癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
ATG4C Antibody
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Application 
| WB, IF, E, IHC-P |
|---|---|
| Primary Accession | Q96DT6 |
| Other Accession | NP_835739, 30410846 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | 52497 Da |
| Concentration (mg/ml) | 1 mg/mL |
| Conjugate | Unconjugated |
| Application Notes | ATG4C antibody can be used for detection of ATG4C by Western blot at 1 - 2 µg/ml. Antibody can also be used for Immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 84938 |
|---|---|
| Other Names | Cysteine protease ATG4C, 3.4.22.-, AUT-like 3 cysteine endopeptidase, Autophagin-3, Autophagy-related cysteine endopeptidase 3, Autophagy-related protein 4 homolog C, ATG4C, APG4C, AUTL1, AUTL3 |
| Target/Specificity | ATG4C; ATG4C antibody is human, mouse and rat reactive. ATG4C is predicted to not cross-react with other ATG4 proteins. |
| Reconstitution & Storage | ATG4C antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
| Precautions | ATG4C Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | ATG4C {ECO:0000303|PubMed:21177865, ECO:0000312|HGNC:HGNC:16040} |
|---|---|
| Function | Cysteine protease that plays a key role in autophagy by mediating both proteolytic activation and delipidation of ATG8 family proteins (PubMed:21177865, PubMed:29458288, PubMed:30661429). The protease activity is required for proteolytic activation of ATG8 family proteins: cleaves the C-terminal amino acid of ATG8 proteins MAP1LC3 and GABARAPL2, to reveal a C-terminal glycine (PubMed:21177865). Exposure of the glycine at the C-terminus is essential for ATG8 proteins conjugation to phosphatidylethanolamine (PE) and insertion to membranes, which is necessary for autophagy (By similarity). In addition to the protease activity, also mediates delipidation of ATG8 family proteins (PubMed:29458288, PubMed:33909989). Catalyzes delipidation of PE-conjugated forms of ATG8 proteins during macroautophagy (PubMed:29458288, PubMed:33909989). Compared to ATG4B, the major protein for proteolytic activation of ATG8 proteins, shows weaker ability to cleave the C-terminal amino acid of ATG8 proteins, while it displays stronger delipidation activity (PubMed:29458288). In contrast to other members of the family, weakly or not involved in phagophore growth during mitophagy (PubMed:33773106). |
| Cellular Location | Cytoplasm {ECO:0000250|UniProtKB:Q8BGE6}. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Autophagy, the process of bulk degradation of cellular proteins through an autophagosomic-lysosomal pathway is important for normal growth control and may be defective in tumor cells. It is involved in the preservation of cellular nutrients under starvation conditions as well as the normal turnover of cytosolic components (1,2). ATG4C, also known as autophagin-3, is one of four mammalian orthologs of the yeast ATG4 protein; all four are cysteine proteases (3). Recent studies have shown that ATG4C and Beclin-1 are regulated by the microRNA miR-376b; overexpression of miR-376b led to decreased mRNA and protein levels, thereby blocking starvation and TOR inhibition-related autophagy (4).
REFERENCES
Gozuacik D and Kimchi A. Autophagy as a cell death and tumor suppressor mechanism. Oncogene 2004; 23:2891-906.
Kisen GO, Tessitore L, Costelli P, et al. Reduced autophagic activity in primary rat hepatocellular carcinoma and ascites hepatoma cells. Carcinogenesis 1993; 14:2501-5.
Marino G, Uria JA, Puente XS, et al. Human autophagins, a family of cysteine proteinases potentially implicated in cell degradation by autophagy. J. Biol. Chem. 2003; 278:3671-8.
Korkmaz G, le Sage C, Tekirdag KA, et al. miR-376b controls starvation and TOR inhibition-related autophagy by targeting ATG4C and BECN1. Autophagy 2012; 8:165-76.
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