• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Normal long bone growth and development in type X collagen-null mice.

作者信息

Rosati R, Horan G S, Pinero G J, Garofalo S, Keene D R, Horton W A, Vuorio E, de Crombrugghe B, Behringer R R

机构信息

Department of Molecular Genetics, University of Texas M.D. Anderson Cancer Center, Houston 77030.

出版信息

Nat Genet. 1994 Oct;8(2):129-35. doi: 10.1038/ng1094-129.

DOI:10.1038/ng1094-129
PMID:7842010
Abstract

To investigate the role of type X collagen in skeletal development, we have generated type X collagen-null mice. Surprisingly, mice without type X collagen were viable and fertile and had no gross abnormalities in long bone growth or development. No differences were detected between the type X collagen-null mice and controls when growth plates of both newborn and 3-week old mice were examined by histology and by immunostaining for extracellular matrix components of bone including osteopontin, osteocalcin and type II collagen. Our results suggest that type X collagen is not required for long bone development. However, mice and humans with dominant acting type X collagen mutations have bone abnormalities, suggesting that only the presence of abnormal type X collagen can modify bone growth and development.

摘要

相似文献

1
Normal long bone growth and development in type X collagen-null mice.
Nat Genet. 1994 Oct;8(2):129-35. doi: 10.1038/ng1094-129.
2
Mouse clavicular development: analysis of wild-type and cleidocranial dysplasia mutant mice.小鼠锁骨发育:野生型和锁骨颅骨发育不全突变小鼠的分析
Dev Dyn. 1997 Sep;210(1):33-40. doi: 10.1002/(SICI)1097-0177(199709)210:1<33::AID-AJA4>3.0.CO;2-2.
3
Restoration of normal bone development by human homologue of collagen type II (COL2A1) gene in Col2a1 null mice.
Dev Dyn. 1999 Jan;214(1):26-33. doi: 10.1002/(SICI)1097-0177(199901)214:1<26::AID-DVDY3>3.0.CO;2-V.
4
Induction of bone-related proteins, osteocalcin and osteopontin, and their matrix ultrastructural localization with development of chondrocyte hypertrophy in vitro.体外软骨细胞肥大发育过程中骨相关蛋白、骨钙素和骨桥蛋白的诱导及其基质超微结构定位。
J Cell Biochem. 1993 Jun;52(2):206-19. doi: 10.1002/jcb.240520212.
5
Retarded skeletal development in transgenic mice with a type II collagen mutation.患有II型胶原蛋白突变的转基因小鼠骨骼发育迟缓。
Am J Pathol. 1996 Dec;149(6):2169-82.
6
Orientation of mineral crystallites and mineral density during skeletal development in mice deficient in tissue nonspecific alkaline phosphatase.组织非特异性碱性磷酸酶缺乏小鼠骨骼发育过程中矿物微晶的取向和矿物密度
J Bone Miner Res. 2003 Jan;18(1):117-25. doi: 10.1359/jbmr.2003.18.1.117.
7
Mice lacking matrilin-1 (cartilage matrix protein) have alterations in type II collagen fibrillogenesis and fibril organization.缺乏Ⅱ型胶原纤维生成和纤维组织的小鼠(软骨基质蛋白)有改变。
Dev Dyn. 1999 Dec;216(4-5):434-41. doi: 10.1002/(SICI)1097-0177(199912)216:4/5<434::AID-DVDY11>3.0.CO;2-X.
8
In situ expression of collagen and proteoglycan genes in notochord and during skeletal development and growth.胶原蛋白和蛋白聚糖基因在脊索以及骨骼发育与生长过程中的原位表达。
Microsc Res Tech. 1994 Aug 15;28(6):470-82. doi: 10.1002/jemt.1070280603.
9
Y-position collagen II mutation disrupts cartilage formation and skeletal development in a transgenic mouse model of spondyloepiphyseal dysplasia.Y 位胶原蛋白 II 突变在脊椎骨骺发育不良的转基因小鼠模型中破坏软骨形成和骨骼发育。
J Bone Miner Res. 2002 Jan;17(1):39-47. doi: 10.1359/jbmr.2002.17.1.39.
10
Skeletal development in transgenic mice expressing a mutation at Gly574Ser of type II collagen.表达II型胶原蛋白Gly574Ser突变的转基因小鼠的骨骼发育
Dev Dyn. 1997 Feb;208(2):170-7. doi: 10.1002/(SICI)1097-0177(199702)208:2<170::AID-AJA4>3.0.CO;2-F.

