Gene: KIR2DS1
Official Full Name: killer cell immunoglobulin like receptor, two Ig domains and short cytoplasmic tail 1provided by HGNC
Gene Summary: Killer cell immunoglobulin-like receptors (KIRs) are transmembrane glycoproteins expressed by natural killer cells and subsets of T cells. The KIR genes are polymorphic and highly homologous and they are found in a cluster on chromosome 19q13.4 within the 1 Mb leukocyte receptor complex (LRC). The gene content of the KIR gene cluster varies among haplotypes, although several "framework" genes are found in all haplotypes (KIR3DL3, KIR3DP1, KIR3DL4, KIR3DL2). The KIR proteins are classified by the number of extracellular immunoglobulin domains (2D or 3D) and by whether they have a long (L) or short (S) cytoplasmic domain. KIR proteins with the long cytoplasmic domain transduce inhibitory signals upon ligand binding via an immune tyrosine-based inhibitory motif (ITIM), while KIR proteins with the short cytoplasmic domain lack the ITIM motif and instead associate with the TYRO protein tyrosine kinase binding protein to transduce activating signals. The ligands for several KIR proteins are subsets of HLA class I molecules; thus, KIR proteins are thought to play an important role in regulation of the immune response. [provided by RefSeq, Jul 2008]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO36919 | KIR2DS1 Knockout cell line (HeLa) | Human | KIR2DS1 | 1:3~1:6 | Negative | Online Inquiry |
KO36920 | KIR2DS1 Knockout cell line (HCT 116) | Human | KIR2DS1 | 1:2~1:4 | Negative | Online Inquiry |
KO36921 | KIR2DS1 Knockout cell line (HEK293) | Human | KIR2DS1 | 1:3~1:6 | Negative | Online Inquiry |
KO36922 | KIR2DS1 Knockout cell line (A549) | Human | KIR2DS1 | 1:3~1:4 | Negative | Online Inquiry |
KIR2DS1 Gene Knockout Cell Lines are genetically engineered cell lines designed to lack the expression of the KIR2DS1 (Killer-cell Immunoglobulin-like Receptor 2DS1) gene, which plays a critical role in modulating immune responses. These cell lines are created through advanced CRISPR/Cas9 gene editing techniques, enabling researchers to investigate the functional role and mechanisms of the KIR2DS1 receptor in various biological processes. The absence of KIR2DS1 allows for deeper insights into its contributions to natural killer (NK) cell activity, immune evasion by tumors, and viral responses.
The key function of the KIR2DS1 receptor is to recognize and potentially enhance the cytotoxicity of NK cells against target cells. By utilizing the KIR2DS1 Gene Knockout Cell Lines, researchers can study the effects of KIR2DS1 signaling—or lack thereof—on both inherent and adaptive immunity, thereby facilitating the understanding of NK cell dynamics in health and disease. These models are invaluable in cancer immunology research, as they help elucidate mechanisms by which tumors manipulate immune checkpoints.
One of the unique selling points of KIR2DS1 Gene Knockout Cell Lines is their specificity and reliability in replicating the KIR2DS1-negative environment, providing a clear experimental framework that distinguishes the effects of this receptor from other KIRs. Compared to alternative cell models, these knockout lines are precisely tailored for targeted studies, reducing confounding variables associated with non-specific gene expression.
The value of these KIR2DS1 Gene Knockout Cell Lines is particularly significant for researchers and clinicians focusing on cancer immunotherapy, infectious diseases, and transplant rejection studies. By providing a robust model to explore immune modulation, these cell lines empower scientists to develop more effective therapeutic strategies and enhance the comprehensiveness of immunological research.
At our company, we pride ourselves on our expertise in genetic engineering and cell line development, ensuring that our products meet the highest scientific standards to support advancing research and clinical applications.
Please note that all services are for research use only. Not intended for any clinical use.
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