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在被劳氏肉瘤病毒转化的鹌鹑视网膜神经元细胞中,谷氨酸脱羧酶活性受到刺激,并受pp60v-src调控。

Glutamic acid decarboxylase activity is stimulated in quail retina neuronal cells transformed by Rous sarcoma virus and is regulated by pp60v-src.

作者信息

Crisanti P, Lorinet A M, Calothy G, Pessac B

出版信息

EMBO J. 1985 Jun;4(6):1467-70. doi: 10.1002/j.1460-2075.1985.tb03804.x.

Abstract

Rous sarcoma virus (RSV) stimulates in quail embryo neuro-retina (NR) cultures the specific activity of glutamic acid decarboxylase (GAD), the enzyme responsible for the synthesis of gamma-aminobutyric acid, a major inhibitory neurotransmitter in NR and in central nervous system. In quail embryo NR cultures transformed by ts NY-68, a thermodependent transformation-defective mutant of RSV, stimulation of GAD activity is regulated by pp60v-src, the product of the src gene of RSV. Fibroblasts and myoblasts have a very low GAD activity that is not stimulated after transformation by RSV. Neuronal clones, previously derived from ts NY-68-transformed established NR cell lines, have a high GAD activity which is regulated by pp60v-src, while other clones have a low GAD activity apparently not regulated by pp60v-src. These data indicate that pp60v-src selectively activates the expression of GAD in distinct neuronal cells of quail embryo NR cultures transformed by RSV. GAD activity is also stimulated in NR cells infected with viruses containing v-mil.

摘要

劳氏肉瘤病毒(RSV)可刺激鹌鹑胚胎神经视网膜(NR)培养物中谷氨酸脱羧酶(GAD)的比活性,GAD是负责合成γ-氨基丁酸的酶,γ-氨基丁酸是NR和中枢神经系统中的一种主要抑制性神经递质。在由ts NY-68(RSV的一种温度依赖性转化缺陷型突变体)转化的鹌鹑胚胎NR培养物中,GAD活性的刺激受RSV src基因产物pp60v-src的调节。成纤维细胞和平滑肌细胞的GAD活性非常低,在被RSV转化后不会受到刺激。先前从ts NY-68转化的已建立NR细胞系衍生而来的神经元克隆具有高GAD活性,该活性受pp60v-src调节,而其他克隆具有低GAD活性,显然不受pp60v-src调节。这些数据表明,pp60v-src在被RSV转化的鹌鹑胚胎NR培养物的不同神经元细胞中选择性激活GAD的表达。感染含v-mil病毒的NR细胞中GAD活性也会受到刺激。

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