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J Clin Endocrinol Metab. 2020 Jun 1;105(6). doi: 10.1210/clinem/dgaa121.
2
Targeting effector pathways in RAC1-driven malignant melanoma.靶向 RAC1 驱动的恶性黑色素瘤中的效应通路。
Small GTPases. 2021 Jul;12(4):273-281. doi: 10.1080/21541248.2020.1728469. Epub 2020 Feb 17.
3
Targeting XPO1 and PAK4 in 8505C Anaplastic Thyroid Cancer Cells: Putative Implications for Overcoming Lenvatinib Therapy Resistance.针对 8505C 间变性甲状腺癌细胞中的 XPO1 和 PAK4:克服仑伐替尼治疗耐药性的潜在意义。
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Cancer Res. 2019 Oct 1;79(19):5074-5087. doi: 10.1158/0008-5472.CAN-19-0244. Epub 2019 Aug 15.
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RAC1 Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.RAC1 通过血清反应因子诱导间充质表型转换,促进黑色素瘤的发展和治疗耐药性。
Cancer Cell. 2019 Jul 8;36(1):68-83.e9. doi: 10.1016/j.ccell.2019.05.015. Epub 2019 Jun 27.
6
MAPK- and AKT-activated thyroid cancers are sensitive to group I PAK inhibition.MAPK 和 AKT 激活的甲状腺癌对 I 组 PAK 抑制敏感。
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Solution structures and biophysical analysis of full-length group A PAKs reveal they are monomeric and auto-inhibited in .全长 A 族 PAK 的溶液结构和生物物理分析表明,它们是单体形式,并在. 中处于自身抑制状态。
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Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer.I 型帕克斯蛋白对于 APC 驱动的结直肠癌模型中的上皮间质转化是必需的。
Nat Commun. 2018 Aug 27;9(1):3473. doi: 10.1038/s41467-018-05935-6.
9
P21 activated kinase signaling in cancer.P21 激活激酶信号通路与癌症。
Semin Cancer Biol. 2019 Feb;54:40-49. doi: 10.1016/j.semcancer.2018.01.006. Epub 2018 Jan 9.
10
Suppression of RAC1-driven malignant melanoma by group A PAK inhibitors.A 组 PAK 抑制剂抑制 RAC1 驱动的恶性黑色素瘤。
Oncogene. 2018 Feb 15;37(7):944-952. doi: 10.1038/onc.2017.400. Epub 2017 Oct 23.

甲状腺癌中的 p21 激活激酶。

p21-Activated Kinases in Thyroid Cancer.

机构信息

Division of Endocrinology, Diabetes, and Metabolism, Department of Internal Medicine, and Cancer Biology Program, The Ohio State University College of Medicine and Arthur G. James Comprehensive Cancer Center, Columbus, Ohio.

Department of Hematology and Medical Oncology, Emory University and Winship Cancer Institute, Atlanta, Georgia.

出版信息

Endocrinology. 2020 Aug 1;161(8). doi: 10.1210/endocr/bqaa105.

DOI:10.1210/endocr/bqaa105
PMID:32609833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7417880/
Abstract

The family of p21-activated kinases (PAKs) are oncogenic proteins that regulate critical cellular functions. PAKs play central signaling roles in the integrin/CDC42/Rho, ERK/MAPK, PI3K/AKT, NF-κB, and Wnt/β-catenin pathways, functioning both as kinases and scaffolds to regulate cell motility, mitosis and proliferation, cytoskeletal rearrangement, and other cellular activities. PAKs have been implicated in both the development and progression of a wide range of cancers, including breast cancer, pancreatic melanoma, thyroid cancer, and others. Here we will discuss the current knowledge on the structure and biological functions of both group I and group II PAKs, as well as the roles that PAKs play in oncogenesis and progression, with a focus on thyroid cancer and emerging data regarding BRAF/PAK signaling.

摘要

p21 激活激酶(PAKs)家族是致癌蛋白,调节关键的细胞功能。PAKs 在整合素/CDC42/Rho、ERK/MAPK、PI3K/AKT、NF-κB 和 Wnt/β-catenin 通路中发挥核心信号作用,既是激酶又是支架,调节细胞迁移、有丝分裂和增殖、细胞骨架重排和其他细胞活动。PAKs 参与了广泛的癌症的发展和进展,包括乳腺癌、胰腺黑色素瘤、甲状腺癌等。在这里,我们将讨论关于 I 组和 II 组 PAKs 的结构和生物学功能的最新知识,以及 PAKs 在致癌和进展中的作用,重点关注甲状腺癌和关于 BRAF/PAK 信号的新兴数据。