Abcam, ab266690, Human SETD2 (KMT3A / HYPB / HIF-1) knockout HEK-293T cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
SETD2 KO cell line available to order. KO validated by Western blot. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 11 bp deletion in exon 3 and 4 bp deletion in exon 3. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 11 bp deletion in exon 3 and 4 bp deletion in exon 3

Product details:
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
patent pages

Properties and Storage Information:
Gene name-SETD2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
KMT3A also known as HYPB (Huntington's disease gene-related protein B) or HIF-1 is a histone methyltransferase enzyme that mechanically transfers methyl groups to histone H3 at lysine 4 and lysine 36. This activity important for chromatin modification influences transcriptional regulation. The molecular mass of KMT3A is approximately 130 kDa. This enzyme is expressed in various tissues such as the brain heart and skeletal muscle highlighting its extensive physiological role.
Biological function summary
KMT3A modifies chromatin structure to regulate gene expression. Its histone methylation function plays a critical role in the modulation of transcriptional activity ensuring that genes are turned on or off when necessary for cellular function. Additionally KMT3A forms part of complex protein networks that mediate gene expression changes in response to cellular signals. The precise regulation of this activity is vital for maintaining normal cellular function and responding to environmental cues.
Pathways
KMT3A engages in significant pathways such as the transcriptional regulation and epigenetic modification pathways. It interacts with various proteins including CoREST and LSD1 within these pathways to modulate gene expression and influence cellular differentiation. Through these interactions KMT3A ensures the correct genetic programs are executed aligning with developmental and homeostatic requirements.
KMT3A has been implicated in neurological conditions such as Huntington's disease. The abnormal regulation or mutation of this target can disrupt its activity and lead to improper chromatin modification which results in altered gene expression and contributes to disease progression. Furthermore KMT3A's interaction with the HIF-1α pathway also links it to cancer as dysregulation can aid in tumor growth and progression by affecting gene expression patterns associated with cell proliferation and survival.