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Expression of TRK-T1 oncogene induces differentiation of PC12 cells.

作者信息

Greco A, Orlandi R, Mariani C, Miranda C, Borrello M G, Cattaneo A, Pagliardini S, Pierotti M A

机构信息

Division of Experimental Oncology A, Istituto Nazionale Tumori, Milan, Italy.

出版信息

Cell Growth Differ. 1993 Jul;4(7):539-46.

PMID:8398895
Abstract

The TRK-T1 oncogene, isolated from a human thyroid carcinoma, represents a rearranged form of the high affinity nerve growth factor (NGF) receptor encoded by the NTRK1 gene; it is created by an intrachromosomal rearrangement fusing the NTRK1 tyrosine kinase domain to the 5' portion of the TPR gene. We have investigated the effect of the TRK-T1 oncogene in PC12 cells, a model system for studying neuronal differentiation and the mechanism of action of NGF. Here, we report that, in PC12 cells, the TRK-T1 oncogene has a differentiating effect that resembles that of NGF and requires the phosphorylation of the oncoprotein. Our results are consistent with the hypothesis that TRK-T1, as well as the original TRK oncogene, induces PC12 differentiation by mimicking the action of NGF bound to its receptor.

摘要

相似文献

1
Expression of TRK-T1 oncogene induces differentiation of PC12 cells.
Cell Growth Differ. 1993 Jul;4(7):539-46.
2
The trk family of oncogenes and neurotrophin receptors.癌基因与神经营养因子受体的trk家族。
Princess Takamatsu Symp. 1991;22:153-70.
3
P53 associates with trk tyrosine kinase.P53与酪氨酸激酶trk相关联。
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Transfection of TRK-A into human neuroblastoma cells restores their ability to differentiate in response to nerve growth factor.将TRK-A转染到人神经母细胞瘤细胞中可恢复其对神经生长因子作出反应而分化的能力。
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Expression of human p140trk receptors in p140trk-deficient, PC12/endothelial cells results in nerve growth factor-induced signal transduction and DNA synthesis.在缺乏p140trk的PC12/内皮细胞中表达人p140trk受体,会导致神经生长因子诱导的信号转导和DNA合成。
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K252a is a selective inhibitor of the tyrosine protein kinase activity of the trk family of oncogenes and neurotrophin receptors.K252a是一种原癌基因trk家族和神经营养因子受体酪氨酸蛋白激酶活性的选择性抑制剂。
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7
Chromosome 1 rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid-specific TRK oncogenes.涉及TPR和NTRK1基因的1号染色体重排产生结构不同的甲状腺特异性TRK致癌基因。
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8
Hierarchical analysis of the nerve growth factor-dependent and nerve growth factor-independent differentiation signaling pathways in PC12 cells with protein kinase inhibitors.利用蛋白激酶抑制剂对PC12细胞中神经生长因子依赖性和非神经生长因子依赖性分化信号通路进行层次分析。
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Differentiation of PC12 cells with v-src: comparison with nerve growth factor.用v-src诱导PC12细胞分化:与神经生长因子的比较。
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引用本文的文献

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Endocrine. 2018 Jul;61(1):36-41. doi: 10.1007/s12020-017-1483-2. Epub 2017 Dec 6.
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Multicellular spheroids from normal and neoplastic thyroid tissues as a suitable model to test the effects of multikinase inhibitors.来自正常和肿瘤性甲状腺组织的多细胞球体作为测试多激酶抑制剂效果的合适模型。
Oncotarget. 2017 Feb 7;8(6):9752-9766. doi: 10.18632/oncotarget.14187.
3
TRKing down an old oncogene in a new era of targeted therapy.
在靶向治疗的新时代追踪一个古老的癌基因。
Cancer Discov. 2015 Jan;5(1):25-34. doi: 10.1158/2159-8290.CD-14-0765. Epub 2014 Dec 19.
4
Role of STAT3 in in vitro transformation triggered by TRK oncogenes.STAT3 在 TRK 癌基因引发的体外转化中的作用。
PLoS One. 2010 Mar 3;5(3):e9446. doi: 10.1371/journal.pone.0009446.
5
Papillary thyroid carcinoma oncogene (RET/PTC) alters the nuclear envelope and chromatin structure.甲状腺乳头状癌致癌基因(RET/PTC)会改变核膜和染色质结构。
Am J Pathol. 1998 Nov;153(5):1443-50. doi: 10.1016/S0002-9440(10)65731-8.
6
A potential pathogenetic mechanism for multiple endocrine neoplasia type 2 syndromes involves ret-induced impairment of terminal differentiation of neuroepithelial cells.2型多发性内分泌腺瘤综合征的一种潜在发病机制涉及ret诱导的神经上皮细胞终末分化受损。
Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7933-7. doi: 10.1073/pnas.93.15.7933.
7
Rearrangements of TRK proto-oncogene in papillary thyroid carcinomas.甲状腺乳头状癌中TRK原癌基因的重排
J Endocrinol Invest. 1995 Feb;18(2):130-3. doi: 10.1007/BF03349721.
8
The DNA rearrangement that generates the TRK-T3 oncogene involves a novel gene on chromosome 3 whose product has a potential coiled-coil domain.产生TRK - T3癌基因的DNA重排涉及3号染色体上的一个新基因,其产物具有潜在的卷曲螺旋结构域。
Mol Cell Biol. 1995 Nov;15(11):6118-27. doi: 10.1128/MCB.15.11.6118.