PDF - peptide deformylase, mitochondrial Gene

中文名称：肽脱甲酰酶，线粒体

种属: Homo sapiens

关于 PDF

功能概要

在甲硫氨酰-tRNA 甲酰基转移酶 (FMT) 对甲硫氨酸进行甲酰化并将带电荷的引发剂 f-met tRNA 转移到核糖体后，蛋白质合成就开始了。在真细菌和真核细胞器中，该基因的产物肽去甲酰基酶 (PDF) 从新生肽的起始甲硫氨酸中去除甲酰基。在真细菌中，新生肽的去甲酰基化是甲硫氨酸氨肽酶随后裂解起始甲硫氨酸所必需的。 PDF 的天然抑制剂放线菌素在某些细菌中充当抗菌剂的发现促使人们对细菌特异性 PDF 抑制剂的设计进行了深入研究。在人类细胞中，只有线粒体蛋白具有起始甲硫氨酸的 N-甲酰化。 PDF 的蛋白抑制剂或 PDF 的 siRNA 可阻断癌细胞系的生长，但对正常细胞生长没有影响。因此，在人类中，PDF 功能可能仅限于快速生长的细胞。[RefSeq 提供，2008 年 11 月]

Protein synthesis proceeds after formylation of methionine by methionyl-tRNA formyl transferase (FMT) and transfer of the charged initiator f-met tRNA to the ribosome. In eubacteria and eukaryotic organelles the product of this gene, peptide deformylase (PDF), removes the formyl group from the initiating methionine of nascent Peptides. In eubacteria, deformylation of nascent Peptides is required for subsequent cleavage of initiating methionines by methionine Aminopeptidase. The discovery that a natural inhibitor of PDF, actinonin, acts as an antimicrobial agent in some bacteria has spurred intensive research into the design of bacterial-specific PDF inhibitors. In human cells, only mitochondrial proteins have N-formylation of initiating methionines. Protein inhibitors of PDF or siRNAs of PDF block the growth of Cancer cell lines but have no effect on normal cell growth. In humans, PDF function may therefore be restricted to rapidly growing cells. [provided by RefSeq, Nov 2008]