TMEM59 蛋白, Human (Cell-Free, His)

TMEM59 Protein actively regulates autophagy during S.aureus infection by promoting LC3 activation through interaction with ATG16L1. This documented interaction facilitates LC3 lipidation, ultimately activating autophagy. Beyond autophagy, TMEM59 crucially modulates O-glycosylation and complex N-glycosylation in Golgi maturation, impacting proteins like APP, BACE1, SEAP, and PRNP. Notably, it hinders APP transport to the cell surface and shedding, forming a pivotal connection in autophagic and glycosylation processes through direct interaction with ATG16L1. TMEM59 Protein, Human (Cell-Free, His) is the recombinant human-derived TMEM59 protein, expressed by E. coli Cell-free, with C-10*His labeled tag. The total length of TMEM59 Protein, Human (Cell-Free, His) is 287 a.a., with molecular weight of 35.5 kDa.

TMEM59 蛋白作为响应金黄色葡萄球菌感染的自噬调节剂发挥作用，积极促进 LC3（MAP1LC3A、MAP1LC3B 或 MAP1LC3C）的激活。这种调节作用是通过与 ATG16L1 相互作用来执行的，导致 LC3 和 ATG16L1 之间形成功能复合物。各种研究记录了这种相互作用，促进 LC3 脂化，最终导致自噬的激活。除了参与自噬调节之外，TMEM59 蛋白还在多种蛋白（包括 APP、BACE1、SEAP 或 PRNP）高尔基体成熟过程中调节 O-糖基化和复杂的 N-糖基化步骤中发挥着至关重要的作用。值得注意的是，它抑制 APP 向细胞表面的转运以及随后的脱落。从分子角度来看，TMEM59 蛋白直接与 ATG16L1 相互作用，特别是通过其 WD 重复序列，在控制自噬过程和糖基化事件的复杂网络中形成关键连接。

Human

E. coli Cell-free

C-10*His

Q9BXS4 (A37-I323)

9528

AFDSVLGDTASCHRACQLTYPLHTYPKEEELYACQRGCRLFSICQFVDDGIDLNRTKLECESACTEAYSQSDEQYACHLGCQNQLPFAELRQEQLMSLMPKMHLLFPLTLVRSFWSDMMDSAQSFITSSWTFYLQADDGKIVIFQSKPEIQYAPHLEQEPTNLRESSLSKMSYLQMRNSQAHRNFLEDGESDGFLRCLSLNSGWILTTTLVLSVMVLLWICCATVATAVEQYVPSEKLSIYGDLEFMNEQKLNRYPASSLVVVRSKTEDHEEAGPLPTKVNLAHSEI

35.5 kDa

Greater than 90% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.