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肥大软骨细胞特异性表达Cre 重组酶转基因小鼠的建立
  • 期刊名称：遗传, 31(1):69-74, 2009
  • 时间：0
  • 相关项目：骨骼发育及其相关疾病的分子机理研究
同期刊论文项目
骨骼发育及其相关疾病的分子机理研究
期刊论文 24 会议论文 9
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成骨细胞特异性表达Cre重组酶转基因小鼠的建立
SMAD4 is required for maintaining normal murine postnatal bone homeostasis
Smad4 is required for the normal organization of the cartilage growth plate
Accelerated re-epithelialization in Dpr2-deficient mice is associated with enhanced response to TGF-
Transforming growth factor-β regulated miR-24 promotes skeletal muscle differentiation
成骨细胞特异性剔除Smad4不影响小鼠造血稳态的维持
Altered Gene Expression in Articular Chondrocytes of Smad3ex8/ex8 Mice Revealed by Gene Profiling Us
The up-regulation of 14-3-3 proteins in Smad4 deficient epidermis and hair follicles at catagen
Transgenic mice that express Cre recombinase in hypertrophic chondrocytes
PTEN deficiency causes dyschondroplasia in mice by enhanced hypoxia-inducible factor-1( signaling an
CollagenI(1 promoter drives the expression of Cre recombinase in Osteoblasts of transgenic mice
Targeting WW domains linker of HECT-type ubiquitin ligase Smurf1 for activation by CKIP-1
TGF-(超家族在软骨发生、发育和维持中的作用
基因打靶技术：开创遗传学新纪元
利用寡核苷酸芯片分析Smad3基因敲除小鼠关节软骨细胞基因表达谱的改变
Smad4介导转化生长因子-β信号调节骨骼发育和稳态维持的功能
Collagenl α1 promoter drives the expression of Cre recombinase in osteoblasts of transgenic mice
TGF—β超家族在软骨发生、发育和维持中的作用
肥大软骨细胞特异性表达Cre重组酶转基因小鼠的建立