R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
STIL (E4U6R) Rabbit mAb #38589
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- WB
Inquiry Info. # 38589
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Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 170 |
| 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
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
STIL (E4U6R) Rabbit mAb recognizes endogenous levels of total STIL protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the carboxy terminus of human STIL protein.
Background
STIL (SCL/TAL-1 interrupting locus) is an integral component of the complex required for centriole duplication during cell division (1). Centrioles are microtubule structures within the centrosome that have a critical role in the assembly of the mitotic spindle and templating the formation of primary cilia. Centriole duplication taking place during cell division involves the transient association of STIL with PLK4 and SAS-6 into a cartwheel structure (2). STIL directly interacts and is phosphorylated by PLK4 (3-7). Deletion of STIL in mice leads to lethality with a loss of centrioles and primary cilia (8). Mutation of the STIL gene in humans leads to neurological defects, including microcephaly (9-11). Expression of STIL has been associated with several cancer types. The STIL locus was originally identified in chromosomal aberration in T-cell leukemias (12). Elevated expression of STIL is observed in several cancer types, where it may contribute to increased mitotic activity, oncogenic signaling pathways, metastatic potential, and poor prognosis (13-18).
- Arquint, C. and Nigg, E.A. (2016) Biochem Soc Trans 44, 1253-1263.
- Gönczy, P. and Hatzopoulos, G.N. (2019) J Cell Sci 132, jcs228833. doi: 10.1242/jcs.228833.
- Arquint, C. et al. (2015) Elife 4, e07888. doi: 10.7554/eLife.07888.
- Ohta, M. et al. (2014) Nat Commun 5, 5267.
- Moyer, T.C. et al. (2015) J Cell Biol 209, 863-78.
- Kratz, A.S. et al. (2015) Biol Open 4, 370-7.
- Dzhindzhev, N.S. et al. (2014) Curr Biol 24, 2526-32.
- David, A. et al. (2014) Cell Cycle 13, 2859-68.
- Kakar, N. et al. (2015) Hum Genet 134, 45-51.
- Kumar, A. et al. (2009) Am J Hum Genet 84, 286-90.
- Bennett, H. et al. (2014) Pediatr Neurol 51, 434-6.
- Aplan, P.D. et al. (1992) Blood 79, 1327-33.
- Ramaswamy, S. et al. (2003) Nat Genet 33, 49-54.
- Erez, A. et al. (2004) Oncogene 23, 5371-7.
- Rabinowicz, N. et al. (2017) Oncotarget 8, 27380-27392.
- Yu, H. et al. (2022) Cancers (Basel) 14, 5777. doi: 10.3390/cancers14235777.
- Wu, X. et al. (2019) Gene 686, 220-227.
- Wang, J. et al. (2019) J Cell Mol Med 23, 5566-5575.
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