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表皮生长因子和环己酰亚胺对肌动蛋白基因转录的特异性刺激。

Specific stimulation of actin gene transcription by epidermal growth factor and cycloheximide.

作者信息

Elder P K, Schmidt L J, Ono T, Getz M J

出版信息

Proc Natl Acad Sci U S A. 1984 Dec;81(23):7476-80. doi: 10.1073/pnas.81.23.7476.

DOI:10.1073/pnas.81.23.7476
PMID:6334309
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC392169/
Abstract

Stimulation of quiescent AKR-2B mouse embryo cells with epidermal growth factor (EGF) results in a rapid and specific induction of actin mRNA sequences. These mRNAs include those coding for both beta- and gamma-cytoskeletal, but not alpha-skeletal muscle, actin isotypes. Elongation of nascent RNA chains in isolated nuclei (run-off transcription) demonstrates that the mRNA accumulation is preceded by an increase in actin gene transcription. This increase is transient, however, and is followed by a rapid attenuation of transcriptional activity. An inhibitor of protein synthesis, cycloheximide, was also found to induce beta- and gamma-actin mRNA accumulation. Furthermore, the simultaneous addition of EGF and cycloheximide produced a synergistic effect on actin sequences in both steady-state nuclear and polysomal RNA. Run-off transcription experiments demonstrate that this synergistic effect results from an increase in the magnitude and duration of actin gene transcription. It is also specific in that alpha-tubulin gene transcription is not similarly affected. These data suggest the existence of a specific labile repressor of actin gene transcription.

摘要

用表皮生长因子(EGF)刺激静止的AKR-2B小鼠胚胎细胞会导致肌动蛋白mRNA序列的快速特异性诱导。这些mRNA包括编码β-和γ-细胞骨架肌动蛋白的序列,但不包括α-骨骼肌肌动蛋白异构体的编码序列。在分离的细胞核中新生RNA链的延伸(径流转录)表明,mRNA积累之前肌动蛋白基因转录增加。然而,这种增加是短暂的,随后转录活性迅速衰减。还发现蛋白质合成抑制剂环己酰亚胺可诱导β-和γ-肌动蛋白mRNA积累。此外,同时添加EGF和环己酰亚胺对稳态核RNA和多聚核糖体RNA中的肌动蛋白序列产生协同作用。径流转录实验表明,这种协同作用是由于肌动蛋白基因转录的幅度和持续时间增加所致。它也是特异性的,因为α-微管蛋白基因转录没有受到类似的影响。这些数据表明存在一种特异性的不稳定的肌动蛋白基因转录抑制因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/6e286754b747/pnas00624-0218-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/d6b2d4840281/pnas00624-0216-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/42d4f1864e99/pnas00624-0216-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/527a86201bac/pnas00624-0217-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/d994e70ef95b/pnas00624-0218-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/dcc13f7eae26/pnas00624-0218-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/6e286754b747/pnas00624-0218-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/d6b2d4840281/pnas00624-0216-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/42d4f1864e99/pnas00624-0216-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/527a86201bac/pnas00624-0217-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/d994e70ef95b/pnas00624-0218-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/dcc13f7eae26/pnas00624-0218-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55cd/392169/6e286754b747/pnas00624-0218-c.jpg

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