SMYD2 KO cell line available now. Free of charge wild type control available.
PC-3
Human
Prostate
Liquid
HSKM-B, Histone methyltransferase SMYD2, KMT3C, Lysine N-methyltransferase 3C, MGC119305, N-lysine methyltransferase SMYD2, SET and MYND domain containing 2, SET and MYND domain-containing protein 2, SMYD2_HUMAN, ZMYND14, Zinc finger MYND domain containing 14
SMYD2 KO cell line available now. Free of charge wild type control available.
HSKM-B, Histone methyltransferase SMYD2, KMT3C, Lysine N-methyltransferase 3C, MGC119305, N-lysine methyltransferase SMYD2, SET and MYND domain containing 2, SET and MYND domain-containing protein 2, SMYD2_HUMAN, ZMYND14, Zinc finger MYND domain containing 14
PC-3
Human
Prostate
Liquid
Adenocarcinoma
SMYD2
Knockout
CRISPR technology
EU: 1 US: 1
Adherent
Male
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.
F-12K + 10% FBS
Cell Freezing Medium-DMSO Serum free media, contains 8.7% DMSO in MEM supplemented with methyl cellulose.
Dry Ice
-196°C
Although we aim to provide customers with a homozygous clone, feasibility will be dependent on the biology of the protein. Should only heterozygous edits be achieved, you will be notified of the outcome and be asked to confirm whether the cell line is acceptable. All clones will be accompanied with DNA sequencing data, and the mutation description.
Recommended control: Human wild-type PC-3 cell line (Human wild-type PC-3 cell line ab290718). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
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.
This supplementary information is collated from multiple sources and compiled automatically.
KMT3C also known as SMYD2 is a lysine methyltransferase enzyme that possesses a unique SET domain responsible for catalyzing the methylation of lysine residues on histone and non-histone proteins. The enzyme has a molecular mass of approximately 52 kDa. SMYD2 shows expression in various tissues including heart skeletal muscle and also liver. It methylates histone H3 on lysine 36 (H3K36) and several non-histone proteins influencing gene expression regulation and protein function.
KMT3C/SMYD2 plays important roles in gene regulation and cellular processes. It functions as a part of a protein complex affecting transcriptional activation and repression via chromatin remodeling. The methylation activity of SMYD2 extends to p53 an important tumor suppressor linking it to the regulation of cell cycle and apoptosis. This enzymatic activity impacts cellular growth and differentiation interfacing with the larger network of cellular gene expression control and protein function modulation.
Research shows KMT3C/SMYD2 being active in the p53 and AKT signaling pathways fundamental to cell survival proliferation and apoptosis. In the context of the p53 pathway SMYD2 methylates p53 which may impact its tumor suppressor functions. SMYD2 also interacts with proteins like RB1 and HDAC1 integrating into broader cell regulatory networks. These interactions facilitate SMYD2's influence on pathways that govern important cellular processes such as growth and DNA damage response.
Mutations and overexpression of KMT3C/SMYD2 associate with various cancers including breast and esophageal cancer. In the case of breast cancer SMYD2 modulates p53 and RB1 activity contributing to tumorigenesis. Furthermore its interaction with HDAC1 connects it with epigenetic dysregulation seen in cancer progression. Altered activity or expression of SMYD2 disrupts normal cellular function providing a link between its biological activity and oncogenic processes.
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