品系名称:C57BL/6-Tg(Zp3-cre)93Knw/J
基本信息
简称:Zp3-cre;
编号:003651 (Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,转基因
繁殖方案:纯合子 x 纯合子(♀ × ♂)
代次: N6 F3p(2016-03-25)
来源:
→ A transgenic construct containing sequence encoding Cre recombinase, a 6Kb sequence of the mouse Zp3 promoter and the metallothionein-1 polyadenylation site sequence was injected into C57BL/6J zygotes to produce the founder line.(来自Jackson网站)
→ 2012年5月从南京大学引进回交6代种鼠;
→ 同胞兄妹交配3代
→ 冷冻精子保存
引种和保存:
2012年5月28日引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Research Tools
Cre-lox System
Cre Recombinase Expression
Cre Recombinase Expression: Germline/Embryonic Expression
Developmental Biology Research
Cre-lox System
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Cre-lox System
Tissue/Cell Markers
Tissue/Cell Markers: Cre-lox System
Reproductive Biology Research
Cre-lox System
oocyte
Genotype: cre related
Research Tools
Cre-lox System
Genetics Research
Mutagenesis and Transgenesis
Mutagenesis and Transgenesis: Cre-lox System(来自Jackson网站)
生物学特征描述:
This is a transgenic line in which cre expression is controlled by the regulatory sequences from the mouse zona pellucida 3 (Zp3) gene. This promoter normally directs expression exclusively in the growing oocyte prior to the completion of the first meiotic division. This strain would be useful for deleting a floxed sequence specifically in the female germ line. The Donating Investigator suggests to accomplish this, females homozygous or heterozygous for the floxed allele, as well as hemizygous for the Zp3cre allele are crossed with wild type males. Progeny will carry the deleted-floxed allele.(来自Jackson网站)
品系名称:B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax
基本信息
简称:APP-PS1;
编号:004462 (Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,转基因
繁殖方案:sibling x Hemizygote(♀ × ♂)
代次:? F2N1F2
来源:
Two expression plasmids (Mo/HuAPP695swe and PS1-dE9) were designed to each be controlled by independent mouse prion protein (PrP) promoter elements, directing transgene expression predominantly to CNS neurons. The Mo/HuAPP695swe transgene expresses a “humanized” mouse amyloid beta (A4) precursor protein gene modified at three amino acids to reflect the human residues and further modified to contain the K595N/M596L (also called K670N/M671L) mutations linked to familial Alzheimers. The PS1-dE9 transgene expresses a mutant human presenilin 1 carrying the exon-9-deleted variant (PSEN1dE9) associated with familial Alzheimer's disease. These constructs were coinjected into B6C3HF2 pronuclei and insertion of the transgenes occured at a single locus. Founder line 85 was obtained and the resulting colony was maintained as a hemizygote by crossing transgenic mice to B6C3F1/J mice.(来自Jackson网站)
→ 首都医科大学基础医学院郑炎委托保种
引种和保存:
从首都医科大学引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Neurobiology Research
Alzheimer's Disease
APP and PSEN1 mutants
Presenilin mutants
strains expressing mutant APP
Behavioral and Learning Defects
Epilepsy
electroconvulsive seizures
Neurodegeneration
Neurobiology Research
Neurodegeneration
Tg(APPswe,PSEN1dE9)85Dbo related
Neurobiology Research
Alzheimer's Disease来自Jackson网站)
生物学特征描述:
Double transgenic mice express a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons. Both mutations are associated with early-onset Alzheimer's disease. The "humanized" Mo/HuAPP695swe transgene allows the mice to secrete a human A-beta peptide. Both the transgenic peptide and holoprotein can be detected by antibodies specific for human sequence within this region (Signet Laboratories' monoclonal 6E10 antibody). The included Swedish mutations (K595N/M596L) elevate the amount of A-beta produced from the transgene by favoring processing through the beta-secretase pathway. This "humanized" Mo/HuAPP695swe protein is immunodetected in whole brain protein homogenates. The transgenic mutant human presenilin protein (PS1-dE9), which in high levels displaces detectable endogenous mouse protein, is also immunodetected in whole brain protein homogenates. The donating investigator reports that transgenic mice develop beta-amyloid deposits in brain by six to seven months of age. These animals also display a slight alteration in their tail phenotype (e.g. kinked tail) that is believed to be due to the mixed genetic background of the strain and is not related to transgene expression. Hemizygous mice on the C57BL/6 background (N9B6) exhibit a high incidence of seizures, as detected by video-EEG. 25% of transgenic mice, 3 to 3.5 months in age, exhibit at least 1 seizure. By 4.5 months of age, seizure incidence increases to 55%.10-15% mortality is reported for transgenic mice on the congenic (N9) C57BL/6 background (Minkeviciene et al. J Neurosci. 