基因编辑鼠_江苏艾菱菲生物科技有限公司

动物资源库

ANIMAL RESOURCE BANK

动物资源库

首页

基因编辑鼠

条件敲除鼠

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

全身敲除鼠

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	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	Trp53bp2）	209456
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

基因敲入鼠

品系背景	基因名称	基因ID	应用说明
C57BL/6	41BB
C57BL/6	CTLA4	12477	Mice homozygous for a knock-out allele exhibit lethality at 3 to 4 weeks of age, decreased T cell numbers, abnormal T cell physiology, inflammation in mutliple organs, abnormal thymus morphology, and lymph node hypoplasia.
SD 大鼠	CYP1A2	13077	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	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	hECM1	1893	Mice homozygous for a knock-out allele exhibit auto-inflammatory disease and do not survive beyond 6 to 8 weeks of age.
C57BL/6	hPear1	375033	Mice homozygous for a knock-out allele show no apparent defects in hemostasis or thrombus formation. Although in vitro dextran sulfate-induced platelet aggregation is impaired, platelet aggregation initiated with physiological agonists is normal.
C57BL/6	Mek1	26395	Homozygous inactivation of this gene leads to reduced embryo size and midgestational lethality due to impaired development and hypovascularization of the placenta with decreased labyrinth cell proliferation and enhanced cell apoptosis. Mutant MEFs fail to exhibit fibronectin-induced migration.
C57BL/6	nedd8	18002
C57BL/6	Pah	18478	Homozygotes for ENU-induced mutations of this gene have altered serum and urine phenylalanine levels and may display reduced body size, microcephaly, microphthalmia, decreased litter size, hypopigmentation, impaired balance/swimming, cognitive deficits, and environmentally-induced seizures.
C57BL/6	PD1	18566	Mice homozygous for disruptions in this gene display abnormalities in leukopoiesis and the immune system which vary considerably depending on the genetic background.
C57BL/6	PPM1K	243382	Mice homozygous for a null allele exhibit defective amino acid metabolism, increased oxidative stress, and increased mortality when subjected to a high-protein diet while in utero and during postnatal development.
C57BL/6	Rab31	106572
C57BL/6	Rosa26-CAG-SCFV+FC
C57BL/6	SLC26A4	23985	Homozygous null mutants are completely deaf with vestibular dysfunction. Mutants show endolymphatic dilatation, degeneration of sensory cells and malformations of otoconia and otoconial membranes. They display unsteady gait and circling and head bobbing.