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Sigma-Aldrich

MITOCHONDRIAL PROTEIN IP KIT

Sufficient for 50 tests

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Synonym(s):
mitochondrial protein immunoprecipitation kit
UNSPSC Code:
12352200
NACRES:
NA.32

form

liquid

technique(s)

immunoprecipitation (IP): suitable

storage temp.

−20°C

General description

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.

Application

MITOCHONDRIAL PROTEIN IP KIT has been used to perform immunoprecipitation and co-immunoprecipitation (Co-IP) of mitochondrial proteins.

Biochem/physiol Actions

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

Signal Word

Danger

Hazard Statements

Hazard Classifications

Acute Tox. 3 Oral - Aquatic Acute 1 - Aquatic Chronic 1 - Eye Dam. 1 - Skin Corr. 1B

WGK

WGK 3

Regulatory Information

监管及禁止进口产品

Certificates of Analysis (COA)

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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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