R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
SNX9 (F9G1M) Rabbit mAb #54984
Filter:
- WB
- IP
Supporting Data
REACTIVITY | H M R Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 78 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Simple Western™ | 1:10 - 1:50 |
Immunoprecipitation | 1:50 |
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
SNX9 (F9G1M) Rabbit mAb recognizes endogenous levels of total SNX9 protein.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human SNX9 protein.
Background
Sorting nexins (SNXs) are a family of cytoplasmic proteins characterized by the presence of a phosphatidylinositol 3-phosphate (PI3P) binding phox (PX) domain. This binding occurs mainly in the early endosome and allows for trafficking of the bound protein to either a degradative or recycling pathway (1). Sorting nexin family member 9 (SNX9) is a multifunctional scaffolding protein that plays an important role in clathrin-mediated endocytosis (CME) (2). In CME, SNX9 binds to the protein clathrin at the plasma membrane and recruits the GTPase dynamin to facilitate membrane fission and vesicle release (3). SNX9 also recruits the protein N-WASP to the cell membrane, a key regulator of actin dynamics (4). SNX9’s function in actin assembly contributes to cancer progression, primarily by affecting cell invasion and metastasis. For instance, SNX9 has been shown to promote metastasis in breast cancer through its interaction with N-WASP and RhoA-ROCK (5). Interestingly, SNX9 has also been shown to have reduced expression in primary tumors relative to healthy tissue (6). In this context, SNX9 downregulation promotes the formation of actin-rich structures known as invadopodia, which are required for cancer cells to invade through the basement membrane (6). SNX9 is also recruited to immunological synapses during T cell activation, where it complexes with N-WASP, p85, and CD28 to internalize CD28 via CME (7,8). Furthermore, targeted knockout of SNX9 has been shown to alleviate CD8+ T cell exhaustion, suggesting its use as a therapeutic target in cancer immunotherapies (9).
- Hanley, S.E. and Cooper, K.F. (2020) Cells 10, 17. doi: 10.3390/cells10010017.
- Bendris, N. and Schmid, S.L. (2017) Trends Cell Biol 27, 189-200.
- Soulet, F. et al. (2005) Mol Biol Cell 16, 2058-67.
- Yarar, D. et al. (2007) Dev Cell 13, 43-56.
- Bendris, N. et al. (2016) Mol Biol Cell 27, 1409-19.
- Bendris, N. et al. (2016) J Cell Sci 129, 2804-16.
- Badour, K. et al. (2007) Proc Natl Acad Sci USA 104, 1593-8.
- Ecker, M. et al. (2022) Elife 11, e67550. doi: 10.7554/eLife.67550.
- Trefny, M.P. et al. (2023) Nat Commun 14, 86.
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