ASXL1 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 9 and 28 bp deletion in exon 9.
ASXL1_HUMAN, Additional sex combs like 1 (Drosophila), Additional sex combs-like protein 1, KIAA0978, Putative Polycomb group protein ASXL1
ASXL1 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon 9 and 28 bp deletion in exon 9.
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, 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 and patent pages.
ASXL1 also known as Additional Sex Combs-Like 1 functions primarily as a core component in chromatin modification processes. This protein has a molecular mass of approximately 165 kDa. ASXL1 is typically expressed in a wide range of tissues including hematopoietic cells indicating its role in diverse biological processes. The protein serves as a regulator of gene expression by influencing how tightly DNA wraps around histones allowing or restricting access to transcriptional machinery.
ASXL1 plays a critical role in epigenetic regulation and is often part of polycomb repressive complexes. These complexes contribute to transcriptional repression particularly during cellular differentiation and development. ASXL1 interacts with other proteins to modify histones thereby affecting the expression of genes involved in growth and differentiation processes. Its function is closely connected to developmental pathways given its impact on regulation at the chromatin level.
ASXL1 interacts with complex epigenetic regulatory networks. It takes part in the PRC2 (Polycomb Repressive Complex 2) pathway an essential pathway for transcriptional silencing via histone methylation. ASXL1 also shows interactions with proteins like EZH2 and SUZ12 within this pathway contributing to the methylation of histone H3 at lysine 27 (H3K27me3). Such interactions underline its role in chromatin remodeling and maintaining gene silencing during development and homeostasis.
ASXL1 mutations are frequently linked to myeloid malignancies such as myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). These mutations often result in loss of function disrupting gene expression regulation and leading to abnormal cellular proliferation. ASXL1’s role connects with the protein RUNX1 in these conditions where impaired regulation can progress to malignancies. Researchers continue to investigate the exact mechanisms through which these interactions contribute to the pathogenesis of these disorders.
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Terms & Conditions.
Allele-2: 1 bp insertion in exon 9.
Allele-1: 28 bp deletion in exon 9.
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