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AB258981

Human MYPN knockout HeLa cell lysate

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MYPN KO cell lysate available now. KO validated. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon2.
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Sanger Sequencing - Human MYPN knockout HeLa cell lysate (AB258981)
  • Sanger seq

Unknown

Sanger Sequencing - Human MYPN knockout HeLa cell lysate (AB258981)

Homozygous : 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

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Complementary Products

Primary Antibodies

AB233039

Anti-MYPN antibody

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-MYPN antibody (AB233039)

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Cell Lines & Lysates

AB266058

Human MYPN knockout HeLa cell line

Sanger Sequencing - Human MYPN knockout HeLa cell line (AB266058)

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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 and patent pages.

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What's included?

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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
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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.
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Quality control

STR analysis

CSF1PO, D13S317, D7S820, D5S818, TH01, D16S539, TPOX

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Cell culture

Biosafety level

EU: 2 US: 2

Adherent/suspension

Adherent

Gender

Female

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Product protocols

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Product promise

We are committed to supporting your work with high-quality reagents, and we're here for you every step of the way. In the unlikely event that one of our products does not perform as expected, you're protected by our Product Promise.
For full details, please see our Terms & Conditions

Please note: All products are 'FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES'.

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