Abcam, ab264499, Human ACTA2 knockout HeLa cell lysate

Size: 1Kit
ACTA2 KO cell lysate available now. KO validated by Immunocytochemistry, Next Generation Sequencing, Western blot. Free of charge wild type control included.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Immunocytochemistry,Next Generation Sequencing,Western blot,
Disease:Adenocarcinoma

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-ACTA2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Immunocytochemistry, Next Generation Sequencing, Western blot, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Alpha smooth muscle actin (α-SMA) also known as ACTA2 is an actin isoform with a specific role in the contractile function of smooth muscle cells. The molecular weight of α-SMA is approximately 42 kDa. This protein is expressed widely in vascular smooth muscle cells the peritoneal lining and myofibroblasts. It often serves as a marker for these cell types. The expression of α-SMA is critical for the mechanical attributes of cells contributing to the rigidity and contractility of tissues where it is present.
Biological function summary
Alpha smooth muscle actin aids in maintaining the structural integrity of tissues by forming part of the actin cytoskeleton an important element in cellular support. It exists in high concentration in stress fibers contributing to cellular movements and shape maintenance. These actions are essential in various dynamic cellular processes such as cell migration and adhesion. Alpha smooth muscle actin does not typically form complexes but it associates with other components of the actin cytoskeleton to ensure cell stability and function.
Pathways
Alpha smooth muscle actin functions significantly within the TGF-beta signaling pathway which influences cell proliferation differentiation and apoptosis. It interacts closely with proteins such as myosin to facilitate cellular contractility and motility. Additionally α-SMA plays a part in the RhoA/Rho kinase (ROCK) pathway connecting with regulators of actin filament organization. These pathways are essential for modulation of smooth muscle contraction and actin filament assembly contributing to vascular development and wound healing.
Alpha smooth muscle actin is importantly involved in fibrotic diseases and vascular diseases like arteriosclerosis. Increased expression of α-SMA is often observed in fibrotic tissues contributing to pathogenesis due to excessive extracellular matrix deposition. In the context of vascular disorders overexpression of α-SMA can lead to abnormal vascular remodeling often seen in diseases like hypertension. Interactions with proteins such as fibronectin and collagens facilitate these pathological changes highlighting the importance of α-SMA in disease development.