Gene: SETDB2
Official Full Name: SET domain bifurcated histone lysine methyltransferase 2provided by HGNC
Gene Summary: This gene encodes a member of a family of proteins that contain a methyl-CpG-binding domain (MBD) and a SET domain and function as histone methyltransferases. This protein is recruited to heterochromatin and plays a role in the regulation of chromosome segregation. This region is commonly deleted in chronic lymphocytic leukemia. Naturally-occuring readthrough transcription occurs from this gene to the downstream PHF11 (PHD finger protein 11) gene. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2016]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO25359 | SETDB2 Knockout cell line (HeLa) | Human | SETDB2 | 1:3~1:6 | Negative | Online Inquiry |
KO25360 | SETDB2 Knockout cell line (HCT 116) | Human | SETDB2 | 1:2~1:4 | Negative | Online Inquiry |
KO25361 | SETDB2 Knockout cell line (HEK293) | Human | SETDB2 | 1:3~1:6 | Negative | Online Inquiry |
KO25362 | SETDB2 Knockout cell line (A549) | Human | SETDB2 | 1:3~1:4 | Negative | Online Inquiry |
SETDB2 Gene Knockout Cell Lines are engineered cellular models designed to facilitate the study of the SETDB2 gene, which plays a critical role in epigenetic regulation and chromatin dynamics. The creation of these knockout cell lines involves targeted gene editing technologies, such as CRISPR/Cas9, which specifically disable the expression of the SETDB2 gene, allowing researchers to investigate its functions and downstream effects in a controlled environment. By eliminating the expression of this gene, scientists can uncover the molecular pathways that SETDB2 regulates and understand its implications in various biological contexts, particularly in cancer and developmental biology.
The key function of SETDB2 is its role in histone methylation, particularly in the tri-methylation of lysine 9 on histone H3 (H3K9me3), a modification associated with gene silencing and regulation of gene expression. The knockout cell lines enable researchers to study the impact of reduced or absent SETDB2 activity on gene expression profiles, chromatin structure, and cellular responses to external stimuli. This systematic approach provides invaluable insights into the epigenetic landscape and its alterations in disease conditions.
In research and clinical settings, SETDB2 Gene Knockout Cell Lines have significant importance, particularly in cancer research, where aberrant epigenetic regulation can lead to tumorigenesis. These models serve as vital tools for understanding the mechanisms of SETDB2 in tumor progression and potential therapeutic approaches targeting epigenetic machinery. Additionally, they can be instrumental for drug screens, molecular pathogenesis studies, and the development of targeted therapies.
Compared to alternative models, the unique selling point of SETDB2 Gene Knockout Cell Lines lies in their precision and specificity. They provide an unparalleled opportunity to dissect the role of this specific gene with minimal off-target effects, ultimately leading to more reliable results in experiments. The customizable nature of these cell lines also allows for versatility across various research applications.
For researchers, clinicians, and biotechnology companies, the value of SETDB2 Gene Knockout Cell Lines is further amplified by their ability to bridge the gap between basic research and clinical applications. They provide a powerful platform to unravel the complexities of gene function and its contributions to disease, fostering innovative solutions and therapeutic strategies.
Our company is dedicated to advancing scientific research through high-quality biological products. With a strong foundation in genetic engineering and cell line development, we empower researchers with tools that enhance their studies and contribute to the advancement of biomedical sciences.
Please note that all services are for research use only. Not intended for any clinical use.
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