| 货号 | 67856S |
| 同种亚型 | Mouse IgG1 |
| 反应种属 | H Mk |
| 来源宿主 | Mouse IgG1 |
| 应用 | W IP IF-IC |
| 目标/特异性 | RCAS1 (D8K2E) Mouse mAb recognizes endogenous levels of total RCAS1 protein. |
| 使用方法 | WB(1:1000) IP (1:50) IF-IC (1:50) |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 背景 | Receptor binding cancer antigen expressed on SiSo cells (RCAS1) is also known as estrogen receptor-binding fragment-associated gene 9 (EBAG9). Originally identified as an estrogen-inducible gene (1), RCAS1 was recently found to play a novel role in the adaptive immune response by negatively regulating the cytolytic activity of cytotoxic T lymphocytes (CTLs) (2). RCAS1 is conserved in phylogeny and is ubiquitously expressed in most human tissues and cells (3,4). There is evidence that tissue expression of RCAS1 is increased in a variety of malignancies, including cancers of the gastrointestinal tract, liver, lung, breast, ovary, endometrium, and cervix. Research studies have shown that levels of RCAS1 tissue expression are negatively correlated with the prognosis of patients harboring the aforementioned malignancies (4). It is also noteworthy that research studies have detected elevated levels of RCAS1 in the sera of cancer patients (4). Initial studies indicated that RCAS1 was secreted from cancer cells and functioned as a ligand for a putative receptor expressed on NK cells, as well as T and B lymphocytes, inducing their apoptosis, which enabled cancer cells to evade immune surveillance (5,6). Subsequent studies have identified RCAS1 as a type III transmembrane Golgi protein with the ability to regulate vesicle formation, secretion, and protein glycosylation (2,7-9). Indeed, it has been shown that RCAS1 overexpression negatively regulates the cytolytic function of CTLs by negatively regulating protein trafficking from the trans-Golgi to secretory lysosomes (2). Furthermore, RCAS1 overexpression delays vesicle transport from the ER to Golgi and causes components of the ER quality control and glycosylation machinery to mislocalize. As a consequence, RCAS1 induces the deposition of tumor-associated glycan antigens on the cell surface, which are thought to contribute to tumor pathogenesis through the mediation of adhesion, invasion, and metastasis (8,9). |
| 运输条件 | 0.75 |
| 存放说明 | -20C |
| 计算分子量 | 32 |
| 参考文献 | 1 . Watanabe, T. et al. (1998) Mol Cell Biol 18, 442-9. 2 . Rüder, C. et al. (2009) J Clin Invest 119, 2184-203. 3 . Tsuchiya, F. et al. (2001) Biochem Biophys Res Commun 284, 2-10. 4 . Giaginis, C. et al. (2009) Histol Histopathol 24, 761-76. 5 . Matsushima, T. et al. (2001) Blood 98, 313-21. 6 . Nakashima, M. et al. (1999) Nat Med 5, 938-42. 7 . Reimer, T.A. et al. (2005) BMC Cancer 5, 47. 8 . Wolf, J. et al. (2010) FASEB J 24, 4000-19. 9 . Engelsberg, A. et al. (2003) J Biol Chem 278, 22998-3007. |
Confocal immunofluorescent analysis of MCF7 cells, untreated (left) or treated with Brefeldin A #9972 (5 μg/ml, 1hr; right), using RCAS1 (D8K2E) Mouse mAb (green). Actin filaments were labeled with DyLight™ 554 Phalloidin #13054 (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye). | |
Western blot analysis of extracts from MCF7 and T47D cells using RCAS1 (D8K2E) Mouse mAb. |
