ATG4 Autophagy Related 4 Homolog B (S. Cerevisiae) (ATG4B) (N-Term) Peptide

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Protein Name
Synonyms Apg4b, APG4B, Aut2b2, apg4b, AUTL1, Autl1, Atg4bl, AW048066, 2510009N07Rik
Protein Region
N-Term
Application
Blocking Peptide (BP)
Pubmed 5 references available
Catalog no. ABIN699805
Quantity 0.1 mg
Price
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Immunogen Synthetic peptide
Specificity The synthetic peptide sequence used to generate the antibody AP1809a was selected from the N-term region of human Autophagy APG4B. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.
Alternative Name APG4B
Background 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). APG4 is a cysteine protease required for autophagy, which cleaves the C-terminal part of either MAP1LC3, GABARAPL2 or GABARAP, allowing the liberation of form I. A subpopulation of form I is subsequently converted to a smaller form (form II). Form II, with a revealed C-terminal glycine, is considered to be the phosphatidylethanolamine (PE)-conjugated form, and has the capacity for the binding to autophagosomes.
Comment

Background: 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). APG4 is a cysteine protease required for autophagy, which cleaves the C-terminal part of either MAP1LC3, GABARAPL2 or GABARAP, allowing the liberation of form I. A subpopulation of form I is subsequently converted to a smaller form (form II). Form II, with a revealed C-terminal glycine, is considered to be the phosphatidylethanolamine (PE)-conjugated form, and has the capacity for the binding to autophagosomes.

Restrictions For Research Use only
Storage 4 °C/-20 °C
Storage Comment Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles
Expiry Date 6 months
Background publications Shintani, Klionsky: "Autophagy in health and disease: a double-edged sword." in: Science (New York, N.Y.), Vol. 306, Issue 5698, pp. 990-5, 2004 (PubMed).

Levine: "Eating oneself and uninvited guests: autophagy-related pathways in cellular defense." in: Cell, Vol. 120, Issue 2, pp. 159-62, 2005 (PubMed).

Lum, DeBerardinis, Thompson: "Autophagy in metazoans: cell survival in the land of plenty." in: Nature reviews. Molecular cell biology, Vol. 6, Issue 6, pp. 439-48, 2005 (PubMed).

Baehrecke: "Autophagy: dual roles in life and death?" in: Nature reviews. Molecular cell biology, Vol. 6, Issue 6, pp. 505-10, 2005 (PubMed).

Greenberg: "Degrade or die: a dual function for autophagy in the plant immune response." in: Developmental cell, Vol. 8, Issue 6, pp. 799-801, 2005 (PubMed).

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