2009). Hemizygous mice, on the congenic C57BL/6J background (N13), 17-18 weeks in age, exhibit epileptiform discharges as detected by video-EEG. Mortality was 38% (6/16) and some mutant mice experienced spontaneous seizures during the experiments. Antiepileptic drugs (carbamazepine, phenytoin, valproate) reduce the frequency of spontaneous electrographic epileptiform discharges (Ziyatdinova et al. Epilepsy Res 2011). These mice may be useful in studies of neurological disorders of the brain, specifically Alzheimer's disease, amyloid plaque formation, and aging.(来自Jackson网站)
品系名称:B6N.129S1-Tlr3tm1Flv/J
基本信息
简称:TIr3-;
编号:009675 (Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,靶突变KO
繁殖方案:Homozygote x Homozygote(♀ × ♂)
代次:N11 F7 F5 (2015-04-27)
来源:
→ A targeting vector containing a loxP site flanked neomycin resistance cassette and a herpes simplex virus thymidine kinase gene was used to disrupt exon 1. The construct was electroporated into 129S1/Sv-Oca2 Tyr KitlSl-J derived W9.5 embryonic stem (ES) cells. This strain was backcrossed to C57BL/6 from the National Cancer Institute (NCI) ten times by the donating laboratory.(来自Jackson网站)
→ 2012年10月从南京大学引进种鼠;
→ 同胞兄妹交配5代;
引种和保存:
2011年10月26日引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Tlr deficiency
Immunodeficiency
Tlr deficiency
Inflammation
Tlr deficiency
Tlr3tm1Flv related
Cell Biology Research
Signal Transduction
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Tlr deficiency
genes regulating susceptibility to infectious disease and endotoxin
Immunodeficiency Associated with Other Defects (来自Jackson网站)
生物学特征描述:
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Northern blot analysis detects a truncated gene product (mRNA), which is not functional. Unlike wildtype macrophages, macrophages derived from these animals fail to produce inflammatory cytokines, IFN-alpha or IFN-beta when challenged with poly(I:C), polyinosine-polycytidylic acid, a synthetic dsRNA analog. Splenocytes isolated from homozygotes do not respond to viral dsRNA and have diminished IL-6 production. Mice homozygous for the mutation are resistant to poly(I:C) induced shock and produce lower levels of IL-12. This mutant mouse strain may be useful in studies of the toll-like receptor pathway of the innate immune response.(来自Jackson网站)
品系名称:B6.B10ScN-Tlr4lps-del/JthJ
基本信息
简称:Tlr4-KO; Tlr4lps-; Tlr4-;
编号:007227 (Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,自发突变
繁殖方案:Homozygote x Homozygote (♀ × ♂)
代次:? F5 (2015-4-27)
来源:
→ Abnormal response to lipopolysaccharide was observed in the inbred strain C57BL/10ScN in the 1970s. The phenotype was subsequently identified as a mutation in the Tlr4 gene. This strain originated from the C57BL/10ScN colony at NCI Frederick and was transferred to the laboratory of Dr. James Thomas, University of Texas Southwestern Medical Center. The allele was introgressed into C57BL/6 by backcrossing for at least five generations. The strain was donated to The Jackson Laboratory Repository in 2008.(来自Jackson网站)
→ 种鼠由维通利华从Jackson实验室引进;
→ 同胞兄妹交配5代,F5代断种
引种和保存:
2011年8月9日引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Tlr deficiency
Immunodeficiency
Tlr deficiency
Inflammation
Tlr deficiency
Tlr4lps-del related
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Tlr deficiency
Immunodeficiency
Tlr deficiency
Inflammation
Tlr deficiency
生物学特征描述:
The stimulation of Toll-like receptor 4 (TLR4) by lipopolysaccharide (LPS) induces the release of proinflammatory cytokines that activate immune responses. The Tlr4Lps-del spontaneous mutation corresponds to a 74723 bp deletion that completely removes the Tlr4 coding sequence. No mRNA or protein is expressed. Homozygous mutants exhibit a defective response to LPS stimulation. The functionally similar Tlr4Lps-d mutation found in C3H/HeJ mice (#000659) is a point mutation that causes an amino acid substitution.
