NTRK3 (TRKC) 信号传导
中文名称
通路描述
NTRK3 (TRKC) 属于神经生长因子受体酪氨酸激酶家族，包括 NTRK1 (TRKA) 和 NTRK2 (TRKB)。NTF3（也称为 NT-3）是 NTRK3 的配体。与其他 NTRK 受体和受体酪氨酸激酶类似，配体结合诱导受体二聚化，随后在受体细胞内（细胞质）保守酪氨酸上发生自磷酸化（Lamballe et al. 1991, Philo et al. 1994, Tsoulfas et al. 1996, Yuen and Mobley 1999, Werner et al. 2014）。这些保守酪氨酸是适配器蛋白的结合位点，触发下游信号级联反应。通过 PLCG1 (Marsh and Palfrey 1996, Yuen and Mobley 1999, Huang and Reichardt 2001)、PI3K (Yuen and Mobley 1999, Tognon et al. 2001, Huang and Reichardt 2001, Morrison et al. 2002, Lannon et al. 2004, Jin et al. 2008) 和 RAS (Marsh and Palfrey 1996, Gunn-Moore et al. 1997, Yuen and Mobley 1999, Gromnitza et al. 2018) 的下游激活的 NTRK3 调节细胞存活、增殖和运动。在没有配体的情况下，NTRK3 作为依赖性受体触发 BAX 和 CASP9 依赖的细胞死亡 (Tauszig-Delamasure et al. 2007, Ichim et al. 2013)。据报道，NTRK3 通过 JAK2 激活 STAT3，但确切机制尚未阐明 (Kim et al. 2016)。据报道，NTRK3 与适配器蛋白 SH2B2 相互作用，但该相互作用在生物学中的作用尚未确定 (Qian et al. 1998)。受体蛋白酪氨酸磷酸酶 PTPRO 和 PTPRS (PTPsigma) 通过去磷酸化 NTRK3 负向调节 NTRK3 信号传导 (Beltran et al. 2003, Faux et al. 2007, Hower et al. 2009, Tchetchelnitski et al. 2014)。除了 NTRK3 的顺式去磷酸化外，前突触 PTPRS 的细胞外域可以与突触后 NTRK3 的细胞外域在反式结合，促进突触形成 (Takahashi et al. 2011, Coles et al. 2014)。
英文描述
Ethanol oxidation Ethanol and related alcohols can be ingested as part of the diet and are formed by microorganisms in the intestinal tract. Ethanol oxidation to acetate occurs primarily in liver cells in a multistep process first described by Racker (1949). First, in the cytosol, ethanol is oxidized to acetaldehyde, with the formation of NADH. Second, in the mitochondrion, acetaldehyde is oxidized to acetate with the formation of NADH. Finally, acetate in the mitochondrion can be condensed with coenzyme A to form acetyl CoA. Polymorphisms in the enzymes catalyzing the first two steps are associated with variation in the efficiency of alcohol catabolism in human populations (Chen et al. 1999; Lange et al. 1976; Jornvall 1985). The molecular mechanism by which cytosolic acetaldehyde enters the mitochondrial matrix is not known (Lemasters 2007).Cytosolic enzymes capable of oxidizing acetaldehyde to acetate have also been identified and characterized in vitro (Inoue et al. 1979) so a purely cytosolic pathway for ethanol oxidation to acetate and conversion to acetyl-CoA can be annotated. The role of this pathway in vivo is unclear, though limited attempts to correlate deficiencies in the cytosolic enzyme with alcohol intolerance have yielded suggestive data (Yoshida et al. 1989). Additional peroxisomal and microsomal pathways for the oxidation of ethanol to acetaldehyde have been described; their physiological significance is unclear and they are not annotated here.
所含基因
12 个基因