PIWI 结合 RNA 生物发生
中文名称
通路描述
在人类和小鼠的生殖细胞中，PIWI 结合 RNA（piRNA）的前体从几百个序列簇、单个转座子、间隔区及基因组中的基因转录而来。这些较长的转录本经加工产生 26-30 个核苷酸的 piRNA，该过程独立于 DICER 酶（负责微 RNA 和小干扰 RNA）。piRNA 的初始加工步骤是 PLD6 酶切割产生成熟的 5' 端。PLD6 切割产物与 PIWIL1（HIWI, MIWI）或 PIWIL2（HILI, MILI）等复合物结合。3'端由未知的外切酶修剪以生成成熟的 piRNA。PIWIL1:piRNA 复合物似乎参与细胞质中的转录后沉默，而 PIWIL2:piRNA 复合物则在细胞质中进一步从转座子转录本和其他转录本生成 piRNA。来自 PIWIL2:piRNA 的切割产物可加载到 PIWIL2 或 PIWIL4（HIWI2, MIWI2）中。加载到 PIWIL2 形成一种称为“乒乓循环”的细胞质扩增循环，从切割的前体 RNA 产生更多的 PIWIL2:piRNA 复合物。加载到 PIWIL4 形成包含 TDRD9 的复合物，该复合物转运至细胞核并指导同源位点的 DNA 甲基化，导致精子发生期间的转录沉默。piRNA 介导的转录沉默有助于限制基因组内内源转座子（如 L1 元件）的转座。
英文描述
TNF receptor superfamily (TNFSF) members mediating non-canonical NF-kB pathway Activation of NF-kB is fundamental to signal transduction by members of the TNFRSF. Expression of NF-kB target genes is essential for mounting innate immune responses to infectious microorganisms but is also important for the proper development and cellular compartmentalization of secondary lymphoid organs necessary to orchestrate an adaptive immune response.
NF-kB transcription factor family is activated by two distinct pathways: the canonical pathway involving NF-kB1 and the non-canonical pathway involving NF-kB2. Unlike NF-kB1 signalling, which can be activated by a wide variety of receptors, the NF-kB2 pathway is typically activated by a subset of receptor and ligand pairs belonging to the tumor necrosis factor receptor (TNF) super family (TNFRSF) members. These members include TNFR2 (Rauert et al. 2010), B cell activating factor of the TNF family receptor (BAFFR also known as TNFRSF13C) (Kayagaki et al. 2002, CD40 (also known as TNFRSF5) (Coope et al. 2002, lymphotoxin beta-receptor (LTBR also known as TNFRSF3) (Dejardin et al. 2002), receptor activator for nuclear factor kB (RANK also known as TNFRSF11A) (Novack et al. 2003), CD27 and Fibroblast growth factor-inducible immediate-early response protein 14 (FN14 also known as TNFRSF12A) etc. These receptors each mediate specific biological roles of the non-canonical NF-kB. These non-canonical NF-kB-stimulating receptors have one thing in common and is the presence of a TRAF-binding motif, which recruits different TNF receptor-associated factor (TRAF) members, particularly TRAF2 and TRAF3, to the receptor complex during ligand ligation (Grech et al. 2004, Bishop & Xie 2007). Receptor recruitment of these TRAF members leads to their degradation which is a critical step leading to the activation of NIK and induction of p100 processing (Sun 2011, 2012).
NF-kB transcription factor family is activated by two distinct pathways: the canonical pathway involving NF-kB1 and the non-canonical pathway involving NF-kB2. Unlike NF-kB1 signalling, which can be activated by a wide variety of receptors, the NF-kB2 pathway is typically activated by a subset of receptor and ligand pairs belonging to the tumor necrosis factor receptor (TNF) super family (TNFRSF) members. These members include TNFR2 (Rauert et al. 2010), B cell activating factor of the TNF family receptor (BAFFR also known as TNFRSF13C) (Kayagaki et al. 2002, CD40 (also known as TNFRSF5) (Coope et al. 2002, lymphotoxin beta-receptor (LTBR also known as TNFRSF3) (Dejardin et al. 2002), receptor activator for nuclear factor kB (RANK also known as TNFRSF11A) (Novack et al. 2003), CD27 and Fibroblast growth factor-inducible immediate-early response protein 14 (FN14 also known as TNFRSF12A) etc. These receptors each mediate specific biological roles of the non-canonical NF-kB. These non-canonical NF-kB-stimulating receptors have one thing in common and is the presence of a TRAF-binding motif, which recruits different TNF receptor-associated factor (TRAF) members, particularly TRAF2 and TRAF3, to the receptor complex during ligand ligation (Grech et al. 2004, Bishop & Xie 2007). Receptor recruitment of these TRAF members leads to their degradation which is a critical step leading to the activation of NIK and induction of p100 processing (Sun 2011, 2012).
所含基因
15 个基因