引用本文的文献

1
The regulatory effect of CoL10A1 to the intracranial vascular invasion and cell proliferation in breast cancer via EMT pathway.胶原蛋白Xα1(CoL10A1)通过上皮-间质转化(EMT)途径对乳腺癌颅内血管侵袭和细胞增殖的调节作用。
Sci Rep. 2025 Apr 1;15(1):11040. doi: 10.1038/s41598-025-87475-w.
2
Congenital Bone Disorders Associated with ERI1-Mediated RNA Metabolism Dysfunction: Spondylo-Epi-Metaphyseal Dysplasia Guo-Campeau Type and Beyond.与ERI1介导的RNA代谢功能障碍相关的先天性骨疾病:郭-坎波型及其他脊柱-骨骺-干骺端发育异常。
Curr Osteoporos Rep. 2025 Feb 13;23(1):9. doi: 10.1007/s11914-025-00903-8.
3
A Collagen10a1 mutation disrupts cell polarity in a medaka model for metaphyseal chondrodysplasia type Schmid.
在施密德型干骺端软骨发育不良的青鳉模型中,胶原蛋白10a1突变会破坏细胞极性。
iScience. 2024 Mar 4;27(4):109405. doi: 10.1016/j.isci.2024.109405. eCollection 2024 Apr 19.
4
Hypertrophic chondrocytes at the junction of musculoskeletal structures.肌肉骨骼结构交界处的肥大软骨细胞。
Bone Rep. 2023 Jul 3;19:101698. doi: 10.1016/j.bonr.2023.101698. eCollection 2023 Dec.
5
Collagen X Is Dispensable for Hypertrophic Differentiation and Endochondral Ossification of Human iPSC-Derived Chondrocytes.胶原蛋白X对于人诱导多能干细胞衍生软骨细胞的肥大分化和软骨内骨化并非必需。
JBMR Plus. 2023 Mar 29;7(5):e10737. doi: 10.1002/jbm4.10737. eCollection 2023 May.
6
Insights into the Cellular and Molecular Mechanisms That Govern the Fracture-Healing Process: A Narrative Review.关于骨折愈合过程的细胞和分子机制的见解:一篇叙述性综述。
J Clin Med. 2021 Aug 12;10(16):3554. doi: 10.3390/jcm10163554.
7
The hypertrophic chondrocyte: To be or not to be.肥大软骨细胞:生存还是毁灭。
Histol Histopathol. 2021 Oct;36(10):1021-1036. doi: 10.14670/HH-18-355. Epub 2021 Jun 17.
8
Gene cloning to clinical trials-the trials and tribulations of a life with collagen.基因克隆到临床试验——胶原相伴的一生的考验与磨难。
Int J Exp Pathol. 2019 Feb;100(1):4-11. doi: 10.1111/iep.12311. Epub 2019 Mar 26.
9
Bone physiology as inspiration for tissue regenerative therapies.骨骼生理学对组织再生疗法的启示。
Biomaterials. 2018 Dec;185:240-275. doi: 10.1016/j.biomaterials.2018.09.028. Epub 2018 Sep 17.
10
The triple helix of collagens - an ancient protein structure that enabled animal multicellularity and tissue evolution.胶原的三螺旋结构——一种古老的蛋白质结构,使动物多细胞性和组织进化成为可能。
J Cell Sci. 2018 Apr 9;131(7):jcs203950. doi: 10.1242/jcs.203950.