ATG13 Antibody
| Code | Size | Price |
|---|
| PSI-5799-0.02mg | 0.02mg | £150.00 |
Quantity:
| PSI-5799-0.1mg | 0.1mg | £449.00 |
Quantity:
Prices exclude any Taxes / VAT
Overview
Host Type: Rabbit
Antibody Isotype: IgG
Antibody Clonality: Polyclonal
Regulatory Status: RUO
Applications:
- Enzyme-Linked Immunosorbent Assay (ELISA)
- Immunofluorescence (IF)
- Immunohistochemistry (IHC)
- Western Blot (WB)
Documents
Further Information
Additional Names:
ATG13 Antibody: KIAA0652, PARATARG8, KIAA0652, Autophagy-related protein 13
Application Note:
ATG13 antibody can be used for detection of ATG13 by Western blot at 1 μg/mL. Antibody can also be used for immunohistochemistry starting at 5 μg/mL. For immunofluorescence start at 20 μg/mL.
Antibody validated: Western Blot in rat samples; Immunohistochemistry in mouse samples and Immunofluorescence in mouse samples. All other applications and species not yet tested.
Antibody validated: Western Blot in rat samples; Immunohistochemistry in mouse samples and Immunofluorescence in mouse samples. All other applications and species not yet tested.
Background:
ATG13 Antibody: 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. This process is negatively regulated by TOR (Target of rapamycin) through phosphorylation of autophagy protein ATG1. ATG13 forms a complex with ULK1 and ULK2, the mammalian homologs of ATG1, and with FIP200. This complex is a target of TOR phosphorylation under normal conditions; inhibition of TOR by rapamycin or leucine deprivation leads to dephosphorylation of ATG13, ULK1 and ULK2, which then leads to autophagy. Knockdown of ATG13 inhibits autophagosome formation.
Background 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.
- Kamada Y, Funakoshi T, Shintani T, et al. Tor-mediated induction of autophagy via Apg1 protein kinase complex. J. Cell. Biol. 2000; 150:1507-13.
- Jung CH, Jun CB, Ro SH, et al. ULK-Atg13-FIP200 complexes mediate mTOR signaling to the autophagy machinery. Mol. Biol. Cell 2009; 20:1992-2003.
Buffer:
ATG13 Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration:
1 mg/mL
Conjugate:
Unconjugated
DISCLAIMER:
Optimal dilutions/concentrations should be determined by the end user. The information provided is a guideline for product use. This product is for research use only.
Homology:
Predicted species reactivity based on immunogen sequence: Bovine: (100%)
Immunogen:
ATG13 antibody was raised against a 15 amino acid synthetic peptide near the carboxy terminus of human ATG13.
The immunogen is located within amino acids 450 - 500 of ATG13.
The immunogen is located within amino acids 450 - 500 of ATG13.
NCBI Gene ID #:
9776
NCBI Official Name:
ATG13 autophagy related 13 homolog (S. cerevisiae)
NCBI Official Symbol:
ATG13
NCBI Organism:
Homo sapiens
Physical State:
Liquid
PREDICTED MOLECULAR WEIGHT:
Predicted: 44, 53, 57, 61 kDa
Observed: 49 kDa
Observed: 49 kDa
Protein Accession #:
NP_001136145
Protein GI Number:
218082953
Purification:
ATG13 Antibody is affinity chromatography purified via peptide column.
Research Area:
Autophagy
SPECIFICITY:
Multiple isoforms of ATG13 are known to exist.
Swissprot #:
O75143
User NOte:
Optimal dilutions for each application to be determined by the researcher.
Related Products
| Product Name | Product Code | Supplier | ATG13 Peptide | PSI-5799P | ProSci | Summary Details | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|