Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker™ Red & Annexin V Alexa Fluor™ 488, for flow cytometry

Citations & References (4)

Invitrogen™

Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker™ Red & Annexin V Alexa Fluor™ 488, for flow cytometry

製品番号（カタログ番号）	数量
V35116	1 kit

製品番号（カタログ番号） V35116

価格（JPY）

111,000

1 kit

お問い合わせください ›

1 kit

このフローサイトメトリー製品は、アポトーシスの2つの特徴であるホスファチジルセリンの外部化とミトコンドリア膜電位の変化に対して迅速かつ便利なアッセイを提供します。提供された結合バッファーでAlexa Fluor™ 488アネキシンVおよびMitoTracker™ Red CMXRos色素を使用して細胞集団を染色した後、生細胞は非常にわずかな緑色蛍光と明るい赤色蛍光を示し、アポトーシスを起こしている細胞は緑色蛍光を示し、赤色蛍光が低下します。これらの集団はフローサイトメーターを使用して簡単に識別でき、アルゴンイオンレーザーの488 nmラインを使用して両方の色素を励起できます。

フローサイトメトリー用のすべてのアポトーシスアッセイの選択ガイドを参照してください。

研究用にのみ使用できます。診断用には使用いただけません。

励起／発光Mitotracker™ red 579⁄599、Alexa Fluor™ 488：499⁄521

フローサイトメーターレーザーライン488

使用対象（アプリケーション）フローサイトメトリー

使用対象 (装置)蛍光顕微鏡、フローサイトメーター

反応数50

製品ラインAlexa Fluor、MitoTracker

製品タイプMitochondrial Membrane Apoptosis Kit

数量1 kit

出荷条件湿氷

コンジュゲートAlexa Fluor™ 488、MitoTracker™ Red

フォーマットチューブ、スライド

Unit Size1 kit

組成および保存条件

1バイアルのアネキシン、Alexa Fluor™ 488コンジュゲート（250 µL）、3バイアルのMitoTracker™ red（1バイアルあたり50 µL）、1ボトルのアネキシン結合バッファー（5倍の溶液、15 mL）、および1バイアルのDMSO（100 µL）を含みます。

冷蔵庫（2～8℃）に保存し、遮光。

よくあるご質問（FAQ）

What are the fluorescence excitation/emission maxima for the dyes contained in the Mitochondrial Membrane Potential Apoptosis Kit, with Mitotracker Red & Alexa Fluor 488 annexin V, for flow cytometry

Alexa Fluor 488 annexin V: 499/521 nm
MitoTracker Red: 579/599 nm

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

I want to study apoptosis using an Annexin V conjugate, but with adherent cells via microscopy instead of flow cytometry. Can this be done?

It has been done, but we don‘t recommend it. Both healthy cells and apoptotic cells possess phosphatidylserine on the cell surface, which can be detected with Annexin V, but apoptotic cells have significantly more of it. You can easily tell the difference between these two populations with flow cytometry, because flow cytometers are more sensitive and have a higher throughput. But with a microscope, you cannot always tell the difference, especially for adherent cells. Instead, for microscopy, we recommend a different technique, such as detecting caspases with CellEvent Caspase Detection Reagents.

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

引用および参考文献 (4)

引用および参考文献

Abstract

Galectin 1 modulates plasma cell homeostasis and regulates the humoral immune response.

Authors:Anginot A, Espeli M, Chasson L, Mancini SJ, Schiff C,

Journal:J Immunol

PubMed ID:23616571

'Galectin-1 (GAL1) is an S-type lectin with multiple functions, including the control of B cell homeostasis. GAL1 expression was reported to be under the control of the plasma cell master regulator BLIMP-1. GAL1 was detected at the protein level in LPS-stimulated B cells and was shown to promote Ig secretion ... More

FGF23 activates injury-primed renal fibroblasts via FGFR4-dependent signalling and enhancement of TGF-ß autoinduction.

Authors:Smith ER, Holt SG, Hewitson TD

Journal:Int J Biochem Cell Biol

PubMed ID:28919046

Bone-derived fibroblast growth factor 23 (FGF23) is an important endocrine regulator of mineral homeostasis with effects transduced by cognate FGF receptor (FGFR)1-a-Klotho complexes. Circulating FGF23 levels rise precipitously in patients with kidney disease and portend worse renal and cardiovascular outcomes. De novo expression of FGF23 has been found in the ... More

High Tidal Volume Induces Mitochondria Damage and Releases Mitochondrial DNA to Aggravate the Ventilator-Induced Lung Injury.

Authors:Lin JY, Jing R, Lin F, Ge WY, Dai HJ, Pan L

Journal:Front Immunol

PubMed ID:30018615

This study aimed to determine whether high tidal volume (HTV) induce mitochondria damage and mitophagy, contributing to the release of mitochondrial DNA (mtDNA). Another aim of the present study was to investigate the role and mechanism of mtDNA in ventilator-induced lung injury (VILI) in rats. ... More

Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells.

Authors:Baykal-Köse S, Acikgoz E, Yavuz AS, Gönül Geyik Ö, Ates H, Sezerman OU, Özsan GH, Yüce Z

Journal:PLoS One

PubMed ID:32106243

Tyrosine kinase inhibitor (TKI) resistance is a major problem in chronic myeloid leukemia (CML). We generated a TKI-resistant K562 sub-population, K562-IR, under selective imatinib-mesylate pressure. K562-IR cells are CD34-/CD38-, BCR-Abl-independent, proliferate slowly, highly adherent and form intact tumor spheroids. Loss of CD45 and other hematopoietic markers reveal these cells have ... More