Rabbit Autophagy Vesicle Nucleation Sampler Kit Monoclonal Antibody

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Cat. No.: DAB-0011836

Size: 20 µL Size: 100 µL Size: Customer Size

Product Information
Clonality	Monoclonal
Host Species	Rabbit
Product Description	Monoclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys630 of human PI3 kinase class III protein, residues surrounding Thr72 of human Beclin-1 protein, residues surrounding Gly502 of human UVRAG protein, residues surrounding Leu210 of human Rubicon protein, or residues surrounding Gly780 of human Atg9A protein.Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly825 of human PIK3R4 protein, residues surrounding Val215 of human Atg14 protein, or residues surrounding Gly129 of human Bif-1 protein. Polyclonal antibodies are purified by protein A and peptide affinity chromatography.
Format	Liquid
Purity	Affinity purity

Target Information
Gene Description	Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents. Autophagy is generally activated by conditions of nutrient deprivation but is also associated with a number of physiological processes including development, differentiation, neurodegeneration, infection and cancer. The molecular machinery of autophagy was largely discovered in yeast and is directed by a number of autophagy-related genes. These proteins are involved in the formation of autophagosomes, cytoplasmic vacuoles that are delivered to lysosomes for degradation. The PIK3R4/PI3K class III complex interacts with Beclin-1 to play a role during several stages of autophagy. Autophagosome formation is stimulated when Atg14 complexes with PIK3R4, PI3K class III, and Beclin-1. The UVRAG protein competes with Atg14 for Beclin-1 binding, forming a mutually exclusive complex with PIK3R4, PI3K class III, and Beclin-1 that regulates autophagosome maturation. Autophagosome maturation is impaired in the presence of the Beclin-1-binding protein Rubicon. Co-expression of PIK3R4 is required for PI3K class III activation and regulation by both Beclin-1/UVRAG and nutrient levels. Bif-1 directly binds to UVRAG, forming a complex with Beclin-1, resulting in increased PI3-kinase class III/Vps34 activity required for autophagosome maturation. Inhibition of GSK-3β, as seen during nutrient deprivation, results in increased expression of Bif-1, and can contribute to autophagic cell death. Atg9A is an integral membrane protein that is required for both the initiation and the expansion of the autophagosome. Recruitment of Atg9A to the autophagosomal membrane is dynamic and transient as Atg9A also cycles between autophagy-related structures known as omegasomes, the trans-Golgi network, and endosomes, and at no point becomes a stable component of the autophagosomal membrane. The precise regulation of Atg9A trafficking is not fully clarified, yet it is suggested to involve p38 mitogen-activated protein kinase -binding protein p38IP and the Beclin-1-binding protein Bif-1.

Target Information

Gene Description

Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents. Autophagy is generally activated by conditions of nutrient deprivation but is also associated with a number of physiological processes including development, differentiation, neurodegeneration, infection and cancer. The molecular machinery of autophagy was largely discovered in yeast and is directed by a number of autophagy-related genes. These proteins are involved in the formation of autophagosomes, cytoplasmic vacuoles that are delivered to lysosomes for degradation. The PIK3R4/PI3K class III complex interacts with Beclin-1 to play a role during several stages of autophagy. Autophagosome formation is stimulated when Atg14 complexes with PIK3R4, PI3K class III, and Beclin-1. The UVRAG protein competes with Atg14 for Beclin-1 binding, forming a mutually exclusive complex with PIK3R4, PI3K class III, and Beclin-1 that regulates autophagosome maturation. Autophagosome maturation is impaired in the presence of the Beclin-1-binding protein Rubicon. Co-expression of PIK3R4 is required for PI3K class III activation and regulation by both Beclin-1/UVRAG and nutrient levels. Bif-1 directly binds to UVRAG, forming a complex with Beclin-1, resulting in increased PI3-kinase class III/Vps34 activity required for autophagosome maturation. Inhibition of GSK-3β, as seen during nutrient deprivation, results in increased expression of Bif-1, and can contribute to autophagic cell death. Atg9A is an integral membrane protein that is required for both the initiation and the expansion of the autophagosome. Recruitment of Atg9A to the autophagosomal membrane is dynamic and transient as Atg9A also cycles between autophagy-related structures known as omegasomes, the trans-Golgi network, and endosomes, and at no point becomes a stable component of the autophagosomal membrane. The precise regulation of Atg9A trafficking is not fully clarified, yet it is suggested to involve p38 mitogen-activated protein kinase -binding protein p38IP and the Beclin-1-binding protein Bif-1.

Shipping & Storage
Shipping	Shipped at 4 °C.
Storage Instructions	Store at +4 °C short term (1-2 weeks). Store at -20 °C long term.
Storage Buffer	Constituent: 100% PBS

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