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c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program [RNA-seq]

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The transcription factor c-Maf is an essential regulator of group 3 ILC homeostasis and effector plasticity. c-Maf limits acquisition of the type 1 program and conversion to the ILC1 fate through restraint of T-bet expression and function. Evaluation of differential expression in Maf--deficient ILC subsets from the small intestine lamina propria. RNA was extracted from three replicate samples of NKp46+ ILC3, CCR6+ ILC3, and ILC2s from cohoused Maf+/+ Il7r-Cre and Maf fl/fl Il7r-Cre mice.

转录因子c-Maf是调控3型固有淋巴细胞(group 3 ILC)稳态与效应可塑性的核心调节因子。c-Maf可通过抑制T-bet的表达与功能,限制细胞获取1型转录程序并向ILC1细胞命运转化。本数据集针对小肠固有层的Maf缺陷型ILC亚群开展基因差异表达分析:从同笼饲养的Maf+/+ Il7r-Cre野生型小鼠与Maf fl/fl Il7r-Cre条件性敲除小鼠的NKp46+ ILC3、CCR6+ ILC3及ILC2细胞中,分别提取了三份生物学重复样本的RNA。

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