Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat.No. | Product Name | Price |
---|---|---|
CLKO-2046 | HAVCR2 KO Cell Lysate-Hela | Inquiry |
CLOE-1443 | Human HAVCR2 HEK293 Cell Lysate | Inquiry |
CLOE-1444 | Human HAVCR2(His) HEK293 Cell Lysate | Inquiry |
CLOE-2247 | Mouse Havcr2 HEK293 Cell Lysate | Inquiry |
CLOE-2250 | Mouse Havcr2(Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC006853 | Panoply™ Human HAVCR2 Knockdown Stable Cell Line | Inquiry |
CSC-RO0013 | Human HAVCR2 Stable Cell Line-CHO | Inquiry |
CSC-RO0119 | Human HAVCR2 Stable Cell Line-HEK293T | Inquiry |
CSC-RO0228 | Monkey HAVCR2 Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0598 | Human HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RO0599 | Monkey HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RT2409 | Human HAVCR2 Knockout Cell Line-Hela | Inquiry |
CSC-SC006853 | Panoply™ Human HAVCR2 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLKO-2046 | HAVCR2 KO Cell Lysate-Hela | Inquiry |
CLOE-1443 | Human HAVCR2 HEK293 Cell Lysate | Inquiry |
CLOE-1444 | Human HAVCR2(His) HEK293 Cell Lysate | Inquiry |
CLOE-2247 | Mouse Havcr2 HEK293 Cell Lysate | Inquiry |
CLOE-2250 | Mouse Havcr2(Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC006853 | Panoply™ Human HAVCR2 Knockdown Stable Cell Line | Inquiry |
CSC-RO0013 | Human HAVCR2 Stable Cell Line-CHO | Inquiry |
CSC-RO0119 | Human HAVCR2 Stable Cell Line-HEK293T | Inquiry |
CSC-RO0228 | Monkey HAVCR2 Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0598 | Human HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RO0599 | Monkey HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RT2409 | Human HAVCR2 Knockout Cell Line-Hela | Inquiry |
CSC-SC006853 | Panoply™ Human HAVCR2 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLKO-2046 | HAVCR2 KO Cell Lysate-Hela | Inquiry |
CLOE-1443 | Human HAVCR2 HEK293 Cell Lysate | Inquiry |
CLOE-1444 | Human HAVCR2(His) HEK293 Cell Lysate | Inquiry |
CLOE-2247 | Mouse Havcr2 HEK293 Cell Lysate | Inquiry |
CLOE-2250 | Mouse Havcr2(Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC006853 | Panoply™ Human HAVCR2 Knockdown Stable Cell Line | Inquiry |
CSC-RO0013 | Human HAVCR2 Stable Cell Line-CHO | Inquiry |
CSC-RO0119 | Human HAVCR2 Stable Cell Line-HEK293T | Inquiry |
CSC-RO0228 | Monkey HAVCR2 Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0598 | Human HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RO0599 | Monkey HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RT2409 | Human HAVCR2 Knockout Cell Line-Hela | Inquiry |
CSC-SC006853 | Panoply™ Human HAVCR2 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLKO-2046 | HAVCR2 KO Cell Lysate-Hela | Inquiry |
CLOE-1443 | Human HAVCR2 HEK293 Cell Lysate | Inquiry |
CLOE-1444 | Human HAVCR2(His) HEK293 Cell Lysate | Inquiry |
CLOE-2247 | Mouse Havcr2 HEK293 Cell Lysate | Inquiry |
CLOE-2250 | Mouse Havcr2(Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC006853 | Panoply™ Human HAVCR2 Knockdown Stable Cell Line | Inquiry |
CSC-RO0013 | Human HAVCR2 Stable Cell Line-CHO | Inquiry |
CSC-RO0119 | Human HAVCR2 Stable Cell Line-HEK293T | Inquiry |
CSC-RO0228 | Monkey HAVCR2 Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0598 | Human HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RO0599 | Monkey HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RT2409 | Human HAVCR2 Knockout Cell Line-Hela | Inquiry |
CSC-SC006853 | Panoply™ Human HAVCR2 Over-expressing Stable Cell Line | Inquiry |
Cat.No. | Product Name | Price |
---|---|---|
CLKO-2046 | HAVCR2 KO Cell Lysate-Hela | Inquiry |
CLOE-1443 | Human HAVCR2 HEK293 Cell Lysate | Inquiry |
CLOE-1444 | Human HAVCR2(His) HEK293 Cell Lysate | Inquiry |
CLOE-2247 | Mouse Havcr2 HEK293 Cell Lysate | Inquiry |
CLOE-2250 | Mouse Havcr2(Fc) HEK293 Cell Lysate | Inquiry |
CSC-DC006853 | Panoply™ Human HAVCR2 Knockdown Stable Cell Line | Inquiry |
CSC-RO0013 | Human HAVCR2 Stable Cell Line-CHO | Inquiry |
CSC-RO0119 | Human HAVCR2 Stable Cell Line-HEK293T | Inquiry |
CSC-RO0228 | Monkey HAVCR2 Stable Cell Line - CHO-K1 | Inquiry |
CSC-RO0598 | Human HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RO0599 | Monkey HAVCR2 Stable Cell Line - THP-1 | Inquiry |
CSC-RT2409 | Human HAVCR2 Knockout Cell Line-Hela | Inquiry |
CSC-SC006853 | Panoply™ Human HAVCR2 Over-expressing Stable Cell Line | Inquiry |
TIM-3, also known as HAVCR2, is part of the larger TIM (T-cell immunoglobulin and mucin domain) family, which plays varied roles in immune response regulation, across autoimmune diseases, cancer immunosurveillance, and more. In humans, this family includes TIM1, TIM3, and TIM4, located on chromosome 5q33.2. TIM-3's function as an immune checkpoint makes it a significant focus in the field of immunotherapy, especially regarding its regulation of T-cell exhaustion in cancer and chronic viral infections.
