ATG16L1 Positive Control for STJ500180 is synthetically produced from the sequence and is suitable for use in western blot applications.
Applications
WB
Note
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Product Properties
Dilution Range
WB: 1:500
Formulation
Provided as 100 uL ready-to-use, in SDS-PAGE sample buffer (Laemelli's buffer) containing Tris, pH 6.8, 1 % SDS, Glycerol and Bromophenolblue blue as tracking dye. The sample is reduced by adding 2% beta mercaptoethanol. The protein concentration is
Storage Instruction
Store at-20°C for long term storage. Avoid freeze-thaw cycles.
This is positive control is recommended for use in combination with ATG16L1 antibody STJ500180.
Additional Info
Post Translational Modifications
Proteolytic cleavage by activated CASP3 leads to degradation and may regulate autophagy upon cellular stress and apoptotic stimuli. Phosphorylation at Ser-139 promotes association with the ATG12-ATG5 conjugate to form the ATG12-ATG5-ATG16L1 complex.
Function
Plays an essential role in both canonical and non-canonical autophagy: interacts with ATG12-ATG5 to mediate the lipidation to ATG8 family proteins (MAP1LC3A, MAP1LC3B, MAP1LC3C, GABARAPL1, GABARAPL2 and GABARAP). Acts as a molecular hub, coordinating autophagy pathways via distinct domains that support either canonical or non-canonical signaling. During canonical autophagy, interacts with ATG12-ATG5 to mediate the conjugation of phosphatidylethanolamine (PE) to ATG8 proteins, to produce a membrane-bound activated form of ATG8. Thereby, controls the elongation of the nascent autophagosomal membrane. As part of the ATG8 conjugation system with ATG5 and ATG12, required for recruitment of LRRK2 to stressed lysosomes and induction of LRRK2 kinase activity in response to lysosomal stress. Also involved in non-canonical autophagy, a parallel pathway involving conjugation of ATG8 proteins to single membranes at endolysosomal compartments, probably by catalyzing conjugation of phosphatidylserine (PS) to ATG8. Non-canonical autophagy plays a key role in epithelial cells to limit lethal infection by influenza A (IAV) virus. Regulates mitochondrial antiviral signaling (MAVS)-dependent type I interferon (IFN-I) production. Negatively regulates NOD1- and NOD2-driven inflammatory cytokine response. Instead, promotes an autophagy-dependent antibacterial pathway together with NOD1 or NOD2. Plays a role in regulating morphology and function of Paneth cell.
CytoplasmPreautophagosomal Structure MembranePeripheral Membrane ProteinEndosome MembraneLysosome MembraneRecruited To Omegasomes Membranes By Wipi2Omegasomes Are Endoplasmic Reticulum Connected Strutures At The Origin Of Preautophagosomal StructuresLocalized To Preautophagosomal Structure (Pas) Where It Is Involved In The Membrane Targeting Of Atg5Localizes Also To Discrete Punctae Along The Ciliary AxonemeUpon Activation Of Non-Canonical AutophagyRecruited To Single-Membrane Endolysosomal Compartments
Alternative Peptide Names
Autophagy-Related Protein 16-1 proteinApg16-Like 1 proteinATG16L1 proteinAPG16L proteinUNQ9393 proteinPRO34307 protein
