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Paradigm shift: the primary function of the Adiponectin Receptors is to regulate cell membrane composition

机译:范式偏移:脂联素受体的主要功能是调节细胞膜组合物

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摘要

The role of PAQR-2 in membrane homeostasis. Conditions that promote membrane rigidification, such as SFA-rich diets or low temperature, stimulate the formation, hence activation, of the PAQR-2/IGLR-2 complex. While PAQR-2 is definitely an ADIPOR ortholog, no functional homolog of IGLR-2 has yet been identified in mammals. Genetic studies reveal that two downstream branches mediate the effects of the PAQR-2/IGLR-2 complex: (1) Branch 1 stimulates the transcription of fatty acid desaturase genes and can be replaced by gain-of-function mutations in NHR-49 (homologous to the mammalian PPARs), MDT-15 or SBP-1; and (2) Branch 2 stimulates the production/incorporation of PUFAs into phospholipids and can be replaced by loss-of-function mutations in FLD-1 (homologous to the mammalian TLCD1/2 proteins) or ACS-13. The ultimate output of PAQR-2 signaling is to increase the UFA content in phospholipids, which promotes fluidity
机译:PAQR-2在膜稳态中的作用。促进致膜刚性的条件,例如富含SFA的饮食或低温,刺激PAQR-2 / IGLR-2复合物的形成,因此激活。虽然PAQR-2绝对是Adipor Ortholog,但在哺乳动物中没有IGLR-2的功能同源物。遗传学研究表明,两个下游分支介导PAQR-2 / IGLR-2复合物的效果:(1)分支1刺激脂肪酸去饱和酶基因的转录,可以通过NHR-49中的功能性突变代替(对哺乳动物PPAR的同源物,MDT-15或SBP-1; (2)分支2刺激Pufas的生产/掺入磷脂,可以通过FLD-1中的功能突变(与哺乳动物TLCD1 / 2蛋白同源)或ACS-13代替。 PAQR-2信号传导的最终输出是增加磷脂中的UFA含量,促进流动性

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