MAP1LC3A
Reactivity: Human
ELISA, FACS
Host: Mouse
Monoclonal
7E9E12
unconjugated
Application Notes
IF: 1:100. WB: 1:1000. IHC-P: 1:10~50
Restrictions
For Research Use only
Format
Liquid
Buffer
Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C,-20 °C
Expiry Date
6 months
Lu, Hsu: "Ambient temperature reduction extends lifespan via activating cellular degradation activity in an annual fish (Nothobranchius rachovii)." in: Age (Dordrecht, Netherlands), Vol. 37, Issue 2, pp. 33, (2015) (PubMed).
Hsu, Chuang, Chan: "Changes in cellular degradation activity in young and old worker honeybees (Apis mellifera)." in: Experimental gerontology, Vol. 50, pp. 128-36, (2014) (PubMed).
Target
MAP1LC3A
(Microtubule-Associated Protein 1 Light Chain 3 alpha (MAP1LC3A))
Macroautophagy is the major inducible pathway for the general turnover of cytoplasmic constituents in eukaryotic cells, it is also responsible for the degradation of active cytoplasmic enzymes and organelles during nutrient starvation. Macroautophagy involves the formation of double-membrane bound autophagosomes which enclose the cytoplasmic constituent targeted for degradation in a membrane bound structure, which then fuse with the lysosome (or vacuole) releasing a single-membrane bound autophagic bodies which are then degraded within the lysosome (or vacuole). MAP1A and MAP1B are microtubule-associated proteins which mediate the physical interactions between microtubules and components of the cytoskeleton. These proteins are involved in formation of autophagosomal vacuoles (autophagosomes). MAP1A and MAP1B each consist of a heavy chain subunit and multiple light chain subunits. MAP1LC3a is one of the light chain subunits and can associate with either MAP1A or MAP1B. The precursor molecule is cleaved by APG4B/ATG4B to form the cytosolic form, LC3-I. This is activated by APG7L/ATG7, transferred to ATG3 and conjugated to phospholipid to form the membrane-bound form, LC3-II.