|Positive WB detected in||mouse thymus tissue, COLO 320 cells|
|Positive IP detected in||COLO 320 cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Sample-dependent, check data in validation data gallery|
13384-1-AP targets AP3B1 in WB, IP, IF,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||AP3B1 fusion protein Ag4225|
|Full Name||adaptor-related protein complex 3, beta 1 subunit|
|Calculated molecular weight||1094 aa, 121 kDa|
|Observed molecular weight||140 kDa|
|GenBank accession number||BC038444|
|Gene ID (NCBI)||8546|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
AP3B1 is the 140-kDa β3A subunit of the adaptor-related protein complex-3 (AP-3), a ubiquitous heterotetrameric complex that is localized to the trans-Golgi network and endosomes and is involved in protein trafficking to lysosomes or specialized endosomal-lysosomal organelles (PMID: 9182526; 9545220). This complex is composed of two lager subunits (δ and β3A or β3B), a medium subunit (μ3A or μ3B), and a small subunit (σ3A or σ3B). The absence of the β3A subunit (AP3B1) results in the loss of stability of AP3 and leads to degradation of μ3A, to which β3A is directly bound, while the other subunits are variably affected (PMID: 16507770). AP3B1 contains three main domains: the N-terminal head domain, the hinge, and the C-terminal ear domain. It has been reported as a target of IP(7)-mediated pyrophosphorylation (PMID: 19934039). Defects in AP3B1 are the cause of Hermansky-Pudlak syndrome type 2 (HPS2) (PMID: 10024875; 16507770).
Defective AP-3-dependent VAMP8 trafficking impairs Weibel-Palade body exocytosis in Hermansky-Pudlak Syndrome type 2 blood outgrowth endothelial cells.
Stem Cell Reports
In Vitro Disease Modeling of Hermansky-Pudlak Syndrome Type 2 Using Human Induced Pluripotent Stem Cell-Derived Alveolar Organoids.
Cellular and molecular defects in a patient with Hermansky-Pudlak syndrome type 5.
Mol Biol Cell
Adaptor protein-3 complex is required for Vangl2 trafficking and planar cell polarity of the inner ear.
Mol Biol Cell
Clathrin-dependent mechanisms modulate the subcellular distribution of class C Vps/HOPS tether subunits in polarized and nonpolarized cells.
Mol Biol Cell
Chemical-Genetic Disruption of Clathrin Function Spares Adaptor Complex 3-Dependent Endosome Vesicle Biogenesis.