首页> 外文期刊>Life sciences >CCK processing by pituitary GH3 cells, human teratocarcinoma cells NT2 and hNT differentiated human neuronal cells evidence for a differentiation-induced change in enzyme expression and pro CCK processing.
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CCK processing by pituitary GH3 cells, human teratocarcinoma cells NT2 and hNT differentiated human neuronal cells evidence for a differentiation-induced change in enzyme expression and pro CCK processing.

机译:垂体GH3细胞,人畸胎瘤细胞NT2和hNT分化的人神经元细胞对CCK的加工证明了分化诱导的酶表达和pro CCK加工变化。

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摘要

Human teratocarcinoma Ntera2/c 1.D1 (NT2) cells express very low levels of the prohormone convertase enzyme PC1, moderate levels of PC2 and significant levels of PC5. When infected with an adenovirus which expresses rat CCK mRNA, several glycine-extended forms were secreted that co-eluted with CCK 33, 22 and 12. Amidated CCK is not produced because these cells appear to lack the amidating enzyme. Pituitary GH3 cells express high levels of PC2 and PC5. CCK adenovirus-infected GH3 cells secrete amidated versions of the same peptides as NT2 cells. Differentiation of NT2 cells into hNT cells with retinoic acid and mitotic inhibitors increased expression of PC5 and decreased expression of PCI and PC2. CCK adenovirus-infected differentiated hNT cells also secrete glycine extended CCK products and the major molecular form produced co-eluted with CCK 8 Gly. These experiments demonstrate that the state of differentiation of this neuronal cell line influences its expression of PC 1,2, and 5 and its cleavage of pro CCK and suggests that these cells may make an interesting model to study how differentiation alters prohormone processing. These results also support the hypothesis that PC5 in differentiated neuronal cells is capable of processing pro CCK to glycine-extended CCK 8.
机译:人畸胎瘤Ntera2 / c 1.D1(NT2)细胞表达极低水平的激素原转化酶PC1,中等水平的PC2和显着水平的PC5。当用表达大鼠CCK mRNA的腺病毒感染时,分泌了几种甘氨酸扩展形式,与CCK 33、22和12共洗脱。由于这些细胞似乎缺乏酰胺化酶,因此不会产生酰胺化的CCK。垂体GH3细胞表达高水平的PC2和PC5。 CCK腺病毒感染的GH3细胞分泌的酰胺化版本与NT2细胞相同。用视黄酸和有丝分裂抑制剂将NT2细胞分化为hNT细胞可增加PC5的表达,并降低PCI和PC2的表达。 CCK腺病毒感染的分化的hNT细胞也分泌甘氨酸扩展的CCK产物,产生的主要分子形式与CCK 8 Gly共洗脱。这些实验表明,该神经元细胞系的分化状态影响其PC 1,2和5的表达及其对pro CCK的切割,并暗示这些细胞可能成为研究分化如何改变激素原加工的有趣模型。这些结果也支持这样的假设,即分化的神经元细胞中的PC5能够将pro CCK加工成甘氨酸延伸的CCK 8。

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