GBP2 (F2Y3F) Rabbit mAb #53311
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 70 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Background
GBPs are IFN-inducible proteins widely distributed among eukaryotes and are involved in innate immune response and inflammasome activation (3,4). During infection, GBP2 can be localized to pathogen-containing vacuoles and act as a positive regulator of inflammasome assembly. GBP2 promotes lysis of pathogen-containing vacuoles, and recruits proteins that mediate bacterial lysis. This process makes ligands available that are detected by inflammasomes, such as lipopolysaccharide (LPS) that activate the non-canonical caspases (through caspase-4 and caspase-11) or double-stranded DNA (dsDNA) that activates inflammasome assembly through AIM2 (5).
In addition to GBP2’s role in immune response, recent work has explored the role of GBP2 in tumor growth and progression (6-8). Increased GBP2 expression is associated with a better prognosis in breast and colon cancers and may result in increased T cell defense against some tumor types (6,7). GBP2 overexpression in mouse fibroblasts inhibited Rac pathway activation and matrix metalloproteinase-9 (MMP-9) expression, highlighting a role for GBP2 in cancer metastasis (6). Conversely, in glioma cells, increased GBP2 enhances proliferation and migration, likely through epidermal growth factor receptor (EGFR) signaling and direct interaction with kinesin superfamily member 22 (KIF22) (7). Given its dual role in immune response and cancer, GBP2 represents a potential therapeutic target.
- Kim, B.H. et al. (2011) Science 332, 717-21.
- Schelle, L. et al. (2023) Med Microbiol Immunol 212, 141-152.
- Braun, E. et al. (2019) Cell Rep 27, 2092-2104.e10.
- Kim, B.H. et al. (2016) Nat Immunol 17, 481-9.
- Dickinson, M.S. et al. (2023) Proc Natl Acad Sci USA 120, e2216028120.
- Zhang, J. et al. (2017) Cell Death Dis 8, e3151.
- Wang, H. et al. (2022) J Immunother Cancer 10, e004302. doi: 10.1136/jitc-2021-004302.
- Ren, Y. et al. (2022) Cell Death Discov 8, 208.
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