• Western blot analysis of lysates from SH-SY5Y cells, primary antibody was diluted at 1:1000, 4°C over night

Anti-IRGM antibody (101-150 aa) (STJ192572)

SKU:
STJ192572

Current Stock:
Host: Rabbit
Applications: WB/ELISA
Reactivity: Human/Rat/Mouse
Note: STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Short Description: Rabbit polyclonal antibody anti-Immunity-related GTPase family M protein (101-150 aa) is suitable for use in Western Blot and ELISA research applications.
Clonality: Polyclonal
Conjugation: Unconjugated
Isotype: IgG
Formulation: Liquid in PBS containing 50% Glycerol and 0.02% Sodium Azide.
Purification: The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration: 1 mg/mL
Dilution Range: WB 1:500-2000
ELISA 1:5000-20000
Storage Instruction: Store at-20°C for up to 1 year from the date of receipt, and avoid repeat freeze-thaw cycles.
Gene Symbol: IRGM
Gene ID: 345611
Uniprot ID: IRGM_HUMAN
Immunogen Region: 101-150 aa
Specificity: IRGM Polyclonal Antibody detects endogenous levels of protein.
Immunogen: Synthesized peptide derived from the human protein at the amino acid range 101-150
Post Translational Modifications Ubiquitinated via 'Lys-63'-linked polyubiquitination in a NOD2-dependent process. 'Lys-63'-linked polyubiquitination is required for interactions with the core autophagy factors.
Function Immunity-related GTPase that plays important roles in innate immunity and inflammatory response. Acts as a dynamin-like protein that binds to intracellular membranes and promotes remodeling and trafficking of those membranes. Required for clearance of acute protozoan and bacterial infections by interacting with autophagy and lysosome regulatory proteins, thereby promoting the fusion of phagosomes with lysosomes for efficient degradation of cargo including microbes. Regulates selective autophagy, including xenophagy and mitophagy, both directly and indirectly. Directly regulates autophagy by acting as a molecular adapter that promotes the coassembly of the core autophagy machinery to mediate antimicrobial defense: IRGM (1) activates AMPK, which in turn phosphorylates ULK1 and BECN1 to induce autophagy, (2) promotes the coassembly of ULK1 and BECN1, enhancing BECN1-interacting partners and (3) influences the composition of the BECN1 complex, by competing with the negative regulators BCL2 and RUBCN, to trigger autophagy. Also activates autophagy by promoting recruitment of STX17 to autophagosomes. In collaboration with ATG8 proteins, regulate lysosomal biogenesis, a fundamental process for any autophagic pathway, by promoting TFEB dephosphorylation. Also modulates autophagy by assisting with autophagosome formation and preventing lysosomal deacidification. While activating autophagy, acts as a key negative regulator of the inflammatory and interferon responses both by (1) promoting mitophagy and (2) mediating autophagy-dependent degradation of effectors of the inflammatory response. Promotes degradation of damaged and IFNG/IFN-gamma-stressed mitochondria via mitophagy, preventing cytosolic release of ligands that activate inflammation. Acts as a suppressor of inflammation by promoting recruitment of inflammation effectors, such as CGAS, RIGI/RIG-I and NLRP3, to autophagosome membranes, leading to their SQSTM1/p62-dependent autophagic degradation. Also directly inhibits assembly of the NLRP3 inflammasome by preventing the association between NLRP3 and PYCARD. Acts as a negative regulator of antiviral innate immune response by suppressing the RIPK2-dependent pro-inflammatory response: mediates recruitment of RIPosomes, composed of RIPK2 and NOD1 or NOD2, to autophagosome membranes, promoting their SQSTM1/p62-dependent autophagic degradation. Isoform IRGMd: Acts as a positive regulator of mitophagy in response to intracellular mycobacteria infection: specifically binds cardiolipin, leading to its translocation to mitochondria, where it promotes affected mitochondrial fission and mitophagy. (Microbial infection) Following infection by hepatitis C virus (HCV), promotes HCV-triggered membrane remodeling, leading to autophagy and Golgi fragmentation, a step required for HCV replication.
Protein Name Immunity-Related Gtpase Family M Protein
Immunity-Related Gtpase Family M Protein 1
Interferon-Inducible Protein 1
Lps-Stimulated Raw 264.7 Macrophage Protein 47 Homolog
Lrg-47
Cellular Localisation Golgi Apparatus Membrane
Cell Membrane
Cytoplasmic Vesicle
Phagosome Membrane
Autophagosome Membrane
Lysosome Membrane
Late Endosome Membrane
Mitochondrion Membrane
Cell Projection
Phagocytic Cup
Behaves Like An Integral Membrane Protein
Recruited To The Plasma Membrane Around Forming Phagocytic Cups
It Remains Associated With Maturing Phagosomes
Association With Phagosomes Is Dependent On Nucleotide-Binding But Is Ifng-Independent
Also Detected In Late Endosomes And Lysosomes
Isoform Irgmd: Mitochondrion
Alternative Antibody Names Anti-Immunity-Related Gtpase Family M Protein antibody
Anti-Immunity-Related Gtpase Family M Protein 1 antibody
Anti-Interferon-Inducible Protein 1 antibody
Anti-Lps-Stimulated Raw 264.7 Macrophage Protein 47 Homolog antibody
Anti-Lrg-47 antibody
Anti-IRGM antibody
Anti-IFI1 antibody
Anti-IRGM1 antibody
Anti-LRG47 antibody

Information sourced from Uniprot.org

12 months for antibodies. 6 months for ELISA Kits. Please see website T&Cs for further guidance