TIM3 antibody (PE)

Catalog No. ABIN2663420

The PE-conjugated Mouse Monoclonal anti-TIM3 antibody (Clone F38-2E2) (ABIN2663420) specifically detects TIM3 in ICFC. The antibody is reactive with Human samples.

Quick Overview for TIM3 antibody (PE) (ABIN2663420)

Target: TIM3 (TIM 3) (Hepatitis A Virus Cellular Receptor 2 (TIM 3))

Reactivity: Human

Host: Mouse

Clonality: Monoclonal

Conjugate: This TIM3 antibody is conjugated to PE

Application: Intracellular Flow Cytometry (ICFC)

Clone: F38-2E2

Product Details anti-TIM3 Antibody (PE)

Cross-Reactivity: Rhesus Monkey

Purification: The antibody was purified by affinity chromatography, and conjugated with PE under optimal conditions. The solution is free of unconjugated PE and unconjugated antibody.

Isotype: IgG1 kappa

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

Buffer: Phosphate-buffered solution, pH 7.2, containing 0.09 % sodium azide and 0.2 % (w/v) BSA .

Preservative: Sodium azide

Precaution of Use: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Handling Advice: Protect from prolonged exposure to light. Do not freeze.

Storage: 4 °C

Storage Comment: The antibody solution should be stored undiluted between 2°C and 8°C.

Target Details for TIM3

Target: TIM3 (TIM 3) (Hepatitis A Virus Cellular Receptor 2 (TIM 3))

Alternative Name: CD366

Target Type: Virus

Background: CD366 (Tim-3) is a transmembrane protein also known as T cell immunoglobulin and mucin domain containing protein-3. Tim-3 is expressed at high levels on activated T cells (preferentially on Th1 cells, monocytes/macrophages, and dendritic cells). Tim-3 has also been shown to exist as a soluble protein. Cells expressing Tim-3 are present at high levels in the CNS of animals at the onset of experimental autoimmune encephalomyelitis (EAE), a disease mediated by lymphocytes secreting Th1-like cytokines. Tim-3 has been proposed to inhibit Th1-mediated immune responses and promote immunological tolerance.

Pathways: Regulation of Lipid Metabolism by PPARalpha, Cancer Immune Checkpoints