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本文引用的文献

1
Enamel proteins and proteases in Mmp20 and Klk4 null and double-null mice.基质金属蛋白酶20(Mmp20)和激肽释放酶4(Klk4)基因敲除及双基因敲除小鼠中的釉质蛋白和蛋白酶
Eur J Oral Sci. 2011 Dec;119 Suppl 1(Suppl 1):206-16. doi: 10.1111/j.1600-0722.2011.00866.x.
2
Matrix metalloproteinase 20 promotes a smooth enamel surface, a strong dentino-enamel junction, and a decussating enamel rod pattern.基质金属蛋白酶20可促进形成光滑的牙釉质表面、坚固的牙本质-牙釉质界以及交叉的牙釉质柱形态。
Eur J Oral Sci. 2011 Dec;119 Suppl 1(Suppl 1):199-205. doi: 10.1111/j.1600-0722.2011.00864.x.
3
Why does enamel in Klk4-null mice break above the dentino-enamel junction?为什么 Klk4 基因敲除小鼠的牙釉质会在牙本质-釉质交界处之上破裂?
Cells Tissues Organs. 2011;194(2-4):211-5. doi: 10.1159/000324260. Epub 2011 May 6.
4
Effect of kallikrein 4 loss on enamel mineralization: comparison with mice lacking matrix metalloproteinase 20.KLK4 缺失对釉质矿化的影响:与 MMP20 缺失小鼠的比较。
J Biol Chem. 2011 May 20;286(20):18149-60. doi: 10.1074/jbc.M110.194258. Epub 2011 Mar 23.
5
How amelogenin orchestrates the organization of hierarchical elongated microstructures of apatite.成釉蛋白如何协调磷灰石的分级长型微结构的组织。
J Phys Chem B. 2010 Feb 18;114(6):2293-300. doi: 10.1021/jp910219s.
6
Consequences for enamel development and mineralization resulting from loss of function of ameloblastin or enamelin.成釉蛋白或釉原蛋白功能丧失对釉质发育和矿化的影响。
Eur J Oral Sci. 2009 Oct;117(5):485-97. doi: 10.1111/j.1600-0722.2009.00666.x.
7
Hypomaturation enamel defects in Klk4 knockout/LacZ knockin mice.Klk4基因敲除/LacZ基因敲入小鼠中的釉质成熟不全缺陷
J Biol Chem. 2009 Jul 10;284(28):19110-21. doi: 10.1074/jbc.M109.013623. Epub 2009 May 6.
8
A mouse model expressing a truncated form of ameloblastin exhibits dental and junctional epithelium defects.表达截短型釉原蛋白的小鼠模型表现出牙齿和结合上皮缺陷。
Matrix Biol. 2009 Jun;28(5):292-303. doi: 10.1016/j.matbio.2009.04.004. Epub 2009 Apr 16.
9
Enamel mineralization in the absence of maturation stage ameloblasts.无成熟阶段成釉细胞的釉质矿化。
Arch Oral Biol. 2009 Apr;54(4):313-21. doi: 10.1016/j.archoralbio.2009.01.007. Epub 2009 Feb 13.
10
Enzymatic Processing of Amelogenin during Continuous Crystallization of Apatite.磷灰石连续结晶过程中釉原蛋白的酶促加工
J Mater Res. 2008 Dec;23(12):3184-3195. doi: 10.1557/JMR.2008.0387.

正常及基因改造小鼠牙釉质发育过程中蛋白质与矿物质的关系。

Relationships between protein and mineral during enamel development in normal and genetically altered mice.

作者信息

Smith Charles E, Hu Yuanyuan, Richardson Amelia S, Bartlett John D, Hu Jan C-C, Simmer James P

机构信息

Facility for Electron Microscopy Research, Department of Anatomy & Cell Biology, and Faculty of Dentistry, McGill University, Montreal, QC, Canada.

出版信息

Eur J Oral Sci. 2011 Dec;119 Suppl 1(Suppl 1):125-35. doi: 10.1111/j.1600-0722.2011.00871.x.

DOI:10.1111/j.1600-0722.2011.00871.x
PMID:22243238
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3295546/
Abstract

The purpose of this study was to quantify and compare the amounts of volatiles (mostly protein) and mineral present in developing incisor enamel in normal mice and in those genetically engineered for absence of intact enamelin, ameloblastin, matrix metalloproteinase 20 (MMP20) or kallikrein-related peptidase 4 (KLK4). Data indicated that all mice showed peaks in the gross weight of volatiles and a similar weight of mineral at locations on incisors normally associated with early maturation. Thereafter, the content of volatiles on normal incisors declined rapidly by as much as 62%, but not by 100%, over 2 mm, accompanied by increases of ≈ threefold in mineral weights. Enamelin heterozygous mice (lower incisors) showed a decrease in volatile content across the maturation stage, yet mineral failed to increase significantly. Mmp20 null mice showed no significant loss of volatiles from maturing enamel, yet the amount of mineral increased. Klk4 null mice showed normal mineral acquisition up to early maturation, but the input of new volatiles in mid to late maturation caused the final mineralization to slow below normal levels. These results suggest that it is not only the amount of protein but also the nature or type of protein or fragments present in the local crystallite environment that affects their volumetric expansion as they mature.

摘要

本研究的目的是量化并比较正常小鼠以及那些因缺乏完整的釉原蛋白、成釉蛋白、基质金属蛋白酶20(MMP20)或激肽释放酶相关肽酶4(KLK4)而进行基因工程改造的小鼠发育中的切牙釉质中挥发性物质(主要是蛋白质)和矿物质的含量。数据表明,所有小鼠的挥发性物质总重量在切牙上通常与早期成熟相关的位置出现峰值,且矿物质重量相似。此后,正常切牙上的挥发性物质含量在2毫米的范围内迅速下降多达62%,但并非100%,同时矿物质重量增加了约三倍。釉原蛋白杂合小鼠(下切牙)在整个成熟阶段挥发性物质含量下降,但矿物质未能显著增加。Mmp20基因敲除小鼠成熟釉质中的挥发性物质没有显著损失,但矿物质含量增加。Klk4基因敲除小鼠在早期成熟前矿物质获取正常,但在成熟中期到后期新挥发性物质的输入导致最终矿化速度低于正常水平。这些结果表明,不仅蛋白质的数量,而且局部微晶环境中存在的蛋白质或片段的性质或类型,都会在其成熟时影响它们的体积膨胀。