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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. 
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