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1
A quest for clarity in bone erosion: The role of sequestosome 1 in Paget's disease of bone.追寻骨侵蚀的清晰认识：自噬体相关蛋白 1 在骨 Paget 病中的作用。
J Biol Chem. 2018 Jun 15;293(24):9542-9543. doi: 10.1074/jbc.H118.003689.
2
p62/sequestosome 1 deficiency accelerates osteoclastogenesis and leads to Paget's disease-like bone phenotypes in mice.p62/自噬体相关蛋白 1 缺乏加速破骨细胞生成，并导致小鼠出现类似 Pagets 病的骨表型。
J Biol Chem. 2018 Jun 15;293(24):9530-9541. doi: 10.1074/jbc.RA118.002449. Epub 2018 Mar 19.
3
A novel mutation (K378X) in the sequestosome 1 gene associated with increased NF-kappaB signaling and Paget's disease of bone with a severe phenotype.在1号聚集体蛋白基因中发现一种新的突变（K378X），其与核因子κB信号增强及具有严重表型的骨佩吉特病相关。
J Bone Miner Res. 2006 Jul;21(7):1136-45. doi: 10.1359/jbmr.060405.
4
Etiology of Paget's disease and osteoclast abnormalities.佩吉特病的病因及破骨细胞异常
J Cell Biochem. 2004 Nov 1;93(4):688-96. doi: 10.1002/jcb.20256.
5
Zoledronic acid prevents pagetic-like lesions and accelerated bone loss in the p62 mouse model of Paget's disease.唑来膦酸可预防 Paget 病 p62 小鼠模型中的 pagetic 样病变和加速骨丢失。
Dis Model Mech. 2018 Aug 23;11(9):dmm035576. doi: 10.1242/dmm.035576.
6
Etiologic factors in Paget's disease of bone.骨佩吉特病的病因因素。
Cell Mol Life Sci. 2006 Feb;63(4):391-8. doi: 10.1007/s00018-005-5473-9.
7
The p62 P392L mutation linked to Paget's disease induces activation of human osteoclasts.与佩吉特病相关的p62 P392L突变可诱导人破骨细胞活化。
Mol Endocrinol. 2009 Oct;23(10):1668-80. doi: 10.1210/me.2009-0066. Epub 2009 Jul 9.
8
Familial Paget's disease of bone: Long-term follow-up of unaffected relatives with and without Sequestosome 1 mutations.家族性骨 Paget 病：有无 Sequestosome 1 突变的未受影响亲属的长期随访。
Bone. 2019 Nov;128:115044. doi: 10.1016/j.bone.2019.115044. Epub 2019 Aug 23.
9
New insights into the role of sequestosome 1/p62 mutant proteins in the pathogenesis of Paget's disease of bone.对骨 Paget 病发病机制中 sequestosome 1/p62 突变蛋白作用的新认识。
Endocr Rev. 2013 Aug;34(4):501-24. doi: 10.1210/er.2012-1034. Epub 2013 Apr 23.
10
Effect of a rare genetic variant of TM7SF4 gene on osteoclasts of patients with Paget's disease of bone.TM7SF4基因罕见遗传变异对骨Paget病患者破骨细胞的影响。
BMC Med Genet. 2017 Nov 16;18(1):133. doi: 10.1186/s12881-017-0495-3.

