Abcam, ab258981, Human MYPN knockout HeLa cell lysate

Size: 1Kit
MYPN KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2.,
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, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-MYPN, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
The MYPN protein also known as myopalladin weighs around 145 kDa. Scientists find MYPN in skeletal and cardiac muscle tissues where it plays a critical role in muscle structure and function. This protein associates with actin filaments and alpha-actinin regulating the organization and stability of the sarcomere the fundamental unit of muscle contraction. By interacting with proteins in the Z-disc MYPN acts as a scaffold which aids in maintaining the architecture necessary for force transmission.
Biological function summary
Myopalladin influences muscle contractility by integrating signals and structural elements in the sarcomere. MYPN forms part of a protein complex involving nebulin and titin which are essential in muscle elasticity and stability. MYPN's presence impacts cellular mechanisms vital in muscle growth and regeneration. It regulates intracellular signaling pathways ensuring muscles respond properly to mechanical stress and maintain their integrity under load.
Pathways
MYPN participates in the MAPK signaling pathway and links with the cytoskeletal regulatory network. In these pathways MYPN works with proteins such as alpha-actinin and titin to mediate cellular responses to mechanical stimuli. These connections highlight its role in maintaining muscle homeostasis. The involvement of MYPN in such pathways signifies its importance in the cellular adaptation process affecting various signal transduction processes and structural developments during muscle contraction and repair.
MYPN mutations associate with conditions like dilated cardiomyopathy and hypertrophic cardiomyopathy. These cardiac diseases show how important MYPN is in maintaining heart muscle function. Mutations can lead to disrupted sarcomere structure causing impaired cardiac function. Additionally the protein connects to titin another sarcomeric protein involved in similar cardiomyopathies highlighting the interplay between sarcomeric proteins in disease mechanisms.