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TRPM7: a unique channel involved in magnesium homeostasis.TRPM7:参与镁稳态的独特通道。
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本文引用的文献

1
Mirk/Dyrk1B maintains the viability of quiescent pancreatic cancer cells by reducing levels of reactive oxygen species.Mirk/Dyrk1B通过降低活性氧水平来维持静止胰腺癌细胞的活力。
Cancer Res. 2009 Apr 15;69(8):3317-24. doi: 10.1158/0008-5472.CAN-08-2903. Epub 2009 Apr 7.
2
Islet oxygen consumption and insulin secretion tightly coupled to calcium derived from L-type calcium channels but not from the endoplasmic reticulum.胰岛的氧消耗和胰岛素分泌与源自L型钙通道而非内质网的钙紧密偶联。
J Biol Chem. 2008 Sep 5;283(36):24334-42. doi: 10.1074/jbc.M802097200. Epub 2008 Jul 1.
3
TRPM7 ion channels are required for sustained phosphoinositide 3-kinase signaling in lymphocytes.瞬时受体电位M型7离子通道是淋巴细胞中持续的磷脂酰肌醇3激酶信号传导所必需的。
Cell Metab. 2008 Jul;8(1):84-93. doi: 10.1016/j.cmet.2008.06.002.
4
Glucose metabolism in lymphocytes is a regulated process with significant effects on immune cell function and survival.淋巴细胞中的葡萄糖代谢是一个受调控的过程,对免疫细胞的功能和存活有重大影响。
J Leukoc Biol. 2008 Oct;84(4):949-57. doi: 10.1189/jlb.0108024. Epub 2008 Jun 24.
5
The Cdk inhibitor p27 in human cancer: prognostic potential and relevance to anticancer therapy.人类癌症中的细胞周期蛋白依赖性激酶抑制剂p27:预后潜力及与抗癌治疗的相关性
Nat Rev Cancer. 2008 Apr;8(4):253-67. doi: 10.1038/nrc2347.
6
CDK inhibitors: cell cycle regulators and beyond.细胞周期蛋白依赖性激酶抑制剂:细胞周期调节剂及其他作用
Dev Cell. 2008 Feb;14(2):159-69. doi: 10.1016/j.devcel.2008.01.013.
7
Orai1 and STIM1 move to the immunological synapse and are up-regulated during T cell activation.Orai1和STIM1迁移至免疫突触,并在T细胞活化过程中上调。
Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2011-6. doi: 10.1073/pnas.0706122105. Epub 2008 Feb 4.
8
ATR signaling can drive cells into senescence in the absence of DNA breaks.在没有DNA断裂的情况下,ATR信号传导可促使细胞进入衰老状态。
Genes Dev. 2008 Feb 1;22(3):297-302. doi: 10.1101/gad.452308.
9
Cellular senescence: when bad things happen to good cells.细胞衰老:当好事发生在好细胞上时。 (注:原英文表述似乎不太符合正常逻辑,正常应该是不好的事情发生在细胞上才会导致衰老,这里按照字面意思翻译)
Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40. doi: 10.1038/nrm2233.
10
Molecular basis of the CRAC channel.CRAC通道的分子基础。
Cell Calcium. 2007 Aug;42(2):133-44. doi: 10.1016/j.ceca.2007.03.002. Epub 2007 May 7.

TRPM7 调节淋巴细胞静息/增殖代谢转换。

TRPM7 regulates quiescent/proliferative metabolic transitions in lymphocytes.

机构信息

Department of Pediatrics and Immunology, University of Washington, Seattle Children's Research Institute, Seattle, WA, USA.

出版信息

Cell Cycle. 2010 Sep 1;9(17):3565-74. doi: 10.4161/cc.9.17.12798. Epub 2010 Sep 25.

DOI:10.4161/cc.9.17.12798
PMID:20724843
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3047620/
Abstract

A unique property of lymphocytes among all body tissues is their capacity for rapid proliferation in the context of responding to infectious challenges. Lymphocyte proliferation involves a transition from a quiescent metabolic state adjusted to maintain cellular energy homeostasis, to a proliferative metabolic state in which aerobic glycolysis is used to generate energy and biosynthetic precursors necessary for the accumulation of cell mass. Here we show that modulation of TRPM7 channel function in tumor B-lymphocytes directly induces quiescent/proliferative metabolic transitions. As TRPM7 is widely expressed outside of the immune system, our results suggest that TRPM7 may play an active role in regulating metabolic transitions associated with rapid cellular proliferation and malignancy.

摘要

淋巴细胞在所有身体组织中具有独特的属性,即它们能够在应对感染性挑战的情况下迅速增殖。淋巴细胞增殖涉及从适应维持细胞能量稳态的静止代谢状态向有氧糖酵解用于产生能量和生物合成前体以积累细胞质量的增殖代谢状态的转变。在这里,我们表明,肿瘤 B 淋巴细胞中 TRPM7 通道功能的调节可直接诱导静止/增殖代谢转变。由于 TRPM7 在免疫系统之外广泛表达,我们的结果表明,TRPM7 可能在调节与快速细胞增殖和恶性肿瘤相关的代谢转变中发挥积极作用。