Normal mouse skin lacking Hras

Oncogenic activating mutations in Ras genes are among the most common drivers of human disease. Treating mouse skin with the chemical carcinogen DMBA induces a characteristic mutation in Hras at codon 61. To understand how skin responds to a constitutive lack of Hras, we generated a cohort of Hras knockout mice. A backcross was generated using male Mus spretus and female FVB/N Hras-/- mice; female F1 hybrids were mated with male FVB/N Hras -/- or Hras -/+ mice to generate a backcross population. This series contains mice that were Hras -/-. Mice were aged to 8 weeks and a tail skin sample was snap frozen.Ras基因的致癌性激活突变是人类最常见的疾病驱动因素之一。使用化学致癌物DMBA处理小鼠皮肤，可在Hras基因的61号密码子处诱导特征性突变。为探究皮肤对Hras组成型缺失的响应机制，我们构建了一组Hras基因敲除小鼠队列。以西班牙小家鼠（Mus spretus）雄性个体与FVB/N背景Hras纯合敲除（Hras-/-）雌性小鼠开展回交，随后将获得的雌性F1杂种与FVB/N背景Hras纯合敲除（Hras-/-）或杂合敲除（Hras-/+）雄性小鼠交配，构建回交群体。本数据集包含Hras-/-基因型的小鼠：将小鼠饲养至8周龄后，取尾部皮肤样本进行速冻冻存。