Leukemia is one of the most deadly diseases, responsible for the highest number of childhood cancer cases. Immunoglobulin-containing and proline-rich receptor-1 (IGPR-1) is a newly identified protein found to play an important role in human colon cancer and angiogenesis. The overall goal of this project was to assess IGPR-1 expression in leukemia cell lines and investigate its possible function in the NF-κB pathway, specifically the role of inhibitor of nuclear factor kappa-B kinase subunit beta (IKKβ) in the phosphorylation of IGPR-1. The NF-κB pathway, among others, plays a critical role in human-T-cell leukemia virus type 1 (HTLV-1) infected T-cells. Our preliminary results indicated that IGPR-1 is expressed in leukemia cell lines at variable levels. Further experiments demonstrated that IKKβ is involved in the phosphorylation of IGPR-1 as treatment of HEK-293 cells ectopically expressing IGPR-1 with an IKKβ inhibitor decreased IGPR-1 phosphorylation at Ser220. Likewise, cells treated with lipopolysaccharide (LPS), which is known to activate IKKβ, also stimulated the phosphorylation of IGPR-1 at Ser220. However, transfection of IGPR-1/HEK293 cells with Tax, an oncogene encoded by HTLV-1, decreased phosphorylation of IGPR-1 at Ser220. Taken together, our data indicates that activation of IKKβ in the NF-κB pathway stimulates phosphorylation of IGPR-1. / 2020-06-17T00:00:00Z
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/36699 |
| Date | 17 June 2019 |
| Creators | Wang, Shawn |
| Contributors | Rahimi, Nader, Franzblau, Carl |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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