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Cat.No.: F4810
| Dilution |
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|
| Application |
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| WB, IHC, FCM |
| Reactivity |
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| Mouse, Human |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
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| 12 kDa 12 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 skeletal muscle tissue; Fetal lung tissue; Human placenta; HEK-293 cells; Neuro-2a cells; Daudi cells |
|---|---|
| Negative Control |
| Specificity |
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| PEN2 Antibody [E13J21] detects endogenous levels of total PEN2 protein. |
| Clone |
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| E13J21 |
| Synonym(s) |
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| PEN2; MDS033; PSENEN; Gamma-secretase subunit PEN-2; Presenilin enhancer protein 2 |
| Background |
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| PEN2 (Presenilin Enhancer 2), an integral membrane glycoprotein essential for γ-secretase complex assembly, features two transmembrane domains with N- and C-termini oriented toward the ER lumen/extracellular space, a conserved D-Y-L-S-F motif in its short C-terminal tail critical for complex stabilization, and key residues like I43 in the cytosolic loop plus charged D90/F94 that fine-tune presenilin endoproteolysis. As the final obligatory subunit binding to the presenilin (PS1/PS2)-nicastrin-APH1 tripartite intermediate, PEN2 triggers PS autoproteolysis at the TMD7-8 junction by stabilizing the catalytic Asp257/Asp385 residues in a horseshoe-shaped water-filled cavity, enabling intramembrane proteolysis of >100 type I transmembrane substrates including amyloid precursor protein (APP) to release Aβ40/42 peptides and Notch receptor to generate NICD transcription factor. This sequential ε→ζ→γ cleavages within the TMD proceed via substrate docking at nicastrin’s large ectodomain followed by lateral cleft entry to the central PS active site, where PEN2 rigidly positions the PS transmembrane bundle to enhance catalytic efficiency and trafficking from ER to plasma membrane/endosomes, critically regulating neuronal differentiation (Notch), synaptic plasticity (APP/Cadherins), and ER homeostasis while contributing to Alzheimer's disease through Aβ plaque formation and cancer via dysregulated Notch/EGFR signaling. |
| References |
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