PE-CF594
Based on 1 Customer Validation
PE-CF594 is a labeled monoclonal antibody conjugate that specifically binds to HLA-DR on the surface of monocytes and B cells, while acting as a signal attenuator. Through steric hindrance and a possible fluorescence resonance energy transfer mechanism, PE-CF594 specifically reduces the fluorescence intensity of PE-CD124 staining, but does not interfere with the staining of other PE-labeled antibodies such as CD40, CD4 or CD14. PE-CF594 can also be used to detect the emission signal of mt-Keima after excitation with a 561-nm laser, thereby effectively evaluating mitophagy activity.
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Stockage:
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
Activité biologique
Description
In Vitro
PE-CF594 enables specific, sensitive detection of mt-Keima fluorescence in HeLa-Parkin cells stably expressing mt-Keima, supporting quantitative flow cytometric analysis of mitophagy activity[2].
PE-CF594 (0-25.0 μg/L; 3 min) can be quantified and discriminated from strongly overlapping fluorochromes using both compensated band pass filters and MOE-based optical computing, with MOE systems enabling multiplexed detection with two elements instead of three discrete filters[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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Appearance Solid
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Color Brown to red
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SMILES
[PE-CF594]
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
Protocole
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Mitophagy Solutions
Mitophagy is the selective autophagic degradation of mitochondria and functions as a mitochondrial quality-control pathway that removes damaged, depolarized, excess, or developmentally programmed mitochondria. The pathway links mitochondrial damage recognition, autophagosome recruitment, lysosomal delivery, and mitochondrial turnover to phenotypes such as mitochondrial homeostasis, oxidative-stress control, metabolic remodeling, differentiation, and neurodegeneration-related mitochondrial fidelity. The best-characterized damage-induced pathway is the PINK1-Parkin axis. Parkin is recruited selectively to impaired mitochondria and promotes their autophagic elimination, while mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, recruits Parkin, and activates Parkin-dependent mitophagy. PINK1 also phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity, and PINK1-driven ubiquitin phosphorylation creates a feed-forward signal for recruiting autophagy machi
Pureté et documentation
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Fiche technique (265 KB)
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SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. De Vita M, et al. Unexpected interference in cell surface staining by monoclonal antibodies to unrelated antigens. Cytometry B Clin Cytom. Published online October 1, 2014. [Content Brief]
[2]. Um JH, et al. Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima. J Vis Exp. 2018;(138):58099. Published 2018 Aug 12. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
PE-CF594 Related Classifications
HY-D3334 Related Classifications
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