Atg13 (D4P1K) Rabbit mAb

• 产品编号：CST-13273S      品牌：CST       原厂货号：13273S
• 产品分类：抗体 > 一抗 > 蛋白特异性一抗
• 应用分类：

描述：

Atg13 (D4P1K) Rabbit mAb 兔单抗能够识别内源性Atg13总蛋白。该单克隆抗体通过合成肽免疫动物制备，这些合成肽序列与人源Atg13蛋白 Asp462位点周围的残基相一致。自噬是自噬溶酶体对其包裹的细胞质内含物进行降解的一种分解代谢过程(1,2)。自噬过程一般是在营养匮乏的条件下被激活，但是也与一些生理过程有关，如发育、分化、神经变性、感染和癌症(3)。在酵母中已阐明自噬的分子机制，这是由许多自噬相关基因(Atg)调控。Atg13/Apg13作为一种固有蛋白，最早在酵母中被发现，其与自噬必须的蛋白激酶Atg1/Apg1存在遗传上的关联性。从Atg13的突变株发现，Atg1的过表达可以抑制自噬缺陷（4）。自噬的发生需要Atg1和Atg13的直接关联，并且通过TOR依赖的磷酸化Atg1的同系物ULK1/2和FIP2000产生抑制，这种蛋白定位于自噬隔离膜上，并且可以调节自噬体的形成（6-8）。mTOR可以将Atg13和ULK1磷酸化，从而抑制ULK1激酶活性和自噬（7-9）。ULK1可以将Atg13的一个未知的位点磷酸化，从而可能促进自噬（7,8）。另一些研究表明，Atg13和FIP200可以不依赖于ULK1和ULK2诱导自噬，但是机理尚不清楚（10）。

1. Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
2. Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18.
3. Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88.
4. Funakoshi, T. et al. (1997) Gene 192, 207-13.
5. Kamada, Y. et al. (2000) J Cell Biol 150, 1507-13.
6. Ganley, I.G. et al. (2009) J Biol Chem 284, 12297-305.
7. Hosokawa, N. et al. (2009) Mol Biol Cell 20, 1981-91.
8. Jung, C.H. et al. (2009) Mol Biol Cell 20, 1992-2003.
9. Kim, J. et al. (2011) Nat Cell Biol 13, 132-41.
10. Alers, S. et al. (2011) Autophagy 7, 1423-33.

原厂资料：

Specificity / Sensitivity

Atg13 (D4P1K) Rabbit mAb recognizes endogenous levels of total Atg13 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asp462 of human Atg13 protein.

Background

Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents (1,2). Autophagy is generally activated by conditions of nutrient deprivation, but has also been associated with a number of physiological processes including development, differentiation, neurodegeneration, infection, and cancer (3). The molecular machinery of autophagy was largely discovered in yeast and referred to as autophagy-related (Atg) genes.

Atg13/Apg13 was originally identified in yeast as a constitutively expressed protein that was genetically linked to Atg1/Apg1, a protein kinase required for autophagy (4). Over-expression of Atg1 suppresses the defects in autophagy observed in Atg13 mutants (4). Autophagy requires a direct association between Atg1 and Atg13, and is inhibited by TOR-dependent phosphorylation of Atg13 under high nutrient conditions (5). 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 (6-8). mTOR phosphorylates both Atg13 and ULK1, suppressing ULK1 kinase activity and autophagy (7-9). ULK1 can directly phosphorylate Atg13 at a yet unidentified site, presumably to promote autophagy (7,8). Additional studies suggest that Atg13 and FIP200 can function independently of ULK1 and ULK2 to induce autophagy through an unknown mechanism (10).

1. Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
2. Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18.
3. Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88.
4. Funakoshi, T. et al. (1997) Gene 192, 207-13.
5. Kamada, Y. et al. (2000) J Cell Biol 150, 1507-13.
6. Ganley, I.G. et al. (2009) J Biol Chem 284, 12297-305.
7. Hosokawa, N. et al. (2009) Mol Biol Cell 20, 1981-91.
8. Jung, C.H. et al. (2009) Mol Biol Cell 20, 1992-2003.
9. Kim, J. et al. (2011) Nat Cell Biol 13, 132-41.
10. Alers, S. et al. (2011) Autophagy 7, 1423-33.

注意事项：

Storage: Supplied in 10 mM sodium HEPES (pH 7.5), 150
mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02%
sodium azide. Store at –20°C. Do not aliquot the antibody.