本文引用的文献

1
p62/sequestosome 1 deficiency accelerates osteoclastogenesis and leads to Paget's disease-like bone phenotypes in mice.p62/自噬体相关蛋白 1 缺乏加速破骨细胞生成，并导致小鼠出现类似 Pagets 病的骨表型。
J Biol Chem. 2018 Jun 15;293(24):9530-9541. doi: 10.1074/jbc.RA118.002449. Epub 2018 Mar 19.
2
p62 is required for stem cell/progenitor retention through inhibition of IKK/NF-κB/Ccl4 signaling at the bone marrow macrophage-osteoblast niche.通过在骨髓巨噬细胞 - 成骨细胞微环境中抑制IKK/NF-κB/Ccl4信号传导，p62对于干细胞/祖细胞的保留是必需的。
Cell Rep. 2014 Dec 24;9(6):2084-97. doi: 10.1016/j.celrep.2014.11.031. Epub 2014 Dec 18.
3
Pathobiology of Paget's Disease of Bone.骨佩吉特病的病理生物学
J Bone Metab. 2014 May;21(2):85-98. doi: 10.11005/jbm.2014.21.2.85. Epub 2014 May 31.
4
Paget's disease of bone.骨 Paget 病。
QJM. 2014 Nov;107(11):865-9. doi: 10.1093/qjmed/hcu075. Epub 2014 Apr 21.
5
A point mutation in the ubiquitin-associated domain of SQSMT1 is sufficient to cause a Paget's disease-like disorder in mice.SQSMT1 泛素相关结构域的点突变足以导致小鼠出现类似 Pagets 病的疾病。
Hum Mol Genet. 2011 Jul 15;20(14):2734-44. doi: 10.1093/hmg/ddr172. Epub 2011 Apr 21.
6
A SQSTM1/p62 mutation linked to Paget's disease increases the osteoclastogenic potential of the bone microenvironment.一种与佩吉特病相关的SQSTM1/p62突变增加了骨微环境的破骨细胞生成潜能。
Hum Mol Genet. 2008 Dec 1;17(23):3708-19. doi: 10.1093/hmg/ddn266. Epub 2008 Sep 2.
7
Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget disease.聚集体小体1（p62）基因的突变会增加破骨细胞生成，但不会诱发佩吉特病。
J Clin Invest. 2007 Jan;117(1):133-42. doi: 10.1172/JCI28267. Epub 2006 Dec 21.
8
p62 ubiquitin binding-associated domain mediated the receptor activator of nuclear factor-kappaB ligand-induced osteoclast formation: a new insight into the pathogenesis of Paget's disease of bone.p62泛素结合相关结构域介导核因子κB受体活化因子配体诱导的破骨细胞形成：对佩吉特骨病发病机制的新见解
Am J Pathol. 2006 Aug;169(2):503-14. doi: 10.2353/ajpath.2006.050960.
9
A novel mutation (K378X) in the sequestosome 1 gene associated with increased NF-kappaB signaling and Paget's disease of bone with a severe phenotype.在1号聚集体蛋白基因中发现一种新的突变（K378X），其与核因子κB信号增强及具有严重表型的骨佩吉特病相关。
J Bone Miner Res. 2006 Jul;21(7):1136-45. doi: 10.1359/jbmr.060405.
10
The atypical PKC-interacting protein p62 is an important mediator of RANK-activated osteoclastogenesis.非典型蛋白激酶C相互作用蛋白p62是RANK激活的破骨细胞生成的重要介质。
Dev Cell. 2004 Feb;6(2):303-9. doi: 10.1016/s1534-5807(03)00403-9.

追寻骨侵蚀的清晰认识：自噬体相关蛋白 1 在骨 Paget 病中的作用。

A quest for clarity in bone erosion: The role of sequestosome 1 in Paget's disease of bone.

机构信息

From the Center for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan 49503.

From the Center for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan 49503

出版信息

J Biol Chem. 2018 Jun 15;293(24):9542-9543. doi: 10.1074/jbc.H118.003689.

DOI:10.1074/jbc.H118.003689
PMID:29907733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6005432/
Abstract

Alterations in the gene are a putative cause of Paget's disease of bone, yet results are conflicting about how these mutations impact osteoclasts, the cell type believed to be the main pathological contributor. In this issue of JBC, Zach provide important new evidence that the protein encoded by , p62, negatively regulates osteoclastogenesis and demonstrate that aged p62-deficient mice develop bone phenotypes similar to those of Paget's disease. These findings help to clarify the role of this important protein and present new opportunities to interrogate bone biology.

摘要

该基因的改变被认为是引起 Pagets 骨病的一个潜在原因，但这些突变如何影响破骨细胞的结果存在争议，破骨细胞被认为是主要的病理性贡献细胞。在本期 JBC 中，Zach 提供了重要的新证据，表明 编码的蛋白 p62 负调节破骨细胞生成，并证明老年 p62 缺陷型小鼠表现出类似于 Pagets 病的骨表型。这些发现有助于阐明该重要蛋白的作用，并为研究骨生物学提供了新的机会。