KIAA0652/ATG13 Rabbit mAb
- 产品详情
- 实验流程
- 背景知识
Application
| WB, FC, IP |
|---|---|
| Primary Accession | O75143 |
| Reactivity | Rat, Human, Mouse |
| Host | Rabbit |
| Clonality | Monoclonal Antibody |
| Isotype | IgG |
| Conjugate | Unconjugated |
| Purification | Affinity Purified |
| Calculated MW | 56572 Da |
| Gene ID | 9776 |
|---|---|
| Other Names | ATG13 |
| Dilution | WB~~1:500-1:1000 FC~~1:50-1:100 IP~~1:20-1:50 |
| Format | Liquid in 50mM Tris-Glycine(pH 7.4), 0.15M NaCl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA. |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
For Research Use Only. Not For Use In Diagnostic Procedures.
| Name | ATG13 |
|---|---|
| Synonyms | KIAA0652 |
| Function | Autophagy factor required for autophagosome formation and mitophagy. Target of the TOR kinase signaling pathway that regulates autophagy through the control of the phosphorylation status of ATG13 and ULK1, and the regulation of the ATG13-ULK1-RB1CC1 complex. Through its regulation of ULK1 activity, plays a role in the regulation of the kinase activity of mTORC1 and cell proliferation. |
| Cellular Location | Cytoplasm, cytosol. Preautophagosomal structure. Note=Under starvation conditions, is localized to puncate structures primarily representing the isolation membrane; the isolation membrane sequesters a portion of the cytoplasm resulting in autophagosome formation |
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
ATG13 is a protein kinase required for autophagy. Overexpression of Atg1 suppresses the defects in autophagy observed in Atg13 mutants. Autophagy requires a direct association between Atg1 and Atg13, and is inhibited by TOR-dependent phosphorylation of Atg13 under high-nutrient conditions. Similarly, mammalian Atg13 forms a complex with the Atg1 homologues ULK1/2, along with FIP200, which localizes to autophagic isolation membranes and regulates autophagosome biogenesis. mTOR phosphorylates both Atg13 and ULK1, suppressing ULK1 kinase activity and autophagy. ULK1 can directly phosphorylate Atg13 at a yet unidentified site, presumably to promote autophagy. Additional studies suggest that Atg13 and FIP200 can function independently of ULK1 and ULK2 to induce autophagy through an unknown mechanism.
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