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AP2S1 Rabbit mAb

Catalog No.: F3323

Application: Reactivity: Human, Mouse, Rat

Usage Information

Dilution
WB1:1000 - 1:10000 IP1:10 - 1:100 IHC1:100

Application
WB, IP, IHC

Source
Rabbit

Reactivity
Human, Mouse, Rat

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
17 kDa 17 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human thyroid carcinoma tissue; Human breast carcinoma tissue; Human colon carcinoma tissue; Human colon carcinoma tissue; Human fetal brain; Mouse brain; Rat brain; Mouse kidney; HeLa cell; HEK-293 cell; SH-SY5Y cell; 293T cell
Negative Control

Datasheet & SDS

Biological Description

Specificity
AP2S1 Rabbit mAb recognizes endogenous levels of total AP2S1 protein.

Uniprot ID
P53680

Clone
L13B7

Synonym(s)
AP17; CLAPS2; AP2S1; AP-2 complex subunit sigma; Adaptor protein complex AP-2 subunit sigma; Adaptor-related protein complex 2 subunit sigma; Clathrin assembly protein 2 sigma small chain; Clathrin coat assembly protein AP17; Clathrin coat-associated protein AP17; HA2 17 kDa subunit; Plasma membrane adaptor AP-2 17 kDa protein; Sigma2-adaptin

Background
AP2S1 encodes the small (~17 kDa) sigma-1 subunit of the adaptor protein complex 2 (AP-2), a heterotetramer essential for clathrin-mediated endocytosis. This complex facilitates cargo selection and vesicle formation at the plasma membrane by bridging clathrin coats with membrane lipids and cargo proteins. AP2S1 has a beta-sandwich fold without enzymatic activity and plays a critical scaffolding role, recognizing sorting motifs such as YxxΦ and dileucine on cargo proteins to ensure selective internalization. AP2S1 also regulates intracellular trafficking by modulating late endosome–lysosome fusion, which influences degradation of proteins like amyloid precursor protein (APP). Silencing AP2S1 enhances this fusion, promoting APP clearance and reducing neurotoxic Aβ42 levels, through interaction with HOPS complex proteins (e.g., VPS41 and VPS16). This mechanism is implicated in Alzheimer’s disease pathology. Additionally, missense mutations at the conserved Arg15 residue of AP2S1 cause familial hypocalciuric hypercalcemia type 3 (FHH3), disrupting calcium-sensing receptor (CaSR) endocytosis and signaling. These mutations reduce adaptor affinity for CaSR dileucine motifs, impair receptor internalization, and alter calcium homeostasis, leading to benign hypercalcemia with low urinary calcium excretion.

Background

AP2S1 encodes the small (~17 kDa) sigma-1 subunit of the adaptor protein complex 2 (AP-2), a heterotetramer essential for clathrin-mediated endocytosis. This complex facilitates cargo selection and vesicle formation at the plasma membrane by bridging clathrin coats with membrane lipids and cargo proteins. AP2S1 has a beta-sandwich fold without enzymatic activity and plays a critical scaffolding role, recognizing sorting motifs such as YxxΦ and dileucine on cargo proteins to ensure selective internalization. AP2S1 also regulates intracellular trafficking by modulating late endosome–lysosome fusion, which influences degradation of proteins like amyloid precursor protein (APP). Silencing AP2S1 enhances this fusion, promoting APP clearance and reducing neurotoxic Aβ42 levels, through interaction with HOPS complex proteins (e.g., VPS41 and VPS16). This mechanism is implicated in Alzheimer’s disease pathology. Additionally, missense mutations at the conserved Arg15 residue of AP2S1 cause familial hypocalciuric hypercalcemia type 3 (FHH3), disrupting calcium-sensing receptor (CaSR) endocytosis and signaling. These mutations reduce adaptor affinity for CaSR dileucine motifs, impair receptor internalization, and alter calcium homeostasis, leading to benign hypercalcemia with low urinary calcium excretion.

References
[1] Wen QX, et al. Traffic. 2023 Jan;24(1):20-33. [2] Hendy GN, et al. J Clin Endocrinol Metab. 2013 Dec;98(12):4666-9.

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3
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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%