||FUNCTION: 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. FUNCTION: May play an important role in the apoptotic process, possibly within the modified cytoskeleton. Its expression is a relatively late event in the apoptotic process, occurring downstream of caspase activity. SUBCELLULAR LOCATION: Cytoplasm. Colocalizes with nonmuscle actin. ALTERNATIVE PRODUCTS: 2 named isoforms produced by alternative splicing. TISSUE SPECIFICITY: Ubiquitous. The mRNA is present at similar levels in viable and apoptotic cells, whereas the protein is dramatically highly expressed in apoptotic cells. INDUCTION: By apoptotic stimuli. PTM: Conjugated to ATG12; which is essential for autophagy, but is not required for association with isolation membrane. SIMILARITY: Belongs to the ATG5 family.
||See product label
||A synthetic peptide corresponding to the C-terminal of human ATG-5L. No immunogenic carrier protein was conjugated to the immunogen. Instead, Adjukine B (see the Adjuvants in biosensis' product list) has been used to orchestrate/boost the immune response.
||Autophagy protein 5; APG5-like; APG 5; APG5; Apoptosis-specific protein; ATG5; APG5L; ASP
||Protein G purified IgG
||Flow Cytometry (2 ug/10^6 cells), IHC, immunofluorescence, WB. Use a dilution of 1:200 to 1:1000 for these applications. Biosensis recommends optimal dilutions/concentrations should be determined by the end user.
||IHC and wb confirmed the specificity for ATG5.
||Human, not yet tested in other species.
||Reconstitute in 500 µl of sterile water. Centrifuge to remove any insoluble material.
||After reconstitution keep aliquots at -20ºC for a higher stability, and at 4ºC with an appropriate antibacterial agent. Glycerol (1:1) may be added for an additional stability. Avoid repetitive freeze/thaw cycles.
||Six months after purchase
||1. Garrido-Maraver J. et al (2012) Screening of effective pharmacological treatments for MELAS syndrome using yeasts, fibroblasts and cybrids models of the disease
Br J Pharmacol. 2012 Jul 2.
2. De la Mata M. et al (2012) Recovery of MERRF fibroblasts and cybrids pathophysiology by Coenzyme Q₁₀
Neurotherapeutics. 2012 Apr;9(2):446-63.
3. Cotán D. et al. (2011) Secondary coenzyme Q10 deficiency triggers mitochondria degradation by mitophagy in MELAS fibroblasts FASEB J. 2011
||1. Mizushima, N et al. (2003) Int J Biochem Cell Biol. 35(5), 553-61
2. Baehrecke EH. Nat Rev Mol Cell Biol. 6(6):505-10. (2005)
3. Lum JJ, et al. Nat Rev Mol Cell Biol. 6(6):439-48. (2005)
4. Greenberg JT. Dev Cell. 8(6):799-801. (2005)