Tlr4 -deficient mice display significantly reduced expression of proinflammatory genes compared to controls 24 h after reperfusion triggered by retinal ischemic injury. These include transcriptional factor p65 (Rela), tumor necrosis factor (Thf), interleukin 6 (Il6), chemokine (C-C motif) ligand 2 (Ccl2), chemokine (C-C motif) ligand 5 (Ccl5), chemokine (C-X-C motif) ligand 10 (Cxcl10), cytochrome b-245, beta polypeptide (Cybb), nitric oxide synthase 2 (Nos2), and intercellular adhesion molecule 1 (Icam1) (Dvoriantchikova et al., 2010).
The effect of TLR4 on tumor progression appears to depend on which cells TLR4 resides and the particular ligand involved. For example, enhanced prostrate tumor progression as a result of TLR4 response to a tumor-derived ligand such as Peroxiredoxin is not seen in the Tlr4 deficient mutant mice (Riddell et al., 2011). Conversely, tumor inhibition seen in wild type mice when B16 melanoma cells were stimulated in vitro with LPS was not seen in mutant mice (Nunez et al., 2012).
TLR4 signaling may also act as innate neuroprotective mechanism through clearance of alpha-synuclein as TLR4 ablation impairs the phagocytic response of microglia to alpha-synuclein and enhances neurodegeneration (Stefanova et al. 2011). (来自Jackson网站)
品系名称:B6.129S1-Tlr5tm1Flv/J
基本信息
简称:TLR5 KO;
编号:008377 (Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,靶突变KO
繁殖方案:Homozygote x Homozygote(♀ × ♂)
代次:N10 F4 ? F5 (2015-04-27)
来源:
→ A targeting vector was used to replace the coding region with a loxP-flanked neomycin resistance cassette inserted in the opposite transcriptional orientation. 129S1/Sv Oca2 Tyr Kitl -derived W9.5 embryonic stem (ES) cells were used to create the mutation. Resultant male chimeric mice were mated to C57BL/6 females. The donating investigator reported that this strain was backcrossed ten times to C57BL/6/Ncr mice (see SNP note below).(来自Jackson网站)
→ 种鼠来源于南京大学;
→ 同胞兄妹交配5代;
引种和保存:
2011年9月16日引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Tlr deficiency
genes regulating susceptibility to infectious disease and endotoxin
Immunodeficiency
Tlr deficiency
Inflammation
Tlr deficiency
Tlr5tm1Flv related
Diabetes and Obesity Research
Hyperglycemia
Insulin Resistance
Immunology, Inflammation and Autoimmunity Research
Inflammation
Internal/Organ Research
Gastrointestinal Defects
Colitis (来自Jackson网站)
生物学特征描述:
The toll-like receptor gene targeted in this strain is a sensor for monomeric flagellin, a component of bacterial flagella known to be a virulence factor. These mice have been used to investigate the mechanism of flagellin detection and signalling in antibacterial immune responses toSalmonella typhimurium and Pseudomonas aeruginosa. The gene has been found to be essential for the recognition of bacterial flagellin both in vivo and ex vivo. Mice that are homozygous for this targeted deletion are viable and fertile. Transcripts of this gene are absent from bone marrow-derived macrophages in homozygotes.
