Oncogenic activation of c-ABL by mutation within its last exon.

A Goga; J McLaughlin; A M Pendergast; K Parmar; A Muller; N Rosenberg; O N Witte

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Oncogenic activation of c-ABL by mutation within its last exon.

机译：c-ABL在其最后一个外显子中的突变致癌激活。

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The c-ABL proto-oncogene is a predominantly nuclear localized tyrosine kinase. A random mutagenesis scheme was used to isolate c-ABL mutants whose expression produced a transformed phenotype in rodent fibroblast cells. An in-frame deletion within the central region of the last exon was identified in one ABL mutant. The mechanism of c-ABL oncogenic activation by mutation within the last exon differs both functionally and structurally from those of v-ABL and BCR/ABL. This class of ABL mutants shows increased tyrosine phosphorylation of cellular proteins in vivo but low levels of autophosphorylation. Last-exon ABL mutants are distinguished from v-ABL or BCR/ABL by their inability to transform primary bone marrow cells or support the growth of transformed pre-B cells. These findings define a new mechanism of oncogenic activation for the ABL kinase through mutations in the last exon which do not require amino-terminal deletions or mutations within the src homology regions.

机译：c-ABL原癌基因主要是核定位的酪氨酸激酶。使用随机诱变方案来分离c-ABL突变体，其表达在啮齿动物成纤维细胞中产生转化的表型。在一个ABL突变体中鉴定出最后一个外显子中心区域内的框内缺失。最后一个外显子中通过突变激活c-ABL致癌的机制在功能和结构上均不同于v-ABL和BCR / ABL。这类ABL突变体显示体内细胞蛋白的酪氨酸磷酸化增加，但自磷酸化水平较低。最后外显子ABL突变体与v-ABL或BCR / ABL的区别在于它们无法转化原代骨髓细胞或无法支持转化的pre-B细胞的生长。这些发现通过最后一个外显子中的突变定义了ABL激酶致癌激活的新机制，该突变不需要src同源区内的氨基末端缺失或突变。

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《Molecular and Cellular Biology》 |1993年第8期|共9页
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A Goga; J McLaughlin; A M Pendergast; K Parmar; A Muller; N Rosenberg; O N Witte;
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中图分类细胞生物学;
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1. Oncogenic activation of c-Abl in non-small cell lung cancer cells lacking FUS1 expression: inhibition of c-Abl by the tumor suppressor gene product Fus1 [J] . J Lin, T Sun, L Ji, Oncogene . 2007,第49期

机译：c-Abl在缺乏FUS1表达的非小细胞肺癌细胞中的致癌激活：肿瘤抑制基因产物Fus1抑制c-Abl
2. Novel types of mutation in the choroideremia ( CHM) gene: a full-length L1 insertion and an intronic mutation activating a cryptic exon. [J] . van den Hurk JA, van de Pol DJ, Wissinger B, Human Genetics . 2003,第3期

机译：脉络膜疾病（CHM）基因中的新型突变类型：全长L1插入和激活隐性外显子的内含子突变。
3. B-Myb represses trans-activation of the Col5A2 collagen promoter indirectly via inhibition of binding of factors interacting with positive elements within the first exon. [J] . Kypreos KE, Marhamati DJ, Sonenshein GE Matrix biology: Journal of the International Society for Matrix Biology . 1999,第3期

机译：B-Myb通过抑制与第一个外显子内与阳性元件相互作用的因子的结合，间接抑制Col5A2胶原启动子的反式激活。
4. Predicting Oncogenic Missense Mutations [C] . Xue Lei, Boshen Wang, Alan Perez-Rathke, IEEE EMBS International Conference on Biomedical Health Informatics . 2019

机译：预测致癌性错义突变
5. Identification of Non-Random Somatic Mutation Clustering While Accounting for Protein Tertiary Structure: Extensions, Novel Methodologies and Applications to Identifying Oncogenic Driver Mutations. [D] . Ryslik, Gregory A. 2014

机译：鉴定蛋白质三级结构时鉴定非随机体细胞突变聚类：扩展，新颖的方法和应用程序，以确定致癌的驱动程序突变。
6. Oncogenic activation of c-ABL by mutation within its last exon. [O] . A Goga, J McLaughlin, A M Pendergast, 1993

机译：c-ABL的最后一个外显子内的突变致癌激活。
7. Oncogenic activation of c-ABL by mutation within its last exon. [O] . Goga, A, McLaughlin, J, Pendergast, A M, 1993

机译：c-ABL的最后一个外显子内的突变致癌激活。

Oncogenic activation of c-ABL by mutation within its last exon.

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