TIM-4 (D3W4F) XP® Rabbit mAb #75484
- WB
- IHC
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous (IHC-P), Transfected (W, F) |
| MW (kDa) | 40-60 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IHC-Immunohistochemistry
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| IHC Leica Bond | 1:100 |
| Immunohistochemistry (Paraffin) | 1:100 |
| Flow Cytometry (Live) | 1:800 |
Storage
For a carrier-free (BSA and azide free) version of this product see product #27337.
Protocol
Specificity / Sensitivity
TIM-4 (D3W4F) XP® Rabbit mAb recognizes endogenous levels of total TIM-4 protein. This antibody does not cross-react with TIM-1 or TIM-3.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro215 of human TIM-4 protein.
Background
T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-4 is expressed by dendritic cells and macrophages (1). Like TIM-1, TIM-4 is a receptor for phosphatidylserine (2). Interaction of TIM-4 with phosphatidylserine exposed by cells undergoing apoptosis leads to uptake of apoptotic cells (2,3). In this way, TIM-4 regulates adaptive immunity by removing apoptotic antigen-specific T cells following clearance of infection. Peritoneal macrophages from mice deficient in TIM-4 fail to effectively clear apoptotic cells leading to hyperactive T and B cells and autoimmunity (4). In addition, TIM-4 expressed by tumor-associated macrophages and dendritic cells leads to autophagy-mediated degradation of dying tumor cells, resulting in reduced antigen presentation and T cell responses (5). TIM-4 was also identified as a ligand for TIM-1, and interaction between these proteins regulates T cell proliferation (1). Finally, TIM-4 is expressed by a subset of proinflammatory B cells that produce IFN-γ and promote Th1 cell differentiation (6).
- Meyers, J.H. et al. (2005) Nat Immunol 6, 455-64.
- Miyanishi, M. et al. (2007) Nature 450, 435-9.
- Kobayashi, N. et al. (2007) Immunity 27, 927-40.
- Rodriguez-Manzanet, R. et al. (2010) Proc Natl Acad Sci U S A 107, 8706-11.
- Baghdadi, M. et al. (2013) Immunity 39, 1070-81.
- Ding, Q. et al. (2017) J Immunol 199, 2585-2595.
Limited Uses
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