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Re: "The 3.6 kb DNA fragment from the rat Col1a1 gene promoter drives the expression of genes in both osteoblast and osteoclast lineage cells" by Boban et al. (Bone 39:1302-1312, 2006).

作者信息

Khosla Sundeep

出版信息

Bone. 2007 Jun;40(6):1671-2; author reply 1673-4. doi: 10.1016/j.bone.2007.02.014. Epub 2007 Feb 23.

DOI:10.1016/j.bone.2007.02.014
PMID:17376754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1952213/
Abstract
摘要

相似文献

1
Re: "The 3.6 kb DNA fragment from the rat Col1a1 gene promoter drives the expression of genes in both osteoblast and osteoclast lineage cells" by Boban et al. (Bone 39:1302-1312, 2006).回复：Boban等人发表的《大鼠Col1a1基因启动子的3.6 kb DNA片段驱动成骨细胞和破骨细胞谱系细胞中基因的表达》（《骨》39:1302 - 1312, 2006年）
Bone. 2007 Jun;40(6):1671-2; author reply 1673-4. doi: 10.1016/j.bone.2007.02.014. Epub 2007 Feb 23.
2
The 3.6 kb DNA fragment from the rat Col1a1 gene promoter drives the expression of genes in both osteoblast and osteoclast lineage cells.来自大鼠Col1a1基因启动子的3.6 kb DNA片段驱动成骨细胞和破骨细胞谱系细胞中基因的表达。
Bone. 2006 Dec;39(6):1302-12. doi: 10.1016/j.bone.2006.06.025. Epub 2006 Aug 30.
3
Overexpression of H1 calponin in osteoblast lineage cells leads to a decrease in bone mass by disrupting osteoblast function and promoting osteoclast formation.成骨细胞系中 H1 钙调宁蛋白的过表达通过破坏成骨细胞功能和促进破骨细胞形成导致骨量减少。
J Bone Miner Res. 2013 Mar;28(3):660-71. doi: 10.1002/jbmr.1778.
4
Col1a1 promoter-targeted expression of p20 CCAAT enhancer-binding protein beta (C/EBPbeta), a truncated C/EBPbeta isoform, causes osteopenia in transgenic mice.p20 CCAAT增强子结合蛋白β（C/EBPβ）是一种截短的C/EBPβ异构体，其在I型胶原蛋白α1（Col1a1）启动子靶向表达可导致转基因小鼠出现骨质减少。
J Biol Chem. 2005 Mar 4;280(9):8117-24. doi: 10.1074/jbc.M410076200. Epub 2004 Dec 14.
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Col1a1-driven transgenic markers of osteoblast lineage progression.由Col1a1驱动的成骨细胞谱系进展的转基因标记物。
J Bone Miner Res. 2001 Jul;16(7):1228-36. doi: 10.1359/jbmr.2001.16.7.1228.
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Col3.6-HSD2 transgenic mice: a glucocorticoid loss-of-function model spanning early and late osteoblast differentiation.Col3.6-HSD2 转基因小鼠：跨越早期和晚期成骨细胞分化的糖皮质激素功能丧失模型。
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本文引用的文献

1
Remodeling and vascular spaces in bone.骨的重塑与血管间隙
J Bone Miner Res. 2007 Jan;22(1):1-6. doi: 10.1359/jbmr.060910.
2
The 3.6 kb DNA fragment from the rat Col1a1 gene promoter drives the expression of genes in both osteoblast and osteoclast lineage cells.来自大鼠Col1a1基因启动子的3.6 kb DNA片段驱动成骨细胞和破骨细胞谱系细胞中基因的表达。
Bone. 2006 Dec;39(6):1302-12. doi: 10.1016/j.bone.2006.06.025. Epub 2006 Aug 30.
3
Endocytosis of tartrate-resistant acid phosphatase by osteoblast-like cells is followed by inactivation of the enzyme.成骨样细胞对酒石酸抗性酸性磷酸酶的内吞作用之后，该酶会失活。
Calcif Tissue Int. 2006 Apr;78(4):248-54. doi: 10.1007/s00223-005-0185-6. Epub 2006 Apr 13.
4
Endogenous expression and endocytosis of tartrate-resistant acid phosphatase (TRACP) by osteoblast-like cells.成骨样细胞对酒石酸抗性酸性磷酸酶（TRACP）的内源性表达及内吞作用。
Bone. 2005 Jun;36(6):1065-77. doi: 10.1016/j.bone.2005.03.005.
5
Eccentric localization of osteocytes expressing enzymatic activities, protein, and mRNA signals for type 5 tartrate-resistant acid phosphatase (TRAP).表达5型抗酒石酸酸性磷酸酶（TRAP）酶活性、蛋白质和mRNA信号的骨细胞的偏心定位。
J Histochem Cytochem. 2004 Nov;52(11):1475-82. doi: 10.1369/jhc.4A6378.2004.
6
Osteoblastic tartrate-resistant acid phosphatase: its potential role in the molecular mechanism of osteogenic action of fluoride.成骨细胞抗酒石酸酸性磷酸酶：其在氟成骨作用分子机制中的潜在作用
J Bone Miner Res. 2003 Oct;18(10):1897-900. doi: 10.1359/jbmr.2003.18.10.1897.
7
Osteoblastic cells regulate the haematopoietic stem cell niche.成骨细胞调节造血干细胞龛。
Nature. 2003 Oct 23;425(6960):841-6. doi: 10.1038/nature02040.
8
Identification of the haematopoietic stem cell niche and control of the niche size.造血干细胞龛的鉴定及龛大小的调控。
Nature. 2003 Oct 23;425(6960):836-41. doi: 10.1038/nature02041.
9
The bone lining cell: its role in cleaning Howship's lacunae and initiating bone formation.骨衬细胞：其在清理Howship陷窝及启动骨形成中的作用。
J Bone Miner Res. 2002 Jan;17(1):77-90. doi: 10.1359/jbmr.2002.17.1.77.
10
Cancellous bone remodeling occurs in specialized compartments lined by cells expressing osteoblastic markers.松质骨重塑发生在由表达成骨细胞标志物的细胞所衬里的特殊区域。
J Bone Miner Res. 2001 Sep;16(9):1575-82. doi: 10.1359/jbmr.2001.16.9.1575.