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Notch1依赖性淋巴瘤发生过程受到前T细胞受体信号传导的辅助,但并非本质上必需。

Notch1-dependent lymphomagenesis is assisted by but does not essentially require pre-TCR signaling.

作者信息

Campese Antonio F, Garbe Annette I, Zhang Fangrong, Grassi Fabio, Screpanti Isabella, von Boehmer Harald

机构信息

Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.

出版信息

Blood. 2006 Jul 1;108(1):305-10. doi: 10.1182/blood-2006-01-0143. Epub 2006 Feb 28.

DOI:10.1182/blood-2006-01-0143
PMID:16507772
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1895839/
Abstract

Overexpression of intracellular Notch plays an important role in the generation of human acute lymphoblastic T cell leukemia (T-ALL). In mouse models, it was shown that Notch-dependent T-ALL required pre-TCR signaling. Here we show that pre-TCR signaling is required to condition mice for Notch-dependent transformation but that it is not required to sustain malignant growth of T-ALL. In contrast to previous studies, we found that disease development does not require pre-TCR but that it can be accelerated in Rag2(-/-) mice by transient mimicking of pre-TCR signals.

摘要

细胞内Notch的过表达在人类急性淋巴细胞性T细胞白血病(T-ALL)的发生中起重要作用。在小鼠模型中,已表明Notch依赖性T-ALL需要前T细胞受体(pre-TCR)信号传导。在此我们表明,pre-TCR信号传导是使小鼠适应Notch依赖性转化所必需的,但维持T-ALL的恶性生长并不需要它。与先前的研究相反,我们发现疾病发展不需要pre-TCR,但通过短暂模拟pre-TCR信号,它可以在Rag2(-/-)小鼠中加速。

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本文引用的文献

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Notch promotes survival of pre-T cells at the beta-selection checkpoint by regulating cellular metabolism.Notch通过调节细胞代谢促进前T细胞在β选择检查点的存活。
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The function of E- and Id proteins in lymphocyte development.E蛋白和Id蛋白在淋巴细胞发育中的作用。
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