Abcam, ab257527, Human MAPK9 knockout HEK-293T cell lysate

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MAPK9 KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 2 and 2 bp insertion in exon 2 and Insertion of the selection cassette in exon 2.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 2 and 2 bp insertion in exon 2 and Insertion of the selection cassette in exon 2.

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-MAPK9, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger 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.
C-Jun N-terminal kinase 2 also known as JNK2 is a member of the MAPK (mitogen-activated protein kinase) family. JNK2 plays a significant role in transmitting signals within cells. It is a protein with a mass of approximately 48 kDa and exists in various tissues including the brain heart and liver. JNK2 is ubiquitously expressed and has two main isoforms produced by alternative splicing. These isoforms are involved in different biological functions emphasizing the protein's versatility.
Biological function summary
C-Jun N-terminal kinase 2 is key in regulating processes such as cell growth apoptosis and differentiation. JNK2 is part of the MAP kinase signal transduction pathways and forms interactions with several proteins including the scaffolding proteins known as JNK-interacting proteins (JIPs). These complexes help coordinate the response of JNK2 in cellular stress and inflammatory responses. JNK2 is also critical in modulating the expression of genes by activating transcription factors such as c-Jun and ATF2.
Pathways
JNK2 operates within the MAPK signaling pathway by integrating various upstream signals to exert effects on gene expression. JNK2 phosphorylates and activates transcription factors playing an important role in cellular responses to stress. It is closely connected to other proteins within the pathway such as JNK1 and JNK3 together contributing to the complex regulation of stress-induced apoptosis and pro-inflammatory responses. These interactions highlight JNK2's essential function across multiple signaling networks.
Research connects c-Jun N-terminal kinase 2 to both cancer and neurodegenerative diseases. Its role in controlling apoptosis and cell proliferation links JNK2 to tumor progression where abnormal JNK2 activity can lead to oncogenesis. Additionally in neurodegenerative diseases like Alzheimer's dysregulated JNK2 signaling may accelerate neuronal death. JNK2's association with other proteins involved in these disorders such as amyloid precursor protein in Alzheimer's disease highlights its influence in pathological processes.