Abcam, ab261667, Human KMT5A knockout HEK-293 cell lysate

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KMT5A KO cell lysate available now. KO validated by Next Generation Sequencing. Free of charge wild type control included. Knockout achieved by CRISPR/Cas9; X = 7 bp deletion, 10 bp deletion and INDEL (25 bp deletion + 11 bp insertion); Frameshift = 96%.
Key facts
Cell type:HEK-293,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Next Generation Sequencing,
Mutation description:Knockout achieved by CRISPR/Cas9; X = 7 bp deletion, 10 bp deletion and INDEL (25 bp deletion + 11 bp insertion); Frameshift = 96%

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-KMT5A, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Next Generation 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.
KMT5A also known as SETD8 or Pr-SET7 is a histone methyltransferase enzyme with a notable role in regulating chromatin dynamics. It specifically catalyzes the monomethylation of histone H4 at lysine 20 (H4K20me1) a modification linked to chromatin compaction and DNA damage response. The molecular mass of KMT5A is approximately 47 kDa. Expression of KMT5A is observed in various tissues including the liver kidney and to some extent in embryonic stem cells indicating its functionality across different stages of development and cell types.
Biological function summary
KMT5A's activity influences several essential cellular processes such as cell cycle progression and DNA repair. As part of a larger chromatin-modulating framework it often functions alongside other chromatin-associated proteins including those from the Polycomb group. It plays a significant role in maintaining genomic stability by marking specific regions of chromatin for certain functions thereby affecting transcription regulation and cellular growth.
Pathways
KMT5A integrates into critical biological mechanisms like the DNA damage response and cell cycle regulation. It links closely with pathways involving p53 and cyclin-dependent kinase (CDK) inhibitors. KMT5A’s histone modification activity influences proteins such as p21 and p16 within the DNA damage signaling network. Its regulatory role here is essential as it facilitates an environment conducive to the DNA repair machinery following genotoxic stress.
KMT5A connects to various pathological states notably cancer and neurodegenerative disorders. Misregulation of KMT5A activity is associated with tumorigenesis where altered levels of H4K20me1 can lead to abnormal cell proliferation. Additionally KMT5A interacts through pathways tied to protein like TP53 influencing cellular responses to stressors typically seen in oncogenesis. Similarly aberrant regulation has implications in cognitive impairments potentially through dysregulated methylation patterns affecting neuronal cell cycle re-entry.