TMEM59 Protein, 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 Protein functions as a regulator of autophagy in response to S.aureus infection, actively promoting the activation of LC3 (MAP1LC3A, MAP1LC3B, or MAP1LC3C). This regulatory role is executed through interaction with ATG16L1, leading to the formation of a functional complex between LC3 and ATG16L1. This interaction, documented in various studies, facilitates LC3 lipidation, ultimately resulting in the activation of autophagy. Beyond its involvement in autophagy regulation, TMEM59 Protein plays a crucial role in modulating the O-glycosylation and complex N-glycosylation steps during the Golgi maturation of several proteins, including APP, BACE1, SEAP, or PRNP. Notably, it inhibits the transport of APP to the cell surface and subsequent shedding. In molecular terms, TMEM59 Protein interacts directly with ATG16L1, specifically through its WD repeats, forming a pivotal connection in the intricate network governing autophagic processes and glycosylation events.

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.