CREB3 因子激活基因
中文名称
通路描述
CREB3 家族成员（也称为 OASIS 家族）是组织特异性蛋白，每个成员都含有转录激活结构域、促进二聚化和 DNA 结合的碱性亮氨酸拉链（bZIP）结构域，以及锚定到内质网膜上的跨膜结构域（参见 Asada 等 2011, Chan 等 2011, Kondo 等 2011, Fox 和 Andrew 2015）。该家族包括 CREB3（LUMAN）、CREB3L1（OASIS）、CREB3L2（BBF2H7, Tisp40）、CREB3L3（CREB-H）和 CREB3L4（CREB4）。当这些蛋白从内质网转运至高尔基体并被 Golgi 驻留蛋白酶 MBTPS1（S1P）和 MBTPS2（S2P）依次切割时，发生受调控的膜内蛋白水解，释放包含转录激活结构域和 bZIP 结构域的胞质区域。该蛋白片段随后从细胞质转运至细胞核，激活靶基因的转录。CREB3L1、CREB3L2 和 CREB3L3 由内质网应激激活，但导致 CREB3 蛋白转运的机制尚未完全阐明。与 ATF6 因子不同，CREB3 蛋白似乎不与 HSPA5（BiP）相互作用，因此似乎不通过 HSPA5 解离来感知未折叠蛋白。
英文描述
Synthesis of Prostaglandins (PG) and Thromboxanes (TX) The bioactive prostaglandin (PG) signalling molecules, including PGA2, PGE2, PGF2a, and PGI2 (prostacyclin) are synthesised from arachidonate and its products by various prostaglandin synthase type enzymes. Prostaglandin H2 (PGH2) is the starting point for the synthesis of Thromboxanes (TXs) (Buczynski et al. 2009, Vance & Vance 2008). PGs and TXs are collectively known as the prostanoids.
Two enzymes, PTGS1 and 2 (COX1 and 2) both catalyze the two-step conversion of arachidonate to PGH2. PTGS1 is constitutively expressed in many cell types while PTGS2 is induced in response to stress and mediates the syntheses of prostaglandins associated with pain, fever, and inflammation. Aspirin irreversibly inactivates both enzymes (though it acts more efficiently on PTGS1), explaining both its antiinflammatory effects and side effects like perturbed gastic acid secretion. Drugs like celecoxib, by specifically inhibiting PTGS2, have a strong anti-inflammatory effect with fewer side effects. These PTGS2-specific drugs, however, probably because of their effects on the balance of prostaglandin synthesis in platelets and endothelial cells, can also promote blood clot formation (Buczynski et al. 2009; Stables & Gilroy 2011).
Two enzymes, PTGS1 and 2 (COX1 and 2) both catalyze the two-step conversion of arachidonate to PGH2. PTGS1 is constitutively expressed in many cell types while PTGS2 is induced in response to stress and mediates the syntheses of prostaglandins associated with pain, fever, and inflammation. Aspirin irreversibly inactivates both enzymes (though it acts more efficiently on PTGS1), explaining both its antiinflammatory effects and side effects like perturbed gastic acid secretion. Drugs like celecoxib, by specifically inhibiting PTGS2, have a strong anti-inflammatory effect with fewer side effects. These PTGS2-specific drugs, however, probably because of their effects on the balance of prostaglandin synthesis in platelets and endothelial cells, can also promote blood clot formation (Buczynski et al. 2009; Stables & Gilroy 2011).
所含基因
15 个基因