TIM-3 is a membrane protein comprising an extracellular domain, a transmembrane domain, and a cytoplasmic tail, consisting of 281 amino acids. Comprising an IgV domain with glycosylation sites, the extracellular area helps to interact with many ligands. Several immune cells express TIM-3: Th1 and Th17 helper T-cells, regulatory T-cells (Treg), dendritic cells (DCs), monocytes, and natural killer (NK) cells. Its prevalence in tumor settings is also shown by its presence in tumor-infiltrating lymphocytes (TILs). TIM-3 production in T-cells usually indicates those with compromised function; it is a hallmark of fatigue particularly about malignancies or persistent infections where immune evasion is common.
TIM-3 interacts with multiple ligands, such as Galectin 9, phosphatidylserine (PtdSer), and CEACAM1, which bind at distinct sites on the IgV domain. Galectin 9 binding may compromise anti-tumor defenses by causing T-cell death and inhibiting Th1-mediated immune responses. Although its precise physiological effect is yet less known, TIM-3 helps to remove apoptotic cells using PtdSer interaction. The association with HMGB1 compromises DNA vaccination effectiveness and chemotherapy results through nucleic acid, hence influencing immune response. TIM-3 is recruited to the immunological synapse of activated T-cells and interacts with BAT3 and LCK kinase to sustain T-cell activation when it is not attached to its ligands.
Figure 1. Models for TIm3–ligand interactions. (Wolf Y, et al., 2022)
In its inhibitory capacity, TIM-3 plays a crucial role in regulating immune responses by modulating T-cell activity. The inhibition of T-helper type 1 (Th1) lymphocytes diminishes auto- and alloimmune responses, promoting immunological tolerance. Conversely, TIM-3 may provoke immunological responses in some situations by increasing TCR-induced signaling in T-cells, which includes ZAP70, LCK, and FYN. Though it may also reduce NK cell-mediated cytotoxicity in certain inflammatory reactions, TIM-3 works as a coreceptor on innate immune cells like NK cells, hence increasing IFN-gamma generation.
The implications of TIM-3 expression extend to cancer, where it is often associated with immune evasion mechanisms. TIM-3 expression has consequences in cancer as well, where it is usually linked with immune evasion mechanisms. Utilizing T-cell mediated response suppression, lets cancer cells escape immune monitoring, hence promoting disease development and treatment resistance. Often, TIM-3 on T-cells in tumor microenvironments indicates an aberrant immune response.
Apart from cancer, TIM-3 also has a function in infectious pathogens and autoimmune disorders. TIM-3 inhibits autoreactive T-cells, hence helping to minimize immune-mediated tissue damage in autoimmune settings. TIM-3 regulates natural immunity during infections, especially with intracellular pathogens, therefore helping to resolve inflammation. Excessive suppression of immune responses, however, may cause infections to persist as well.
Immunotherapy research depends much on TIM-3, as other immune checkpoints such as CTLA4 and PD-1. Pharmaceutical firms are aggressively looking for TIM-3 targeting therapies given no authorized medications. Focusing on illnesses like acute myeloid leukemia and non-small cell lung cancer, these treatments are in different clinical trial stages. Combining TIM-3 inhibitors with current therapies could provide more therapeutic advantages.
Therapeutic use of TIM-3 and PD-1/PD-L1 pathways together might strengthen immune responses against cancers. Engaging a larger immune assault on cancer cells, several therapeutic studies investigate dual-specific antibodies targeting both TIM-3 and PD-1 or PD-L1. These medicines provide a more complete immune modulation strategy meant to offset adaptive resistance mechanisms seen with anti-PD-1 therapy. Early research has shown encouraging outcomes in lowering tumor loads and increasing immune cell penetration into malignancies.
While targeting TIM-3 presents considerable promise, challenges remain in understanding its complex biology and interactions. The therapeutic potential of TIM-3 inhibitors, especially in combination with other immunomodulators, continues to attract scientific interest. Researchers are exploring the precise mechanisms by which TIM-3 influences different immune cell types and its role under various pathological conditions to design more effective interventions.
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