注册 | 登录
点击这里给我发消息
所有产品
  • 所有产品
  • 一抗
  • 裂解液
>   首页   >   产品   >   一抗   >   精选抗体   >   细胞自噬抗体   >   ATG16L Antibody (C-term)   

ATG16L Antibody (C-term)

Purified Rabbit Polyclonal Antibody (Pab)

     
  • 1 - ATG16L Antibody (C-term) AP1817c
    Western blot analysis of hAPG16L-K366 (Cat.#AP1817c) in NIH-3T3, HepG2, Hela, Jurkat and NCI-H460 cell line lysates (35ug/lane). APG16L (arrow) was detected using the purified Pab.
  • 14 - ATG16L Antibody (C-term) AP1817c
    Formalin-fixed and paraffin-embedded human colon carcinoma tissue reacted with Autophagy APG16L antibody (C-term), which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated.
  • 产品详情
  • 文献引用 : 1
  • 实验流程
  • 背景知识
Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IHC-P, E
Primary Accession Q676U5
Reactivity Human
Host Rabbit
Clonality Polyclonal
Isotype Rabbit IgG
Calculated MW 68265 Da
Antigen Region 454-483 aa
Additional Information
Gene ID 55054
Other Names Autophagy-related protein 16-1, APG16-like 1, ATG16L1, APG16L
Target/Specificity This ATG16L antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 454-483 amino acids from the C-terminal region of human ATG16L.
Dilution WB~~1:1000
IHC-P~~1:100~500
E~~Use at an assay dependent concentration.
Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.
StorageMaintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsATG16L Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
Name ATG16L1 {ECO:0000303|PubMed:17200669, ECO:0000312|HGNC:HGNC:21498}
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) (PubMed:23376921, PubMed:23392225, PubMed:24553140, PubMed:24954904, PubMed:27273576, PubMed:29317426, PubMed:30778222, PubMed:33909989). Acts as a molecular hub, coordinating autophagy pathways via distinct domains that support either canonical or non- canonical signaling (PubMed:29317426, PubMed:30778222). 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 (PubMed:23376921, PubMed:23392225, PubMed:24553140, PubMed:24954904, PubMed:27273576). Thereby, controls the elongation of the nascent autophagosomal membrane (PubMed:23376921, PubMed:23392225, PubMed:24553140, PubMed:24954904, PubMed:27273576). 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 (By similarity). 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 (PubMed:33909989). Non-canonical autophagy plays a key role in epithelial cells to limit lethal infection by influenza A (IAV) virus (By similarity). Regulates mitochondrial antiviral signaling (MAVS)-dependent type I interferon (IFN-I) production (PubMed:22749352, PubMed:25645662). Negatively regulates NOD1- and NOD2-driven inflammatory cytokine response (PubMed:24238340). Instead, promotes an autophagy-dependent antibacterial pathway together with NOD1 or NOD2 (PubMed:20637199). Plays a role in regulating morphology and function of Paneth cell (PubMed:18849966).
Cellular Location Cytoplasm. Preautophagosomal structure membrane; Peripheral membrane protein. Endosome membrane; Peripheral membrane protein. Lysosome membrane; Peripheral membrane protein. Note=Recruited to omegasomes membranes by WIPI2 (By similarity). Omegasomes are endoplasmic reticulum connected strutures at the origin of preautophagosomal structures (By similarity). Localized to preautophagosomal structure (PAS) where it is involved in the membrane targeting of ATG5 (By similarity). Also localizes to discrete punctae along the ciliary axoneme (By similarity). Upon activation of non-canonical autophagy, recruited to single-membrane endolysosomal compartments (PubMed:29317426). Under starved conditions, the ATG12-ATG5-ATG16L1 complex is translocated to phagophores driven by RAB33B (PubMed:32960676). {ECO:0000250|UniProtKB:Q8C0J2, ECO:0000269|PubMed:29317426, ECO:0000269|PubMed:32960676}
Research Areas

For Research Use Only. Not For Use In Diagnostic Procedures.

BACKGROUND

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.

REFERENCES

Baehrecke EH. Nat Rev Mol Cell Biol. 6(6):505-10. (2005)
Lum JJ, et al. Nat Rev Mol Cell Biol. 6(6):439-48. (2005)
Greenberg JT. Dev Cell. 8(6):799-801. (2005)
Levine B. Cell. 120(2):159-62. (2005)
Shintani T and Klionsky DJ. Science. 306(5698):990-5. (2004)

FeedBack

终于等到您。ABCEPTA(百远生物)抗体产品。
点击下方“我要评价 ”按钮提交您的反馈信息,您的反馈和评价是我们最宝贵的财富之一,
我们将在1-3个工作日内处理您的反馈信息。

如有疑问,联系:0512-88856768 tech-china@abcepta.com.


我要评价