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.
商品は「研究用試薬」です。人や動物の医療用・臨床診断用・食品用の製品ではありません。
研究用途以外に使用した場合、当社は一切の責任を負いかねます。
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保管条件:
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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生物活性
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化学情報
- プロトコル
- 純度とドキュメンテーション
- 参考文献
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Help & FAQs
生物活性
製品説明
体外実験
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.
化学情報
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性状 Solid
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Color Brown to red
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SMILES
[PE-CF594]
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
4°C, protect from light
* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
プロトコル
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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
純度とドキュメンテーション
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データシート (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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取扱説明書 (2659 KB)
参考文献
[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
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)
PE-CF594 関連分類
HY-D3334 関連分類
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