Relative to controls, homozygotes have increased fat mass throughout the body, particularly in visceral fat, a substantial increase in serum triglyceride and cholesterol levels, increased blood pressure, and higher than normal production of pro-inflammatory cytokines interferon gamma and interleukin 1 beta in adipose tissue. Basal insulin levels and insulin production in response to a glucose challenge are significantly elevated, and the response to exogenous insulin is reduced compared with that of controls. The ability to restore blood glucose to baseline levels after administration of a bolus of glucose is impaired, and a mild elevation in blood glucose levels is found after an overnight fast. After 8 weeks on a high fat diet fasting glucose concentrations exceed 120 mg/dL, inflammatory infiltrates are found in the pancreatic islets, and hepatic steatosis is observed.
Homozygotes offer a model of metabolic syndrome for which the hyperphagia, obesity, hyperglycemia, insulin resistance, colomegaly, and increased pro-inflammatory cytokines can be transferred from diseased homozygotes to wild-type hosts by tranplanting gut microbiota. Treatment of homozygotes with broad spectrum antibiotics for 12 weeks corrects the metabolic syndrome. Hysterectomy re-derivation to upgrade the microbial flora of homozygotes results in diminished severity of colitis and a more uniform phenotype of mild inflammation and obesity, including a 20% increase in body mass at 20 weeks of age.(来自Jackson网站)
品系名称:NOD.Cg-PrkdcscidB2mtm1Unc/J
基本信息
简称:NODSCID
编号:002570(Jackson)
科技资源标识:
分类:小鼠,基因工程小鼠,靶突变KO
繁殖方案:Homozygote x Homozygote(♀ × ♂)
代次:? F22 F2(2015-03-25)
来源:
→ The B2mtm1Unc targeted mutant strain was developed in the laboratory of Dr. Beverly Koller and Dr. Oliver Smithies at the University of North Carolina at Chapel Hill. It was generated by a targeted disruption of the B2m gene. The 129-derived E14TG2a ES cell line was used. This strain carrying both B2m and sci mutations was generated in the laboratory of Dr. Leonard Shultz at the Jackson Laboratory by backcrossing the B2mtm1Unc mutation 10 generations to the NOD/LtSz-Prkdcscid strain.(来自Jackson网站)
→ 种鼠来自南京大学;
→ 同胞兄妹交配2代;
引种和保存:
2014年10月引入本单位
功能及用途:
This mouse can be used to support research in many areas including:
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
NOD Congenics with Mutations Affecting Immunocompetence
Research Tools
Immunology, Inflammation and Autoimmunity Research
B and T cell deficiency
B2mtm1Unc related
Hematological Research
