous for disruptions in this gene exhibit reduced body weight, brain weight, size of forebrain commissures, locomotor activity, forelimb grip strength, and spatial learning scores. Many mice also exhibit agenesis of the corpus callosum, and extensive reactive gliosis.
C57BL/6 AQP1 11826 Homozygous mutation of this gene results in urine hypoosmality.
C57BL/6 ASIC1a 11419 Homozygous mutation of this gene results in absence of H+-gated currents in hippocampal neurons, impaired long term potentiation, reduced excitatory postsynaptic potentials, and defective spatial learning and eye blink conditioning.
SD 大鼠 ASIC3 171209 Homozygotes for targeted null mutations exhibit reduced latency to onset of pain responses, increased sensitivity to light touch, but decreased sensitivity to noxious pinch and responses of acid- and noxious heat-sensitive nociceptors.
C57BL/6 ASPP2Symbol
Trp53bp2
209456 Homozygous mutation is lethal by 30 days of age, although majority die embryonically. Heterozygotes show increased susceptibility to spontaneous and induced tumors of the lymphoma and sarcoma types
C57BL/6 ATM 11920 Homozygotes for null mutations may exhibit locomotor abnormalities, motor learning deficits, growth retardation, sterility due to meiotic arrest, and susceptibility to thymic lymphomas. Mice homozygous for a kinase dead allele exhibit early embryonic lethality associated with genetic instability.
C57BL/6 ATPIF1 11983 Mice exhibit normal growth and breeding and are protected from TAC-pressure overload and isoproterenol infusion.
C57BL/6 Capn3 12335 Homozygous mutation of this gene results in muscle dystrophy. The psoas, soleus, and deltoid muscles are the most severely affected. The mutant allele appears to be preferentially transmitted resulting in ratio distortion.
B6N.129S2 Caspase1 12362 Homozygous targeted mutants fail to produce mature IL1A and IL1B and are resistant to LPS-induced endotoxin shock and to FAS antibody-induced apoptosis.
C57BL/6 Caspase8 12370 Homozygotes for a targeted null mutation exhibit impaired cardiac muscle development, cardiac erythrocyte congestion, low numbers of colony-forming cells, and prenatal lethality. T-cell restricted knockout mice are viable, but immunodeficient.
C57BL/6 Cav1 12389 Homozygous targeted mutants displayed vascular system dysfunctions and thickening of lung aveloar septa from hyperproliferation and fibrosis, ultimately causing the mice physical limitations. Mice also display increased incidence of calcium calculi, kidney stones, and decreased adiposity.
C57BL/6 CB1Cnr1 12801 Mice homozygous for a null allele exhibit abnormal behaviors, altered long term depression and susceptibility to induced seizure.
C57BL/6 Cb2 12802 Macrophages from homozygous mutant animals are resistant to the inhibitory effects of delta9-Tetrahydrocannabinol. Alopecia is seen in some but not all homozygotes.
C57BL/6 CCk-1R    
FVB CCL3 20302 Animals homozygous for a mutation in this gene exhibit resistance to Coxsackie virus-induced myocarditis and reduced pneumonitis following infection with influenza virus.
C57BL/6 CD24 12484 Homozygous mutation of this gene results in slight impairment of B cell development. Mutant erythrocytes have increased tendency to aggregate.
C57BL/6 Cflar  21939 Homozygous inactivation of this gene may cause impaired immunoglobulin class switching and germinal center formation, reduced susceptibility to type II hypersensitivity reaction, impaired priming of T cells and control of M. tuberculosis infection, and altered response to transplant.
C57BL/6 CHL1 12661 Homozygous mutation of this gene results in enlargement of the lateral ventricles and altered hippocampal mossy fiber organization. Mutant animals exhibit altered exploratory behavior.
C57BL/6 CNGA1 12788  
C57BL/6 CNR2 CB2  12802 Macrophages from homozygous mutant animals are resistant to the inhibitory effects of delta9-Tetrahydrocannabinol. Alopecia is seen in some but not all homozygotes.
C57BL/6 CNTNAP1 53321 Homozygous mutant mice exhibit reduced body size and nervous system defects, including impaired balance, hypoactivity, and ataxia.
C57BL/6 CRAMP 12796 Mice homozygous for a knock-out allele are more susceptible to necrotic skin infection caused by Group A Streptococcus and urinary tract infection caused by uropathogenic E. coli and F. solani-induced keratitis.
C57BL/6 Cx3cl1 20312 Mice homozygous for a knock-out allele show a specific reduction in Gr1(low) monocyte levels, and increased neuronal cell loss in a neurotoxin (MPTP)-induced model of Parkinson disease. Mice homozygous for a different knock-out allele are less susceptible to cerebral ischemia-reperfusion injury.
C57BL/6 Cxcl1 14825 Targeted mutations in this gene when combine with targeted mutation of Ldlr decreases susceptibility to atherosclerotic lesions.
C57BL/6 CXCR3 12766 Mice homozygous or hemizygous for disruptions in this gene display immune system abnormalities. Hemizygous male mice exhibit elevated serum glucose levels.
C57BL/6 CXCR4 12767 Homozygous targeted null mutants exhibit altered viability, lungs, kidneys, immune system, hematopoiesis, myelopoiesis, cerebellar foliation, neuronal cell layer development, susceptibility to diet-induced obesity and adaptive thermogenesis.
C57BL/6 Cxcr6  80901 A small percentage of mice that are heterozygous or homozygous for a knock-out allele develop medulloblastomas in the cerebellum after 12 months of age.
C57BL/6 Cyp1a1 13076 Mice homozygous for a null allele display resitance to some signs of TCDD induced toxicity but do not display any gross abnormalities in the abscence of treatment.
