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糖原合酶激酶3调节盘基网柄菌中的细胞命运。

Glycogen synthase kinase 3 regulates cell fate in Dictyostelium.

作者信息

Harwood A J, Plyte S E, Woodgett J, Strutt H, Kay R R

机构信息

Medical Research Council, Laboratory of Molecular Biology, Cambridge, England.

出版信息

Cell. 1995 Jan 13;80(1):139-48. doi: 10.1016/0092-8674(95)90458-1.

Abstract

Extracellular cyclic AMP (cAMP) induces the formation of prespore cells in Dictyostelium but inhibits stalk cell formation. We have cloned gskA, which encodes the Dictyostelium homolog of glycogen synthase kinase 3 (GSK-3), and discovered that it is required for both cAMP effects. Disruption of gskA creates a mutant that aggregates but forms few spores and an abnormally high number of stalk cells. These stalk cells probably arise from an expanded prestalk B (pstB) cell population, which normally produces the basal disc of the fruiting body. In cultured mutant cells, cAMP neither inhibits pstB cell differentiation nor induces efficient prespore cell differentiation. We propose that cAMP acts through a common pathway that requires GSK-3 and determines the proportion of prespore and pstB cells.

摘要

细胞外环磷酸腺苷(cAMP)可诱导盘基网柄菌中前孢子细胞的形成,但会抑制柄细胞的形成。我们克隆了gskA基因,它编码糖原合酶激酶3(GSK-3)的盘基网柄菌同源物,并发现它是cAMP两种作用所必需的。gskA基因的破坏产生了一种突变体,该突变体能够聚集,但形成的孢子很少,且柄细胞数量异常多。这些柄细胞可能源自扩大的前柄B(pstB)细胞群体,该群体通常产生子实体的基盘。在培养的突变细胞中,cAMP既不抑制pstB细胞分化,也不诱导有效的前孢子细胞分化。我们提出,cAMP通过一条需要GSK-3的共同途径发挥作用,并决定前孢子细胞和pstB细胞的比例。

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