R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
TSPO (D1N7Z) Rabbit mAb #70358
Filter:
- WB
- IP
- IHC
- IF
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 18 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:100 |
Immunohistochemistry (Paraffin) | 1:50 - 1:200 |
Immunofluorescence (Immunocytochemistry) | 1:200 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
TSPO (D1N7Z) Rabbit mAb recognizes endogenous levels of total TSPO protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly160 of human TSPO protein.
Background
Translocator protein (TSPO) is an 18 kDa mitochondrial drug- and cholesterol-transporting protein involved in steroid hormone synthesis and mitochondrial homeostasis in various cell types (1,2). Originally thought to play a role exclusively in steroid synthesis in steroidogenic cells, subsequent research studies have implicated TSPO in a variety of pathologies in a broad range of tissues, including progression of breast cancer, neuroinflammation, and neurological disorders (1,3-5). TSPO was first identified by its ability to bind benzodiazepines in peripheral tissues and glial cells, hence its alternate name, Peripheral Benzodiazepine Receptor (PBR).
TSPO has been shown to modulate an array of cellular functions; it is critical for steroidogenesis, modulates mitochondrial function and metabolism, and plays a role in both cell proliferation and apoptosis (2,6,7). TSPO is found in the outer mitochondrial membrane where it coordinates with Steroidogenic Acute Regulatory Factor (StAR) to transport cholesterol into the mitochondria and is critical for steroidogenesis and tumor progression (8,9). This is illustrated by studies that show the non-aggressive, hormone-dependent cell line, MCF7, expresses low levels of TSPO whereas the more aggressive, metastatic, and hormone-independent cell line, MDA-MB-231, expresses high levels of TSPO (9). This study, and others, suggest that TSPO may be an important regulator of hormone-dependent tumor progression. Numerous investigations have concluded that due to its high affinity for pharmacological compounds and upregulation in disease, TSPO is an attractive target for diagnosis and treatment of tumor progression, neuroinflammation, neurodegeneration, and neurological/psychiatric disorders (10-14).
TSPO has been shown to modulate an array of cellular functions; it is critical for steroidogenesis, modulates mitochondrial function and metabolism, and plays a role in both cell proliferation and apoptosis (2,6,7). TSPO is found in the outer mitochondrial membrane where it coordinates with Steroidogenic Acute Regulatory Factor (StAR) to transport cholesterol into the mitochondria and is critical for steroidogenesis and tumor progression (8,9). This is illustrated by studies that show the non-aggressive, hormone-dependent cell line, MCF7, expresses low levels of TSPO whereas the more aggressive, metastatic, and hormone-independent cell line, MDA-MB-231, expresses high levels of TSPO (9). This study, and others, suggest that TSPO may be an important regulator of hormone-dependent tumor progression. Numerous investigations have concluded that due to its high affinity for pharmacological compounds and upregulation in disease, TSPO is an attractive target for diagnosis and treatment of tumor progression, neuroinflammation, neurodegeneration, and neurological/psychiatric disorders (10-14).
- Batarseh, A. and Papadopoulos, V. (2010) Mol Cell Endocrinol 327, 1-12.
- Gatliff, J. and Campanella, M. (2012) Curr Mol Med 12, 356-68.
- Sileikyte, J. et al. (2011) J Biol Chem 286, 1046-53.
- Mukherjee, S. and Das, S.K. (2012) Curr Mol Med 12, 443-57.
- Da Pozzo, E. et al. (2012) Curr Mol Med 12, 426-42.
- Riond, J. et al. (1991) Eur J Biochem 195, 305-11.
- Veenman, L. and Gavish, M. (2012) Curr Mol Med 12, 398-412.
- Papadopoulos, V. et al. (1997) Steroids 62, 21-8.
- Batarseh, A. et al. (2012) Biochim Biophys Acta 1819, 38-56.
- Scarf, A.M. and Kassiou, M. (2011) J Nucl Med 52, 677-80.
- Rupprecht, R. et al. (2010) Nat Rev Drug Discov 9, 971-88.
- Venneti, S. et al. (2013) Glia 61, 10-23.
- Politis, M. et al. (2012) Front Pharmacol 3, 96.
- Calabresi, P.A. and Bohnen, N.I. (2012) Neurology 79, 496-7.
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