KMT5A KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9; X = 7 bp deletion, 10 bp deletion and INDEL (25 bp deletion + 11 bp insertion); Frameshift = 96%.
H4 K20 specific histone methyltransferase, H4-K20-HMTase, H4-K20-HMTase SETD8, Histone H4 K20 methyltransferase, Histone lysine N methyltransferase H4 lysine 20 specific, Histone-lysine N-methyltransferase SETD8, Lysine N-methyltransferase 5A, N-lysine methyltransferase SETD8, PR-Set7, PR/SET domain containing protein 8, PR/SET domain-containing protein 07, PR/SET07, Pr SET 7, PrSET7, SET 07, SET 8, SET domain containing (lysine methyltransferase) 8, SET domain containing 8, SET domain containing lysine methyltransferase 8, SET domain-containing protein 8, SETD 8, SETD8_HUMAN
KMT5A KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided. Knockout achieved by CRISPR/Cas9; X = 7 bp deletion, 10 bp deletion and INDEL (25 bp deletion + 11 bp insertion); Frameshift = 96%.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
We will provide viable cells that proliferate on revival.
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 and patent pages.
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.
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.
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.
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X = 7 bp deletion, 10 bp deletion and INDEL (25 bp deletion + 11 bp insertion)
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