|Application ||WB, IF|
|Calculated MW||14272 Da|
|Positive Control||WB: 293 cell lysate, IF: U251 cells|
|Application & Usage||Western blot: 1:1000, IF: 1:200.|
|Other Names||MAP1LC3A; Microtubule-associated proteins 1A/1B light chain 3A; Autophagy-related protein LC3 A; Autophagy-related ubiquitin-like modifier LC3 A; MAP1 light chain 3-like protein 1; MAP1A/MAP1B light chain 3 A; Microtubule-associated protein 1 light chain 3 alpha|
|Formulation||Supplied in PBS with 0.09% (W/V) sodium azide.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||LC3 (APG8A) (Isoform A specific) Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Ubiquitin-like modifier involved in formation of autophagosomal vacuoles (autophagosomes) (PubMed:20713600, PubMed:24290141). Whereas LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation (PubMed:20713600).|
|Cellular Location||Cytoplasm, cytoskeleton. Endomembrane system; Lipid-anchor. Cytoplasmic vesicle, autophagosome membrane; Lipid-anchor. Cytoplasmic vesicle, autophagosome Note=LC3-II binds to the autophagic membranes|
|Tissue Location||Most abundant in heart, brain, liver, skeletal muscle and testis but absent in thymus and peripheral blood leukocytes.|
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Provided below are standard protocols that you may find useful for product applications.
Autophagy is an alternative process of proteasomal degradation for some long-lived proteins or organelles. Alterations in the autophagic-lysosomal compartment have been linked to neuronal death in many neurodegenerative disorders as well as in transmissible neuronal pathologies (prion diseases). Genetic studies in yeast have shown that Autophagy-defective Gene-8 (Atg-8) represents a specific marker for autophagy. Among the four families of mammalian Atg8-related proteins only LC3 (Microtubule-associated Protein1 Light Chain 3) is expressed at sufficient high levels and efficiently recruited to autophagic vesicles in cells and tissues. During autophagy the cytoplasmic form, LC3-I is processed and recruited to autophagosomes, where LC3-II is generated by site specific proteolysis near to the C-terminus. Autophagic vacuoles have been also reported frequently in cardiomyopathies or muscle cells exposed to different experimental settings.
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