REGULATION OF TRACE METAL UPTAKE IN BACTERIA

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 NikR是依赖于镍酶如尿素酶和NiFe氢化酶生存的病原微生物的关键调节转录因子。 如果没有适量的Ni 2+，这些细菌无法在某些条件下生存，例如低pH或厌氧环境。 然而，过量的Ni 2+可引起细胞凋亡，因此调节细胞中Ni 2+的浓度是非常重要的。 出于这些原因，我们研究了细菌Ni 2+调节转录因子，NikR。 迄今为止，我们已经发表了许多大肠杆菌NikR（EcNikR）的结构，这些结构有助于阐明NikR的整体结构，金属结合过程和NikR-DNA结合机制。 这些结构包括：全长apo-EcNikR和Ni 2+结合的调节结构域（Schreiter等人，Nature Structural Biology 10（2003），794）、全长镍活化的EcNikR和EcNikR-操纵基因DNA复合物（Schreiter等人，PNAS 103（2006），13676）和EcNikR的apo、Cu 2 +-和Zn 2 +-结合的金属结合结构域（MBD）（菲利普斯，et al.，Biochemistry 47（2008），1938）。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. NikR is a key regulatory transcription factor for pathogenic microorganisms that depend on nickel enzymes such as urease and NiFe-hydrogenase for survival. Without a proper amount of Ni2+ these bacteria are unable to survive in certain conditions, such as low pH or anaerobic environments. However, an excess of Ni2+ in the cell can cause apoptosis, thus regulating the concentration of Ni2+ in the cell is of great importance. For these reasons we study the bacterial Ni2+-regulatory transcription factor, NikR. To date, we have published a number of structures of Escherichia coli NikR (EcNikR) that have helped elucidate the overall structure of NikR, the metal binding processes, and NikR-DNA binding mechanism. These structures include: the full-length apo-EcNikR and the Ni2+-bound regulatory domain (Schreiter et al., Nature Structural Biology 10 (2003), 794), full-length nickel-activated EcNikR and the EcNikR-operator DNA complex (Schreiter, et al., PNAS 103 (2006), 13676), and apo, Cu2+-, and Zn2+-bound metal binding domain (MBD) of EcNikR (Phillips, et al., Biochemistry 47 (2008), 1938).