Wang, Chen, Yeo, Karsli-Uzunbas, White, Mizushima, Virgin, Guan: "Elevated p62/SQSTM1 determines the fate of autophagy-deficient neural stem cells by increasing superoxide." in: The Journal of cell biology, Vol. 212, Issue 5, pp. 545-60, (2016) (PubMed).
Zhang, Li, Zhang, Zhang, Teves, Liu, Strauss, Pazour, Foster, Hess, Zhang: "Intraflagellar transport protein IFT20 is essential for male fertility and spermiogenesis in mice." in: Molecular biology of the cell, (2016) (PubMed).
Wu, Zhang, Lu, Xia, Zhou, Petrof, Claud, Chen, Chang, Carmeliet, Sun: "Intestinal epithelial vitamin D receptor deletion leads to defective autophagy in colitis." in: Gut, Vol. 64, Issue 7, pp. 1082-94, (2015) (PubMed).
Wang, Mendonsa, Symington, Zhang, Cadwell, Virgin, Mysorekar: "Atg16L1 deficiency confers protection from uropathogenic Escherichia coli infection in vivo." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 109, Issue 27, pp. 11008-13, (2012) (PubMed).
Nascimento-Ferreira, Santos-Ferreira, Sousa-Ferreira, Auregan, Onofre, Alves, Dufour, Colomer Gould, Koeppen, Déglon, Pereira de Almeida: "Overexpression of the autophagic beclin-1 protein clears mutant ataxin-3 and alleviates Machado-Joseph disease." in: Brain : a journal of neurology, Vol. 134, Issue Pt 5, pp. 1400-15, (2011) (PubMed).
Travassos, Carneiro, Ramjeet, Hussey, Kim, Magalhães, Yuan, Soares, Chea, Le Bourhis, Boneca, Allaoui, Jones, Nuñez, Girardin, Philpott: "Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry." in: Nature immunology, Vol. 11, Issue 1, pp. 55-62, (2009) (PubMed).
Nomura, Uzawa, Yamano, Fushimi, Ishigami, Kouzu, Koike, Siiba, Bukawa, Yokoe, Kubosawa, Tanzawa: "Overexpression and altered subcellular localization of autophagy-related 16-like 1 in human oral squamous-cell carcinoma: correlation with lymphovascular invasion and lymph-node metastasis." in: Human pathology, Vol. 40, Issue 1, pp. 83-91, (2008) (PubMed).
Target
ATG16L1
(ATG16 Autophagy Related 16-Like 1 (ATG16L1))
APG16L antikoerper, ATG16A antikoerper, ATG16L antikoerper, IBD10 antikoerper, WDR30 antikoerper, 1500009K01Rik antikoerper, Apg16l antikoerper, Atg16l antikoerper, Wdr30 antikoerper, atg16 antikoerper, atg16l antikoerper, fb57e05 antikoerper, wu:fb57e05 antikoerper, zgc:110147 antikoerper, autophagy related 16 like 1 antikoerper, autophagy related 16-like 1 (S. cerevisiae) antikoerper, autophagy related 16-like 1 antikoerper, autophagy related 16 like 1 S homeolog antikoerper, ATG16 autophagy related 16-like 1 (S. cerevisiae) antikoerper, ATG16L1 antikoerper, Atg16l1 antikoerper, atg16l1 antikoerper, atg16l1.S antikoerper
Hintergrund
Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). The APG12-APG5-APG16L complex is esential for the elongation of autophagic isolation membranes. This complex initially associates in uniform distribution with small vesicle membranes. During membrane elongation, the complex partitions, with a great concentration building on the outer side of the isolation membrane. Upon completion of the formation of the autophagosome, the APG12-APG5-APG16L dissociates from the membrane.