TIM-4 (D3W4F) XP® Rabbit mAb (BSA and Azide Free) #27337
- 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
This product is the carrier-free version of product #75484. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN, or CUT&Tag assays. If you require a carrier-free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
For standard formulation of this product see product #75484.
Storage
Specificity / Sensitivity
TIM-4 (D3W4F) XP® Rabbit mAb (BSA and Azide Free) 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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