SD 大鼠 Cyp1a1+Cyp1a2    
SD 大鼠 Cyp2e1 13106 Mice homozygous for a null allele exhibit altered responses to xenobiotics including decreased urethane-induced tumors and allylnitrile- or acetamenophen-associated mortality but increased allylnitrile-induced vestibular function loss.
C57BL/6 CYP4V3 102294 Homozygous null mice exhibit corneoretinal crystal accumulation and systemic dyslipidemia characteristic of Bietti Crystalline Dystrophy.
C57BL/6 Cyp4x1 81906 Mice homozygous for a knock-out allele exhibit a mildly obese phenotype.
C57BL/6 D1 13370 Mice homozygous for a disruption in this gene display elevated thyroxine (T4) and reverse triiodothyronine (rT3) levels and changes in the metabolism and excretion of iodothyronines.
C57BL/6 D5    
C57BL/6 Dkk3 50781 Mice homozygous for a knock-out allele are viable, fertile and euthyroid but exhibit hyperactivity, a slight but significant decrease in the frequency of natural killer cells, and significantly increased IgM, hemoglobin, and hematocrit levels.
C57BL/6 Dusp18 75219  
C57BL/6 Eif4b  75705  
C57BL/6 EPHA4 13838 Mutants are known for their "hopping gait". Homozygotes for targeted null mutations show loss of limb alternation in locomotion and axon guidance defects of the corticospinal tract within medulla and spinal cord, resulting in aberrant midline projections. Heterozygotes show less severe phenotype.
C57BL/6 Erk1 26417 Mice homozygous for a targeted null mutation are hyperactive with impaired T cell maturation and proliferation. Mice homozygous for a knock-out allele on a CD-1 background exhibit normal Mendelian ratios, growth, and no obvious abnormalities.
C57BL/6 EXO1 26909 Homozygous mutation of this gene results in reduced life span, lymphoma development, and male/female sterilty due to defective meiosis.
SD 大鼠 F8    
C57BL/6 F9 14071 Male hemizygotes for targeted null mutations are subject to fatal blood loss after tail snipping, and some affected males spontaneously die from umbilical cord bleeding. Carrier females show reduced levels of factor IX.
C57BL/6 Fadd 14082 Mice homozygous for a knock-out allele exhibit embryonic lethality associated with abnormal embryogenesis.
SD 大鼠 Fah 14085 Homozygotes for targeted, deletion, and ENU-induced mutations die perinatally with liver and kidney dysfunction, hypoglycemia, and grossly altered liver mRNA expression. Mice homozygous for a mutation of this gene exhibit inappropriate bouts of activity during the light period of the circadian cycle.
C57BL/6 Fcer1g 14127 Homozygotes for targeted null mutations exhibit impairments in macrophage phagocytosis, NK cell-mediated antibody-coated cytotoxicity, mast cell degranulation, IgE-mediated systemic anaphylaxis, and neutrophil recruitment and migration.
C57BL/6 Fcer2a 14128 Mice homozygous for mutations in this gene are essentially normal although IgE levels or IgE mediated responses may be abnormal.
C57BL/6 Figla  26910 Inactivation of this locus results in female sterility owing to an absence of primordial follicles and oocyte depletion. Mutant males are fertile and exhibit no apparent defects of the reproductive system.
C57BL/6 Fmo3 14262  
C57BL/6 Fpr2 14289 Mice homozygous for a targeted reporter allele exhibit altered leukocyte responses and experimentally induced inflammation.
C57BL/6 Fyn 14360 Different targeted allele homozygotes show different defects, including seizure susceptibility, anxiety, impaired suckling, myelination, LTP and spatial learning, and defects in immune system, circadian rhythm, testes weight and olfactory bulb formation.
C57BL/6 Gab2 14389 Homozygotes for targeted null mutations exhibit impairments in passive cutaneous and systemic anaphylaxis, Fc gamma receptor-mediated phagocytosis, and mast cell development.
C57BL/6 Gfi1 14581 Homozygotes for targeted null mutations exhibit loss of inner ear hair cells, ataxia, circling, and deafness. Mutants also show a block in granulocyte and neutrophil maturation, and are hypersensitive to endotoxin stimulation.
C57BL/6 Gm6760  627470  
C57BL/6 Gnai3 14679 Mice homozygous for a knock-out allele exhibit normal basal cardiac function and beta-adrenergic sensitivity. Mice homozygous for a different knock-out allele exhibit enhanced T cell migration toward CXCR3 agonists.
C57BL/6 Gpr103 229214 Mice homozygous for a mutation diisplay kyphosis with abnormal vertebrae morphology and development including osteopenia of the vertebrae.
C57BL/6 GPR116  224792 Mice homozygous for a knock-out allele exhibit premature death, decreased body weight and respiratory distress associated with pulmonary alveolar proteinosis.
C57BL/6 Gpr119 236781 Mice homozygous for a knock-out allele exhibit normal growth and glucose homeostasis except lowered body weight when fed a low-fat diet and decreased insulin levels post-glucose load.
C57BL/6 Gpr120 107221 Homozygotes for a null allele show altered taste responses to fatty acids. Homozygotes for another null allele develop obesity, liver steatosis, and impaired glucose metabolism, adipogenesis and lipogenesis on a high-fat diet. Homozygotes for a third allele show altered islet somatostatin secretion.
C57BL/6 Gpr131/TGR5 227289 Mutations in this gene result in abnormal cholesterol, bile, and insulin homeostasis.
C57BL/6 Gpr132 56696 Mice homozygous for disruptions in this gene display a generally normal phenotype but eventually develop a "late onset lymphoproliferative autoimmune syndrome"
C57BL/6 Gpr146 80290 Mice exhibit normal susceptibility to VSV infection.
C57BL/6 Gpr171 229323  
C57BL/6 Gpr30
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