Epidermal growth factor and glucagon receptors in mice homozygous for a lethal chromosomal deletion.
Epidermal growth factor and glucagon receptors in mice homozygous for a lethal chromosomal deletion.
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致死性染色体缺失纯合小鼠的表皮生长因子和胰高血糖素受体。
DOI：
10.1073/pnas.80.17.5379
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发表时间：
1983
影响因子：
11.1
通讯作者：
Gluecksohn-Waelsch,S
中科院分区：
文献类型：
--
作者：
Shaw,PA;Gluecksohn-Waelsch,S
表皮生长因子（EGF）和胰高血糖素与其受体的结合已在单细胞悬液中进行了研究，这些悬液取自新生小鼠的肝脏和其他器官，这些小鼠为围产期致死性缺失纯合子，包括7号染色体上的白化病（c）位点。125I标记的和非放射性EGF和Scatchard平衡结合数据分析的竞争实验表明，肝细胞从缺失纯合子只有约等于20%的特定EGF受体的数量存在于细胞从正常窝。与此相反，表皮生长因子结合到单细胞悬浮液从器官以外的肝脏是正常的缺失纯合子。类似的结果，在竞争性置换实验与125碘标记和非放射性胰高血糖素：肝细胞缺失突变体显示只有约等于30%的特定胰高血糖素结合位点的细胞中发现正常的同窝出生。在EGF的情况下，结合减少是由于每个细胞胰高血糖素受体的数量减少，而不是受体亲和力的改变，胰高血糖素结合到来自肝脏以外的器官的单细胞悬浮液在缺失突变体中是正常的。EGF和胰高血糖素受体数量的减少是肝细胞特异性的，正如先前描述的这些突变体的超微结构和生化异常一样。细胞膜的完整性和受体相互作用的控制正常肝细胞分化的意义进行了讨论。
The binding of epidermal growth factor (EGF) and of glucagon to their receptors has been examined in single-cell suspensions obtained from livers and other organs of newborn mice homozygous for a perinatally lethal deletion that includes the albino (c) locus on chromosome 7. Competition experiments with 125I-labeled and nonradioactive EGF and Scatchard analysis of equilibrium binding data showed that hepatocytes from deletion homozygotes had only approximately equal to 20% of the number of specific EGF receptors present in cells from normal littermates. In contrast, EGF binding to single-cell suspensions from organs other than the liver was normal in deletion homozygotes. Similar results were obtained in competitive displacement experiments with 125I-labeled and nonradioactive glucagon: hepatocytes from deletion mutants showed only approximately equal to 30% of the specific glucagon binding sites found in cells from normal littermates. As in the case of EGF, the decreased binding was due to decreased numbers of glucagon receptors per cell rather than alterations in receptor affinity, and glucagon binding to single-cell suspensions from organs other than the liver was normal in the deletion mutants. The reductions in numbers of EGF and glucagon receptors are liver-cell specific as are the previously described ultrastructural and biochemical abnormalities in these mutants. The significance of cell membrane integrity and hormone-receptor interactions in the control of normal liver cell differentiation is discussed.