- CITATIONS: 96
|Application ||WB, IHC-P, IF, E|
|Other Accession||A6NCE7, O41515, Q9CQV6|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||14688 Da|
|Antigen Region||1-30 aa|
|Other Names||Microtubule-associated proteins 1A/1B light chain 3B, Autophagy-related protein LC3 B, Autophagy-related ubiquitin-like modifier LC3 B, MAP1 light chain 3-like protein 2, MAP1A/MAP1B light chain 3 B, MAP1A/MAP1B LC3 B, Microtubule-associated protein 1 light chain 3 beta, MAP1LC3B, MAP1ALC3|
|Target/Specificity||This LC3 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human LC3.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||LC3 Antibody (APG8B) (N-term) 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). Plays a role in mitophagy which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production (PubMed:28017329). In response to cellular stress and upon mitochondria fission, binds C-18 ceramides and anchors autophagolysosomes to outer mitochondrial membranes to eliminate damaged mitochondria (PubMed:22922758). While LC3s are involved in elongation of the phagophore membrane, the GABARAP/GATE-16 subfamily is essential for a later stage in autophagosome maturation. Promotes primary ciliogenesis by removing OFD1 from centriolar satellites via the autophagic pathway. Through its interaction with the reticulophagy receptor TEX264, participates in the remodeling of subdomains of the endoplasmic reticulum into autophagosomes upon nutrient stress, which then fuse with lysosomes for endoplasmic reticulum turnover (PubMed:31006538, PubMed:31006537).|
|Cellular Location||Cytoplasm, cytoskeleton. Endomembrane system; Lipid-anchor. Cytoplasmic vesicle, autophagosome membrane; Lipid-anchor. Note=LC3-II binds to the autophagic membranes. LC3-II localizes with the mitochondrial inner membrane during Parkin-mediated mitophagy (PubMed:28017329). Localizes also to discrete punctae along the ciliary axoneme|
|Tissue Location||Most abundant in heart, brain, skeletal muscle and testis. Little expression observed in liver|
Provided below are standard protocols that you may find useful for product applications.
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. MAP1LC3b 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.
References for protein:
1.Baehrecke EH. Nat Rev Mol Cell Biol. 6(6):505-10. (2005)
2.Lum JJ, et al. Nat Rev Mol Cell Biol. 6(6):439-48. (2005)
3.Greenberg JT. Dev Cell. 8(6):799-801. (2005)
4.Levine B. Cell. 120(2):159-62. (2005)
5. Shintani T and Klionsky DJ. Science. 306(5698):990-5. (2004)
6.Tanida I., et al. Int. J. Biochem. Cell Biol. 36:2503-2518(2004)
7.He H., et al. J. Biol. Chem. 278:29278-29287(2003)
8.Tanida I., et al. J. Biol. Chem. 279:36268-36276(2004)
References for U251 cell line:
1. Westermark B.; Pontén J.; Hugosson R. (1973).” Determinants for the establishment of permanent tissue culture lines from human gliomas”. Acta Pathol Microbiol Scand A. 81:791-805. [PMID: 4359449].
2. Pontén, J.,Westermark B. (1978).” Properties of Human Malignant Glioma Cells in Vitro”. Medical Biology 56: 184-193.[PMID: 359950].
3. Geng Y.;Kohli L.; Klocke B.J.; Roth K.A.(2010). “Chloroquine-induced autophagic vacuole accumulation and cell death in glioma cells is p53 independent”. Neuro Oncol. 12(5): 473–481.[ PMID: 20406898].
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