|Recombinant Mouse TIMD4 protein (Catalog#50388-M08H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Mouse TIMD4 (rM TIMD4; Catalog#50388-M08H; NP_848874.3; Met 1-Thr 279). Total IgG was purified by Protein A affinity chromatography.|
ELISA: 0.5-1 μg/mL
This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Mouse TIMD4. The detection limit for Mouse TIMD4 is 0.0049 ng/well.
Anti-Histone H3 rabbit monoclonal antibody at 1:200 dilution
Lane A: NIH3T3 Whole Cell Lysate
Lane B: Hela Whole Cell Lysate
Lysates/proteins at 30 μg per lane.
Goat Anti-Rabbit IgG (H+L)/HRP at 1/10000 dilution.
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size:15 kDa
Observed band size:17 kDa
A type I transmembrane protein called TIM4 (T-cell immunoglobulin- and mucin-domain-containing molecule; also known as TIMD4), which belongs to the immunoglobulin superfamily and TIM family. TIM4 is involved in regulating T-cell proliferation and lymphotoxin signaling. It is a ligand for HAVCR1/TIMD1. Recent reports indicate that dendritic cell (DC)-derived T-cell immunoglobulin and mucin domain molecule (TIM)-4, which is expressed on dendritic cells and macrophages, plays an important role in the initiation of T(H)2 polarization. TIM4 bound apoptotic cells by recognizing phosphatidylserine via its immunoglobulin domain. The expression of TIM4 in fibroblasts enhanced their ability to engulf apoptotic cells. TIM4 is phosphatidylserine receptor for the engulfment of apoptotic cells, and may also be involved in intercellular signalling in which exosomes are involved. Modulation of TIM4 production in dendritic cells (DCs) represents a novel therapeutic approach for the treatment of peanut allergy. The interaction of TIM1/TIM4 played a critical role in sustaining the polarization status of Th2 cells in allergic rhinitis (AR) patients. Cross-linking FcgammaRI by antigen/IgG complexes increased the production of TIM4 by dendritic cells via upregulating tumor necrosis factor-alpha in DCs. Specific immunotherapy (SIT) suppresses the skewed Th2 responses via disrupting the interaction of TIM1/TIM4 in antigen-specific Th2 cells.