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C3G自我调节机制揭示:对造血系统恶性肿瘤的影响

C3G self-regulatory mechanism revealed: implications for hematopoietic malignancies.

作者信息

Carabias Arturo, Guerrero Carmen, de Pereda José M

机构信息

Centro de Investigación del Cáncer and Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)- Universidad de Salamanca, Salamanca, Spain.

Structural Molecular Biology Group, Novo Nordisk Foundation Centre for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen N, Denmark.

出版信息

Mol Cell Oncol. 2020 Dec 1;8(1):1837581. doi: 10.1080/23723556.2020.1837581.

DOI:10.1080/23723556.2020.1837581
PMID:33553598
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7849780/
Abstract

Abnormally increased signaling by the GTPase RAP1 favors progression of diverse tumors. We have characterized the auto-regulation and activation of C3G (RAPGEF1), an activator of RAP1. This led us to discover mutations in non-Hodgkin's lymphomas that activate C3G-RAP1 constitutively, suggesting that deregulation of C3G may favor the dissemination of tumor cells.

摘要

GTP酶RAP1的信号异常增强有利于多种肿瘤的进展。我们已经对RAP1的激活剂C3G(RAPGEF1)的自动调节和激活进行了表征。这使我们发现了非霍奇金淋巴瘤中激活C3G-RAP1的突变,提示C3G的失调可能有利于肿瘤细胞的扩散。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8df/7849780/40f1d0084b1a/KMCO_A_1837581_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8df/7849780/40f1d0084b1a/KMCO_A_1837581_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8df/7849780/40f1d0084b1a/KMCO_A_1837581_F0001_OC.jpg

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C3G contributes to platelet activation and aggregation by regulating major signaling pathways.C3G 通过调节主要信号通路促进血小板的活化和聚集。
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Calcium-RasGRP2-Rap1 signaling mediates CD38-induced migration of chronic lymphocytic leukemia cells.
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Signalling to actin: role of C3G, a multitasking guanine-nucleotide-exchange factor.信号转导至肌动蛋白:C3G,一种多功能鸟嘌呤核苷酸交换因子的作用。
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