Mouse Autophagy protein 5 (ATG5) ELISA Kit | ATG5 elisa kit

Mouse Autophagy protein 5 (ATG5) ELISA Kit

Cat. Num. AAA7227851

• Reactivity: Mouse
• Synonyms: Autophagy protein 5 (ATG5); Mouse Autophagy protein 5 (ATG5) ELISA Kit; ATG5 elisa kit

• Reactivity: Mouse
• Specificity: This assay has high sensitivity and excellent specificity for detection of ATG5. No significant cross-reactivity or interference between ATG5 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ATG5 and all the analogues, therefore, cross reaction may still exist in some cases.

• Samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
• Assay Type: Quantitative Competitive
• Sensitivity: 0.1 ng/mL
• Preparation and Storage: Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for ATG5 elisa kit

Intended Uses: This ATG5 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse ATG5. This ELISA kit for research use only, not for therapeutic or test applications!

Principle of the Assay: ATG5 ELISA kit applies the competitive enzyme immunoassay technique utilizing an anti-ATG5 antibody and an ATG5-HRP conjugate. The assay sample and buffer are incubated together with ATG5-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the ATG5 concentration since ATG5 from samples and ATG5-HRP conjugate compete for the anti-ATG5 antibody binding site. Since the number of sites is limited, as more sites are occupied by ATG5 from the sample, fewer sites are left to bind ATG5-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ATG5 concentration in each sample is interpolated from this standard curve.

NCBI and Uniprot Product Information

• NCBI GI #: 62079231
• NCBI GeneID: 365601
• NCBI Accession #: NP_001014272.1
• NCBI GenBank Nucleotide #: NM_001014250.1
• Molecular Weight: 32,398 Da
• NCBI Official Full Name: autophagy protein 5
• NCBI Official Synonym Full Names: autophagy related 5
• NCBI Official Symbol: Atg5
• NCBI Protein Information: autophagy protein 5; ATG5 autophagy related 5 homolog
• UniProt Protein Name: Autophagy protein 5
• Protein Family: Autophagy protein
• UniProt Gene Name: Atg5
• UniProt Entry Name: ATG5_RAT

Uniprot Description

ATG5: Required for autophagy. Conjugates to ATG12 and associates with isolation membrane to form cup-shaped isolation membrane and autophagosome. The conjugate detaches from the membrane immediately before or after autophagosome formation is completed. The ATG5-ATG12 conjugate forms a complex with several units of ATG16. Interacts with TECPR1; the interaction is direct and does not take place when ATG16 is associated with the ATG5- ATG12 conjugate. By apoptotic stimuli. Ubiquitous. The mRNA is present at similar levels in viable and apoptotic cells, whereas the protein is dramatically highly expressed in apoptotic cells. Belongs to the ATG5 family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Ubiquitin conjugating system; Autophagy; Apoptosis

Cellular Component: protein complex; membrane; cytoplasm; pre-autophagosomal structure membrane; autophagic vacuole; axoneme

Molecular Function: protein binding; APG8 conjugating enzyme activity

Biological Process: response to drug; response to fungus; apoptosis; ventricular cardiac muscle cell development; C-terminal protein lipidation; post-translational protein modification; vasodilation; regulation of release of sequestered calcium ion into cytosol; cellular response to nitrogen starvation; heart contraction; regulation of cytokine secretion during immune response; mitochondrion degradation; autophagy; innate immune response; blood vessel remodeling; negative regulation of protein ubiquitination; otolith development; autophagic vacuole formation; negative regulation of apoptosis