背景品系 | 基因名称 | 基因ID | 应用说明 |
C57BL/6 | A20(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. |
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 |
ASPP2(Symbol 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 | CB1(Cnr1) | 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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