Actin Polymerization/Depolymerization Assay Kit (ab239724)
Key features and details
- Detection method: Fluorescent
- Platform: Microplate reader
Overview
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Product name
Actin Polymerization/Depolymerization Assay Kit -
Detection method
Fluorescent -
Product overview
Actin Polymerization/Depolymerization Assay Kit (ab239724) can be used to study the effect of different compounds, proteins and tissue extracts on Actin polymerization and depolymerization.
The kit utilizes a proprietary Pyrene-labeled Actin molecule that develops a higher fluorescent signal if it undergoes polymerization. The signal can be easily detected using a fluorescence microplate reader. The assay is simple, high- throughput compatible, and can be completed in less than three hours.
Samples: Protein, Tissue Extracts, Compounds/Chemotherapeutic Agents.
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Platform
Microplate reader
Properties
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Storage instructions
Store at -20°C. Please refer to protocols. -
Components Identifier 100 tests ATP (100 mM) 2 x 100µl Buffer G 1 x 20ml Buffer P (10X) 1 x 1.5ml Labeled Rabbit Muscle Actin Blue cap 1 x 4 vials -
Research areas
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Function
Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells. -
Involvement in disease
Defects in ACTA1 are the cause of nemaline myopathy type 3 (NEM3) [MIM:161800]. A form of nemaline myopathy. Nemaline myopathies are muscular disorders characterized by muscle weakness of varying severity and onset, and abnormal thread-or rod-like structures in muscle fibers on histologic examination. The phenotype at histological level is variable. Some patients present areas devoid of oxidative activity containg (cores) within myofibers. Core lesions are unstructured and poorly circumscribed.
Defects in ACTA1 are a cause of myopathy congenital with excess of thin myofilaments (MPCETM) [MIM:161800]. A congenital muscular disorder characterized at histological level by areas of sarcoplasm devoid of normal myofibrils and mitochondria, and replaced with dense masses of thin filaments. Central cores, rods, ragged red fibers, and necrosis are absent.
Defects in ACTA1 are a cause of congenital myopathy with fiber-type disproportion (CFTD) [MIM:255310]; also known as congenital fiber-type disproportion myopathy (CFTDM). CFTD is a genetically heterogeneous disorder in which there is relative hypotrophy of type 1 muscle fibers compared to type 2 fibers on skeletal muscle biopsy. However, these findings are not specific and can be found in many different myopathic and neuropathic conditions. -
Sequence similarities
Belongs to the actin family. -
Cellular localization
Cytoplasm > cytoskeleton. - Information by UniProt
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Alternative names
- a actin
- a-actin
- ACTA
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Images
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Actin Polymerization is induced by Buffer P.
The process is inhibited by Latrunculin A (23 μM). Assays were performed following the kit protocol. Note: Latrunculin A is Actin polymerization inhibitor in vitro and in vivo by the formation of a 1:1 complex with monomeric G-actin. Latrunculin A acts a depolymerization agent acting on Actin filaments (Factin).
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Polymerized Actin is depolymerized by Latrunculin A (23 µM).Assays were performed following the kit protocol. Note: Latrunculin A is Actin polymerization inhibitor in vitro and in vivo by the formation of a 1:1 complex with monomeric G-actin. Latrunculin A acts a depolymerization agent acting on Actin filaments (Factin).
