形式
liquid
技术
immunoprecipitation (IP): suitable
储存温度
−20°C
一般描述
The mitochondrial protein immunoprecipitation (IP) kit contains a ready-to-use mitochondria protein IP buffer, optimized for immunoprecipitation (IP and co-IP) using mitochondria and mitochondrial extracts. The buffer is a gentle formulation, which maintains the stability of mitochondrial complexes.
应用
MITOCHONDRIAL PROTEIN IP KIT has been used to perform immunoprecipitation and co-immunoprecipitation (Co-IP) of mitochondrial proteins.
生化/生理作用
The mitochondrial protein immunoprecipitation (IP) kit also provides choices of detergents, N-dodecyl-β-D-maltoside, Triton X-100, and digitonin, to achieve different stringency conditions for protein-protein interaction studies. Triton X-100 is the most commonly used detergent, especially for membrane protein solubilization. The mitochondrial protein immunoprecipitation (IP) kit may be used for the following:
- optimized for compatibility with immunoprecipitation (IP and co-IP) and pull-down using tagged proteins
- gentle formulation for maintenance of stable mitochondrial complexes
- compatible with sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS PAGE), 2D gel, native gel, and mass spectrometry
- functional assays and enzymatic assays
警示用语：
Danger
危险声明
危险分类
Acute Tox. 3 Oral - Aquatic Acute 1 - Aquatic Chronic 1 - Eye Dam. 1 - Skin Corr. 1B
储存分类代码
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
法规信息
监管及禁止进口产品
Jinchul Kim et al.
Cancer cell, 35(2), 191-203 (2019-02-05)
The tumor suppressor p53 is somatically mutated in half of all human cancers. Paradoxically, the wild-type p53 (WTp53) is often retained in certain human cancers, such as hepatocarcinoma (HCC). We discovered a physiological and oncogenic role of WTp53 in suppressing
Rongli Zhang et al.
Journal of molecular and cellular cardiology, 112, 64-73 (2017-09-09)
Heart failure is associated with mitochondrial dysfunction so that restoring or improving mitochondrial health is of therapeutic importance. Recently, reduction in NAD+ levels and NAD+-mediated deacetylase activity has been recognized as negative regulators of mitochondrial function. Using a cardiac specific
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