线粒体自噬 - 动物
中文名称
通路描述
线粒体是细胞的能量工厂，对于真核细胞的生长和功能至关重要。然而，氧化磷酸化过程中产生的有害副产物称为活性氧（ROS），会导致线粒体功能障碍。如果损伤过重无法修复，这些线粒体会被特定的自噬模式选择性识别并靶向降解，称为线粒体自噬。线粒体膜电位丧失可诱导线粒体自噬，涉及激酶 PINK1 和 E3 泛素连接酶 Parkin。PINK1 作为线粒体去极化的传感器，招募 Parkin，随后通过泛素依赖性方式招募线粒体自噬受体。此外，还存在几种 PINK1/Parkin 无关的线粒体自噬途径，其中需要一组含有 LIR 的受体，以应对不同的刺激。线粒体自噬有助于维持健康的线粒体网络并防止程序性细胞死亡。
英文描述
FASTK family proteins regulate processing and stability of mitochondrial RNAs Fas-activated serine/threonine kinase (FASTK) and its homologs FASTKD1-5 each contain three conserved domains (FAST_1, FAST_2, and RAP) that bind RNA (Castello et al. 2012, Baltz et al. 2012). FASTKD1-5 and the short isoform of FASTK localize to mitochondria where they participate in regulating the processing and stability of RNA (Simarro et al. 2010, reviewed in Jourdain et al. 2017).
FASTK interacts with the 3' end of the MT-ND6 mRNA and protects the mRNA from degradation by the degradosome, SUPV3L1:PNPT1 (Jourdain et al. 2015). The MT-ND6 mRNA is unusual in being processed from the large L-strand precursor without flanking tRNA genes and thus without canonical processing by RNAse P and RNase Z. FASTK may, therefore, participate in an uncharacterized non-canonical mechanism of RNA processing or protect 3' ends produced by such a mechanism.
FASTKD1 acts to reduce the abundance of the MT-ND3 mRNA by an uncharacterized mechanism (Boehm et al. 2017).
FASTKD2 binds the 16S rRNA and the MT-ND6 mRNA and participates in their processing and expression (Antonicka and Shoubridge 2015, Popow et al. 2015). FASTKD2 interacts with several mitochondrial proteins including MTERFD1, TRUB2, WBSCR16, and NGRN (Antonicka et al. 2017).
FASTKD3 increases levels of five mitochondrial mRNAs (MT-ND2, MT-ND3, MT-CYB, MT-CO2, and the MT-ATP8/6 bicistronic mRNA) and increases translation of MT-CO1 mRNA through uncharacterized mechanisms (Boehm et al. 2016, Ohkubo et al. 2021).
TBRG4 (FASTKD4) binds most RNAs transcribed from the H-strand and enhances the expression levels of MT-ATP8/6, MT-CO1, MT-CO2, MT-CO3, MT-ND3, MT-CYB, and MT-ND5 mRNAs (Wolf and Mootha 2014, Boehm et al. 2017, Ohkubo et al. 2021). TBRG4 stabilizes MT-CO1, MT-ND3, and MT-CO2 mRNAs and assists the processing of MT-ND5 and MT-CYB mRNAs (Boehm et al. 2017, Ohkubo et al. 2021).
FASTKD5 binds 12S rRNA and all mRNAs except MT-ND3 and reduces levels of MT-ATP8/6, MT-CO1, MT-CO3, MT-ND5, and MT-CYB mRNAs (Antonicka and Shoubridge 2015, Ohkubo et al. 2021). .
FASTK interacts with the 3' end of the MT-ND6 mRNA and protects the mRNA from degradation by the degradosome, SUPV3L1:PNPT1 (Jourdain et al. 2015). The MT-ND6 mRNA is unusual in being processed from the large L-strand precursor without flanking tRNA genes and thus without canonical processing by RNAse P and RNase Z. FASTK may, therefore, participate in an uncharacterized non-canonical mechanism of RNA processing or protect 3' ends produced by such a mechanism.
FASTKD1 acts to reduce the abundance of the MT-ND3 mRNA by an uncharacterized mechanism (Boehm et al. 2017).
FASTKD2 binds the 16S rRNA and the MT-ND6 mRNA and participates in their processing and expression (Antonicka and Shoubridge 2015, Popow et al. 2015). FASTKD2 interacts with several mitochondrial proteins including MTERFD1, TRUB2, WBSCR16, and NGRN (Antonicka et al. 2017).
FASTKD3 increases levels of five mitochondrial mRNAs (MT-ND2, MT-ND3, MT-CYB, MT-CO2, and the MT-ATP8/6 bicistronic mRNA) and increases translation of MT-CO1 mRNA through uncharacterized mechanisms (Boehm et al. 2016, Ohkubo et al. 2021).
TBRG4 (FASTKD4) binds most RNAs transcribed from the H-strand and enhances the expression levels of MT-ATP8/6, MT-CO1, MT-CO2, MT-CO3, MT-ND3, MT-CYB, and MT-ND5 mRNAs (Wolf and Mootha 2014, Boehm et al. 2017, Ohkubo et al. 2021). TBRG4 stabilizes MT-CO1, MT-ND3, and MT-CO2 mRNAs and assists the processing of MT-ND5 and MT-CYB mRNAs (Boehm et al. 2017, Ohkubo et al. 2021).
FASTKD5 binds 12S rRNA and all mRNAs except MT-ND3 and reduces levels of MT-ATP8/6, MT-CO1, MT-CO3, MT-ND5, and MT-CYB mRNAs (Antonicka and Shoubridge 2015, Ohkubo et al. 2021). .
所含基因
3 个基因