首页> 外文期刊>Bulletin of experimental biology and medicine >Genetic Determination of Regressive Pattern of Walker 256 Carcinosarcoma in Rats with Hypothalamic Diabetes Insipidus
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Genetic Determination of Regressive Pattern of Walker 256 Carcinosarcoma in Rats with Hypothalamic Diabetes Insipidus

机译:下丘脑尿崩症大鼠Walker 256癌肉瘤消退模式的遗传测定

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摘要

We studied the growth dynamics of Walker 256 carcinosarcoma in recombinant progeny of dihybrid crosses of Brattleboro and WAG rats. A mutation in the vasopressin gene determining hypothalamic diabetes insipidus was detected in Brattleboro rats. WAG rats are carriers of normal vasopressin gene. Another interlinear difference was linked to tyrosinase gene controlling melanin synthesis. WAG rats express mutant allele determining albino phenotype. Brattleboro rats had normal working tyrosinase gene. F2 segregation yielded phenotypic classes with two patterns of tumor growth: linear growth or regression. Tumors regression was not linked to tyrosinase activity and was observed only in rats with diabetes insipidus. Analysis of mutants in next generations F3 and F4 confirmed this regularity in the Walker 256 carcinosarcoma growth pattern.
机译:我们研究了 Walker 256 癌肉瘤在 Brattleboro 和 WAG 大鼠双杂交杂交重组后代中的生长动态。在Brattleboro大鼠中检测到决定下丘脑尿崩症的加压素基因突变。WAG大鼠是正常加压素基因的携带者。另一个线间差异与控制黑色素合成的酪氨酸酶基因有关。WAG大鼠表达突变等位基因,决定白化表型。Brattleboro大鼠具有正常工作的酪氨酸酶基因。F2 分离产生具有两种肿瘤生长模式的表型类别:线性生长或消退。肿瘤消退与酪氨酸酶活性无关,仅在尿崩症大鼠中观察到。对下一代 F3 和 F4 突变体的分析证实了 Walker 256 癌肉瘤生长模式的这种规律性。

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