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TIM-3/HAVCR2/CD366 (BSB-163)
TIM-3/HAVCR2/CD366 (BSB-163)
- 中文名称：
- TIM-3/HAVCR2/CD366 (BSB-163)
- 英文名称：
- TIM-3/HAVCR2/CD366 (BSB-163)
- 品牌：
- AAA Biotech
- 品牌介绍：
- AAA Biotech专注于为全球生命科学研究提供高品质的蛋白质研究工具，核心产品包括经严格验证的抗体、重组蛋白及ELISA试剂盒。
- 货号：
- AAA59395
- 规格：
- 5 Slides|3 mL (RTU)|0.1 mL (Concentrate)|7 mL (RTU)|0.5 mL (Concentrate)
- 保存建议：
- Store at 2-8 degree C (Control Slides: Store at 20-25 degree C)
- 货期：
- 6-8周
- 来源宿主：
- Mouse
- 反应种属：
- Human
- 免责声明：
- *本产品仅供科研实验使用，不得用于临床诊断。*
- 其他：
克隆性:Monoclonal
同型:IgG2c
克隆号:[BSB-163]
特异性:N/A
纯度:N/A
形式：Paraffin, Frozen
TIM-3 is a mouse monoclonal antibody derived from cell culture supernatant that is concentrated, dialyzed, filter sterilized and diluted in buffer pH7.5, containing BSA and sodium azide as a preservative.
浓度：N/A
- 说明书：
T-cell Immunoglobulin and Mucin-domain Containing-3 (TIM-3), also known as Hepatitis A virus cellular receptor 2 (HAVCR2), is a protein that in humans is encoded by the HAVCR2 gene. TIM-3 is an immune checkpoint and together with other inhibitory receptors including programmed cell death protein 1 (PD-1) and lymphocyte activation gene 3 protein (LAG3) mediate CD8+ T-cell exhaustion. TIM-3 expression is up-regulated in tumor-infiltrating lymphocytes in Lung, Gastric, Head & Neck Cancers, Schwannoma, Melanoma and Follicular B-cell Non-Hodgkin Lymphoma. The TIM-3 pathway may interact with the PD-1 pathway in the dysfunctional CD8+ T cells and Tregs in cancer. TIM-3 is mainly expressed on activated CD8+ T cells and suppresses macrophage activation following PD-1 inhibition.
Upregulation has been observed in tumors progressing after anti-PD-1 therapy. It has been reported that early breast cancer patients with TIM-3+ iTILs have significantly improved breast cancer-specific survival whereas TIM-3+ sTILs did not reach statistical significance and it was concluded that the presence of TIM-3+ iTILs is an independent favorable prognostic factor in the whole cohort as well as among ER negative patients. In myelogenous leukemia (AML), upregulated TIM-3 during AML could reduce cytokine production. Co-expression of PD-1 and TIM-3 was correlated with AML progression. In follicular B-cell non-Hodgkin lymphoma, TIM-3 was expressed on nearly 35% of lymph node CD4+ and CD8+ T cells and could mediate T-cells exhaustion. In glioma patients, TIM-3 was correlated with cancer immune escape and might be a potent target. In colorectal cancer, upregulation of TIM-3 could restrict T-cell responses and might participate in tumorigenesis. The expression of TIM-3 antibody might be an independent prognostic factor for colorectal cancer.