Anemia, Iron Deficiency and Transport Defects
hemochromatosis
Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
MHC class I deficiency
Internal/Organ Research
Liver Defects
hemochromatosis
Metabolism Research
Hemochromatosis
iron metabolism defects
Research Tools
Immunology, Inflammation and Autoimmunity Research
MHC class I deficiency
Prkdcscid related
Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
B and T cell deficiency
Internal/Organ Research
Lymphoid Tissue Defects
B and T cell deficiency
Research Tools
Cancer Research
B and T cell deficiency, xenograft/transplant host
Toxicology Research
xenograft/transplant host
Virology Research
B and T Cell Deficiency
AIDS research tool (来自Jackson网站)
生物学特征描述:
Mice homozygous for both the B2mtm1Unc and Prkdcscid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies.(来自Jackson网站)
品系名称:C57BL/6J-ACE2em6(hACE2)/Nifdc
基本信息
简称:hACE2-KI humanized mouse
编号:NR01007
科技资源标识:CSTR:15497.09.NR01007
分类:小鼠,基因工程小鼠,靶突变KI
繁殖方案:纯合子繁殖
代次:
来源:
引种和保存:
功能及用途:
生物学特征描述:
hACE2-KI/Nifdc人源化小鼠模型由中国食品药品检定研究院自主设计并研发成功。采用CRISPR/Cas9技术构建,将hACE2基因插入纯的C57BL/6遗传背景小鼠的mACE2基因启动子之下,并共表达荧光标记基因tdTomato。经过近2年的繁育观察,发现外源基因hACE2表达高且稳定,外源基因准确插入小鼠X染色体GRC.m38.p6位点,为单拷贝插入。是目前全球首个hACE2的人源化小鼠模型。
品系名称:Nifdc:新西兰白兔
基本信息
简称:新西兰白兔
编号:NR040200001
科技资源标识:CSTR:15497.09.NR040200001
分类:兔,封闭群
繁殖方案:采用完全循环交配方法
代次:
来源:
2000年,中国药品生物制品检定所实验动物中心通过对普通级新西兰白兔实施剖腹产、人工饲乳,获得净化新西兰白兔。随后通过人工饲菌、悉生化,建立了SPF级新西兰白兔种群。
引种和保存:
功能及用途:
应用于皮肤反应试验、热源实验、眼科研究、生殖生理和避孕药研究、免疫学研究等。
生物学特征描述:
新西兰白兔被毛全白,头宽圆而粗短,耳较宽厚而直立,臀圆,腰肋部肌肉丰满,四肢粗壮有力,性情温驯,易于管理。体形中等,成兔体重4~5kg,繁殖力强,平均每胎产仔7~8只。
品系名称:青紫蓝兔
基本信息
简称:
编号:NR040200002
科技资源标识:CSTR:15497.09.NR040200002
分类:兔,封闭群
繁殖方案:采用完全循环交配方法
代次:
来源:
青紫蓝兔由法国育种家戴葆斯基用噶伦兔分别与喜玛拉雅兔和蓝色贝韦伦兔杂交,然后将两类杂种兔进行横交并经过不断选育于20世纪初育成。后来经改进毛色和体重,在欧美的部分国家又曾导入弗郎德巨兔等其他兔种血缘,最终形成青紫蓝兔的标准型、美国型和巨型3个类型。
由于青紫蓝兔被毛浓密、富有光泽,毛纤维颜色分段,风吹被毛时呈现旋涡状、形似花朵而走俏国际毛皮市场,因此,最初是以著名的皮用品种向世界推广的,而后随其产肉性能的改善,以皮肉兼用品种分布在世界各地。
青紫蓝兔批量引入我国的时间较早,在20世纪60-70年代已成为我国杂交改良本地兔的主要 品种 。 我国引入最多的是标准型青紫蓝兔和美国型青紫蓝兔 。
引种和保存:
功能及用途:
应用于眼科研究,免疫学研究等。
生物学特征描述:
属于皮肉兼用型兔,其外貌特征是被毛整体为蓝灰色,耳尖及尾面为黑色,眼圈,尾底、腹下和后额三角区呈灰白色。单根纤维自基部至毛梢的颜色依次为深灰色、乳白色、珠灰色、雪白色和黑色,被毛中夹杂有全白或全黑的针毛。眼睛为茶褐色或蓝色。耳下垂,母兔颌下有肉髯。大型体重可达4-6公斤。体健壮,耐寒,适应性强,生长快。
品系名称:日本大耳白兔
基本信息
简称:大耳白兔
编号:NR040200003
科技资源标识:CSTR:15497.09.NR040200003
分类:兔,封闭群
繁殖方案:采用完全循环交配方法
代次:
来源:
日本使用中国白兔和日本兔杂交选育而成的。
引种和保存:
功能及用途:
适用于注射和采血,是理想的实验用兔
生物学特征描述:
兔体格强健,较耐粗饲,适应性强,体型较大,生长发育较快。该兔头大小适中,额宽,面凸,被毛白且浓密而柔软,皮张面积大,质地良好,眼红色,颈较粗,母兔颈下有肉髯。体型中等偏大,成兔体重4-5kg。繁殖力强,每胎产仔8-10只,初生重60g左右。兔母性好,泌乳量大。生长发育较快,2月龄平均重1.4kg,4月龄3kg。耳大、耳根细、耳端尖、耳薄,形同柳叶并向后竖立,血管明显,适用于注射和采血。