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本文引用的文献

1
G-protein stimulatory subunit alpha and Gq/11α G-proteins are both required to maintain quiescent stem-like chondrocytes.G蛋白刺激亚基α和Gq/11α G蛋白都是维持静止的干细胞样软骨细胞所必需的。
Nat Commun. 2014 Apr 30;5:3673. doi: 10.1038/ncomms4673.
2
Regulation of chondrogenesis by protein kinase C: Emerging new roles in calcium signalling.蛋白激酶C对软骨形成的调控:钙信号传导中的新作用初现
Cell Signal. 2014 May;26(5):979-1000. doi: 10.1016/j.cellsig.2014.01.011. Epub 2014 Jan 17.
3
Role of regulator of G protein signaling proteins in bone.G 蛋白信号转导调节蛋白在骨中的作用。
Front Biosci (Landmark Ed). 2014 Jan 1;19(4):634-48. doi: 10.2741/4232.
4
Parathyroid hormone/parathyroid hormone-related protein receptor signaling is required for maintenance of the growth plate in postnatal life.甲状旁腺激素/甲状旁腺激素相关蛋白受体信号对于维持出生后的生长板是必需的。
Proc Natl Acad Sci U S A. 2011 Jan 4;108(1):191-6. doi: 10.1073/pnas.1005011108. Epub 2010 Dec 20.
5
Osteoblast precursors, but not mature osteoblasts, move into developing and fractured bones along with invading blood vessels.成骨细胞前体,而不是成熟的成骨细胞,会与入侵的血管一起进入正在发育和骨折的骨骼。
Dev Cell. 2010 Aug 17;19(2):329-44. doi: 10.1016/j.devcel.2010.07.010.
6
Parathyroid hormone-related peptide represses chondrocyte hypertrophy through a protein phosphatase 2A/histone deacetylase 4/MEF2 pathway.甲状旁腺激素相关肽通过蛋白磷酸酶2A/组蛋白去乙酰化酶4/MEF2途径抑制软骨细胞肥大。
Mol Cell Biol. 2009 Nov;29(21):5751-62. doi: 10.1128/MCB.00415-09. Epub 2009 Aug 24.
7
The transcriptional activity of Sox9 in chondrocytes is regulated by RhoA signaling and actin polymerization.软骨细胞中Sox9的转录活性受RhoA信号传导和肌动蛋白聚合作用的调控。
Mol Cell Biol. 2009 Aug;29(15):4262-73. doi: 10.1128/MCB.01779-08. Epub 2009 May 26.
8
G(12)/G(13)-mediated signalling in mammalian physiology and disease.G(12)/G(13)介导的信号传导在哺乳动物生理学和疾病中的作用
Trends Pharmacol Sci. 2008 Nov;29(11):582-9. doi: 10.1016/j.tips.2008.08.002. Epub 2008 Sep 22.
9
Beta2-adrenergic receptors expressed on murine chondrocytes stimulate cellular growth and inhibit the expression of Indian hedgehog and collagen type X.
J Cell Biochem. 2008 May 15;104(2):545-53. doi: 10.1002/jcb.21646.
10
Heterotrimeric G protein activation by G-protein-coupled receptors.G蛋白偶联受体介导的异源三聚体G蛋白激活
Nat Rev Mol Cell Biol. 2008 Jan;9(1):60-71. doi: 10.1038/nrm2299.

G蛋白在骨骺软骨细胞分化中的作用。

Role of G-proteins in the differentiation of epiphyseal chondrocytes.

作者信息

Chagin Andrei S, Kronenberg Henry M

机构信息

Department of Physiology and PharmacologyKarolinska Institutet, Nanna Svartz Vagen 2, Stockholm 17177, SwedenEndocrine UnitMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114-2696, USA

Department of Physiology and PharmacologyKarolinska Institutet, Nanna Svartz Vagen 2, Stockholm 17177, SwedenEndocrine UnitMassachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114-2696, USA.

出版信息

J Mol Endocrinol. 2014 Oct;53(2):R39-45. doi: 10.1530/JME-14-0093. Epub 2014 Jun 30.

DOI:10.1530/JME-14-0093
PMID:24982242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4152416/
Abstract

Herein, we review the regulation of differentiation of the growth plate chondrocytes by G-proteins. In connection with this, we summarize the current knowledge regarding each family of G-protein α subunit, specifically, Gα(s), Gα(q/11), Gα(12/13), and Gα(i/o). We discuss different mechanisms involved in chondrocyte differentiation downstream of G-proteins and different G-protein-coupled receptors (GPCRs) activating G-proteins in the epiphyseal chondrocytes. We conclude that among all G-proteins and GPCRs expressed by chondrocytes, Gα(s) has the most important role and prevents premature chondrocyte differentiation. Receptor for parathyroid hormone (PTHR1) appears to be the major activator of Gα(s) in chondrocytes and ablation of either one leads to accelerated chondrocyte differentiation, premature fusion of the postnatal growth plate, and ultimately short stature.

摘要

在此,我们综述了G蛋白对生长板软骨细胞分化的调控。与此相关,我们总结了目前关于G蛋白α亚基各家族的知识,具体而言,包括Gα(s)、Gα(q/11)、Gα(12/13)和Gα(i/o)。我们讨论了G蛋白下游参与软骨细胞分化的不同机制,以及骨骺软骨细胞中激活G蛋白的不同G蛋白偶联受体(GPCR)。我们得出结论,在软骨细胞表达的所有G蛋白和GPCR中,Gα(s)具有最重要的作用,并可防止软骨细胞过早分化。甲状旁腺激素受体(PTHR1)似乎是软骨细胞中Gα(s)的主要激活剂,二者任一缺失都会导致软骨细胞分化加速、出生后生长板过早融合,并最终导致身材矮小。