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Building bone with a SOST-PTH partnership.

作者信息

Sims Natalie A

机构信息

St. Vincent's Institute and Department of Medicine at St. Vincent's Hospital, The University of Melbourne, Fitzroy, Victoria, Australia.

出版信息

J Bone Miner Res. 2010 Feb;25(2):175-7. doi: 10.1002/jbmr.53.

DOI:10.1002/jbmr.53
PMID:20175218
Abstract
摘要

相似文献

1
Building bone with a SOST-PTH partnership.通过硬化蛋白-甲状旁腺激素联合作用构建骨骼。
J Bone Miner Res. 2010 Feb;25(2):175-7. doi: 10.1002/jbmr.53.
2
Sclerostin: a gem from the genome leads to bone-building antibodies.硬化素:来自基因组的瑰宝催生促骨生成抗体。
J Bone Miner Res. 2010 Sep;25(9):1897-904. doi: 10.1002/jbmr.161.
3
SOST is a target gene for PTH in bone.硬化蛋白是甲状旁腺激素在骨骼中的一个靶基因。
Bone. 2005 Aug;37(2):148-58. doi: 10.1016/j.bone.2005.03.018.
4
Downregulation of SOST/sclerostin by PTH: a novel mechanism of hormonal control of bone formation mediated by osteocytes.甲状旁腺激素对骨硬化蛋白(SOST)的下调作用:一种由骨细胞介导的激素控制骨形成的新机制。
J Musculoskelet Neuronal Interact. 2006 Oct-Dec;6(4):358-9.
5
Parathyroid hormone (PTH)-induced bone gain is blunted in SOST overexpressing and deficient mice.甲状旁腺激素(PTH)诱导的骨量增加在 SOST 过表达和缺乏的小鼠中受到抑制。
J Bone Miner Res. 2010 Feb;25(2):178-89. doi: 10.1359/jbmr.090730.
6
Bone anabolic effects of parathyroid hormone are blunted by deletion of the Wnt antagonist secreted frizzled-related protein-1.通过缺失分泌型卷曲相关蛋白-1(一种Wnt拮抗剂),甲状旁腺激素的骨合成代谢作用会减弱。
J Cell Physiol. 2007 Feb;210(2):352-7. doi: 10.1002/jcp.20834.
7
Identification of the disease-causing gene in sclerosteosis--discovery of a novel bone anabolic target?骨硬化症致病基因的鉴定——发现一个新的骨合成代谢靶点?
J Musculoskelet Neuronal Interact. 2004 Jun;4(2):139-42.
8
Early response of the human SOST gene to stimulation by 1α,25-dihydroxyvitamin D.人类SOST基因对1α,25 - 二羟基维生素D刺激的早期反应。
J Steroid Biochem Mol Biol. 2016 Nov;164:369-373. doi: 10.1016/j.jsbmb.2015.12.006. Epub 2015 Dec 9.
9
Human genetics of SOST.硬化抑制素的人类遗传学
J Musculoskelet Neuronal Interact. 2006 Oct-Dec;6(4):355-6.
10
Bone morphogenetic proteins and their antagonists: the sclerostin paradigm.骨形态发生蛋白及其拮抗剂:硬化素范例
J Endocrinol Invest. 2005;28(8 Suppl):15-7.

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1
T cells, osteoblasts, and osteocytes: interacting lineages key for the bone anabolic and catabolic activities of parathyroid hormone.T细胞、成骨细胞和骨细胞:甲状旁腺激素骨合成与分解代谢活动的关键相互作用谱系
Ann N Y Acad Sci. 2016 Jan;1364(1):11-24. doi: 10.1111/nyas.12969. Epub 2015 Dec 10.
2
Estrogen alone or in combination with parathyroid hormone can decrease vertebral MEF2 and sclerostin expression and increase vertebral bone mass in ovariectomized rats.单独使用雌激素或与甲状旁腺激素联合使用,可降低去卵巢大鼠的椎骨MEF2和硬化蛋白表达,并增加椎骨骨量。
Osteoporos Int. 2014 Dec;25(12):2743-54. doi: 10.1007/s00198-014-2818-y. Epub 2014 Jul 30.
3
Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease.
骨免疫学:抑瘤素M作为健康与疾病中骨形成和骨吸收的多效性调节因子
Bonekey Rep. 2014 May 14;3:527. doi: 10.1038/bonekey.2014.22. eCollection 2014.
4
Aging periosteal progenitor cells have reduced regenerative responsiveness to bone injury and to the anabolic actions of PTH 1-34 treatment.衰老的骨膜祖细胞对骨损伤及甲状旁腺激素1-34(PTH 1-34)治疗的合成代谢作用的再生反应性降低。
Bone. 2014 May;62:79-89. doi: 10.1016/j.bone.2014.02.002. Epub 2014 Feb 12.
5
The sclerostin-independent bone anabolic activity of intermittent PTH treatment is mediated by T-cell-produced Wnt10b.间歇性甲状旁腺激素治疗的不依赖硬化素的骨合成代谢活性由T细胞产生的Wnt10b介导。
J Bone Miner Res. 2014 Jan;29(1):43-54. doi: 10.1002/jbmr.2044.
6
Parathyroid hormone treatment improves the cortical bone microstructure by improving the distribution of type I collagen in postmenopausal women with osteoporosis.甲状旁腺激素治疗通过改善Ⅰ型胶原的分布改善绝经后骨质疏松症妇女的皮质骨微观结构。
J Bone Miner Res. 2012 Mar;27(3):702-12. doi: 10.1002/jbmr.1497.
7
Consequences of daily administered parathyroid hormone on myeloma growth, bone disease, and molecular profiling of whole myelomatous bone.甲状旁腺激素每日给药对骨髓瘤生长、骨病和整个骨髓瘤骨的分子谱分析的影响。
PLoS One. 2010 Dec 20;5(12):e15233. doi: 10.1371/journal.pone.0015233.
8
The immune system and bone.免疫系统与骨骼。
Arch Biochem Biophys. 2010 Nov 1;503(1):41-53. doi: 10.1016/j.abb.2010.05.027. Epub 2010 Jun 17.