Data |
Western Blotting

|
Clonality |
Monoclonal
|
Clone |
1F12 |
Isotype
(Immunized Animal)
|
Mouse IgG1 κ
|
Applications |
- WB
- 1 µg/mL
 - FCM*
- reported. (PMID: 25597631)
 - IH*
- reported. (PMID: 24089213)

|
Immunogen
(Antigen) |
Recombinant Human ATG16L1 TV2 (85-588 a.a.)
|
Reactivity
[Gene ID] |
Human[55054], Mouse[77040], Rat[363278] |
Storage buffer |
1 mg/mL in PBS/50% glycerol, pH 7.2
|
Storage temp. |
-20°C
|
Conjugate |
Unlabeled |
Manufacturer |
MBL |
Alternative names |
ATG16L1, autophagy related 16-like 1 (S. cerevisiae), IBD10, WDR30, APG16L, ATG16A, Apg16l
|
Background |
Autophagy is a process of intracellular bulk degradation in which cytoplasmic components including organelles are sequestered within double-membrane vesicles that deliver the contents to the lysosome/vacuole for degradation. Autophagy has two ubiquitin-like conjugation systems, the Atg12 and LC3-II systems. In the Atg12 conjugation system, the Atg16L-Atg12-Atg5 forms 800 kDa complex that elongates autophagic isolation membrane. After completion of the formation of the autophagosome, the Atg12-Atg5-Atg16L complex dissociates from the membrane. In recent study, nonsynonymous SNP analysis has indicated that ATG16L1 is a Crohn's disease susceptibility gene. |
Related products |
8485 Autophagy Ab Sampler Set PM040 Anti-Atg16L pAb M151-3 Anti-Atg10 (Human) mAb M154-3 Anti-Atg12 (Human) mAb M153-3 Anti-Atg5 mAb PM050 Anti-Atg5 pAb PM036 Anti-LC3 pAb M152-3 Anti-LC3 mAb PD017 Anti-Beclin 1 pAb PM072 Anti-VMP1 pAb PM045 Anti-p62 (SQSTM1) pAb M133-3 Anti-Atg3 mAb PM039 Anti-Atg7 (Human) pAb
|
Citations |
Western Blotting - Adolph TE et al. Paneth cells as a site of origin for intestinal inflammation. Nature 503, 272-6 (2013)(PMID:24089213)
- Myeku N et al. Dynamics of the degradation of ubiquitinated proteins by proteasomes and autophagy: association with sequestosome 1/p62. J Biol Chem 286, 22426-40 (2011)(PMID:21536669)
- Murthy A et al. A Crohn's disease variant in Atg16l1 enhances its degradation by caspase 3. Nature 506, 456-62 (2014)(PMID:24553140)
- Boada-Romero E et al. The T300A Crohn's disease risk polymorphism impairs function of the WD40 domain of ATG16L1. Nat Commun. 7, 11821 (2016)(PMID:27273576)
- Diamanti MA et al. IKKα controls ATG16L1 degradation to prevent ER stress during inflammation. J Exp Med. 214, 423-437 (2017)(PMID:28082356)
- Slowicka K et al. Physical and functional interaction between A20 and ATG16L1-WD40 domain in the control of intestinal homeostasis. Nat Commun. 10, 1834 (2019)(PMID:31015422)
- Shizukuishi S et al. Streptococcus pneumoniae hijacks host autophagy by deploying CbpC as a decoy for Atg14 depletion. EMBO Rep. 21, e49232 (2020)(PMID:32239622)
Immunoprecipitation - Serramito-Gómez I et al. Regulation of cytokine signaling through direct interaction between cytokine receptors and the ATG16L1 WD40 domain. Nat Commun. 11, 5919 (2020)(PMID:33219218)
Flow Cytometry - Morozova K et al. Annexin A2 promotes phagophore assembly by enhancing Atg16L+ vesicle biogenesis and homotypic fusion. Nat Commun. 6, 5856 (2015)(PMID:25597631)
Immunocytochemistry - Kucharewicz K et al. Simultaneous induction and blockade of autophagy by a single agent. Cell Death Dis. 9, 353 (2018)(PMID:29500364)
- Chu J et al. ATG4B inhibitor FMK-9a induces autophagy independent on its enzyme inhibition. Arch Biochem Biophys. 644, 29-36 (2018)(PMID:29510087)
Immunohistochemistry - Adolph TE et al. Paneth cells as a site of origin for intestinal inflammation. Nature 503, 272-6 (2013)(PMID:24089213)
- Asai E et al. Spatiotemporal alterations of autophagy marker LC3 in rat skin fibroblasts during wound healing process. Fukushima J Med Sci. 64, 15-22 (2018)(PMID:29343655)
Immunofluorescence - Morozova K et al. Annexin A2 promotes phagophore assembly by enhancing Atg16L+ vesicle biogenesis and homotypic fusion. Nat Commun. 6, 5856 (2015)(PMID:25597631)
|
Product category |
- Research area
- Autophagy
|