Protein Sample Production Facility, Max-Delbrück-Centrum für Molekulare Medizin, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
Cell Mol Life Sci. 2011 Sep;68(18):3121-31. doi: 10.1007/s00018-010-0618-x. Epub 2011 Feb 3.
Krueppel-like factor 4 (Klf4) belongs to the Sp/Klf family of zinc-finger transcription factors and is indispensable for terminal maturation of epithelial tissues. Furthermore, it is part of a small set of proteins that are used to generate pluripotent embryonic stem cells from differentiated tissues. Herein, we describe that a Klf4 zinc-finger domain mutant induces self-renewal and block of maturation, while wild-type Klf4 induces terminal macrophage differentiation. Moreover, we present the crystal structure of the zinc-finger domain of Klf4 bound to its target DNA, revealing that primarily the two C-terminal zinc-finger motifs are required for site specificity. Lack of those two zinc fingers leads to deficiency of Klf4 to induce macrophage differentiation. The first zinc finger, on the other hand, inhibits the otherwise cryptic self-renewal and block of differentiation activity of Klf4. Our data show that impairing the DNA binding could potentially contribute to a monocytic leukemia.
Krueppel 样因子 4(Klf4)属于 Sp/Klf 家族的锌指转录因子,对于上皮组织的终末成熟是必不可少的。此外,它是一小部分蛋白质中的一员,这些蛋白质可用于从分化组织中生成多能胚胎干细胞。在此,我们描述了 Klf4 锌指结构域突变体诱导自我更新和成熟阻滞,而野生型 Klf4 诱导终末巨噬细胞分化。此外,我们还展示了 Klf4 的锌指结构域与其靶 DNA 结合的晶体结构,揭示了主要是两个 C 末端锌指基序对于位点特异性是必需的。缺乏这两个锌指会导致 Klf4 缺乏诱导巨噬细胞分化的能力。另一方面,第一个锌指抑制 Klf4 的自我更新和分化阻滞活性,否则这种活性是隐蔽的。我们的数据表明,破坏 DNA 结合可能有助于单核细胞白血病的发生。