Sehgal Pravin B
Department of Cell Biology & Anatomy, New York Medical College, Valhalla, NY 10595, United States.
Semin Cell Dev Biol. 2008 Aug;19(4):329-40. doi: 10.1016/j.semcdb.2008.07.003. Epub 2008 Jul 24.
In recent years several of the key tenets of the original cytokine-STAT-signaling paradigm had to be revised. First, the notion that nonphosphorylated "inactive" STATs are present in the cytoplasm as free monomers which dimerized only subsequent to Tyr-phosphorylation has been replaced by the understanding that nonphosphorylated STATs in the cytoplasm exist largely as dimers and high molecular mass "statosome" complexes. Second, the notion that phosphorylation, either of Tyr or Ser residues or both, in STAT species is required for transcriptional activation has been replaced by the realization that nonphosphorylated STATs can be transcriptionally active albeit with respect to sets of target genes distinct from phosphorylated STATs. Third, the notion that it is the activation by phosphorylation of STATs at the plasma membrane that then leads to their import into the nucleus has been replaced by the recognition that even nonphosphorylated STATs shuttle between the cytoplasm and nucleus at all times in a constitutive manner. Fourth, the notion that the trans-cytoplasmic transit of STATs from the plasma membrane to the nuclear import machinery takes place exclusively as a free cytosolic process has been replaced by the understanding that at least a portion of this trans-cytoplasmic transit is mediated via membrane-associated caveolar and endocytic trafficking (the "signaling endosome" hypothesis). Fifth, the targeting and sequestration of activated STAT3 to long-lived endosomes in the cytoplasm requires consideration of STAT3-mediated "signal transduction" from the plasma membrane to cytoplasmic membrane destinations potentially for function(s) in the cytoplasm. Indeed, in tissue sections many discrete histologic cell types display PY-STAT3 almost exclusively in the cytoplasm with little, if any, in the nucleus. New challenges include determining the structural bases for the recruitment of nonphosphorylated dimeric STAT species to the cytosolic face of membranes including at the cytoplasmic tails of respective receptor complexes, the conformational changes subsequent to phosphorylation and the structural bases for the targeting and functions of STAT proteins within the cytoplasm per se.
近年来,原始细胞因子-信号转导和转录激活因子(STAT)信号转导模式的几个关键原则不得不进行修订。首先,非磷酸化的“无活性”STATs以游离单体形式存在于细胞质中,仅在酪氨酸磷酸化后才二聚化的观念,已被细胞质中未磷酸化的STATs主要以二聚体和高分子量“信号转导体”复合物形式存在的认识所取代。其次,STAT家族中酪氨酸或丝氨酸残基或两者的磷酸化是转录激活所必需的观念,已被非磷酸化的STATs也可具有转录活性这一认识所取代,尽管其作用的靶基因集与磷酸化的STATs不同。第三,STATs在质膜上通过磷酸化激活后再导入细胞核的观念,已被即使是非磷酸化的STATs也始终以组成性方式在细胞质和细胞核之间穿梭的认识所取代。第四,STATs从质膜到核输入机制的跨细胞质转运仅作为游离的胞质过程发生的观念,已被至少部分这种跨细胞质转运是通过与膜相关的小窝和内吞运输介导的(“信号内体”假说)这一认识所取代。第五,激活的STAT3靶向并隔离到细胞质中长寿的内体需要考虑STAT3介导的从质膜到细胞质膜目的地的“信号转导”,这可能在细胞质中发挥作用。实际上,在组织切片中,许多离散的组织学细胞类型几乎仅在细胞质中显示磷酸化的STAT3,细胞核中则很少(如果有的话)。新的挑战包括确定将非磷酸化二聚体STAT种类募集到膜的胞质面(包括各自受体复合物的细胞质尾部)的结构基础、磷酸化后的构象变化以及STAT蛋白在细胞质内靶向和功能的结构基础。