| Project/Area Number |
20791364
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Functional basic dentistry
|
|---|
| Research Institution | The Nippon Dental University |
|---|
Principal Investigator |
MAEDA Genta The Nippon Dental University, 生命歯学部, 助教 (80434140)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
|---|
| Keywords | IKKα / MALT1 / NFκB / メチレーション / エピジェネティック / GATA3 / 扁平上皮癌 / 分化 / 転写因子 |
|---|
| Research Abstract |
Mucosa-associated lymphoid tissue1 (MALT1) activates nuclear factor -kB (NFκB) in lymphocyte lineages and have an effect on differentiation of epithelium. However, its expression and role in the pathology of malignant tumors of epithelial origin is not known. I examined MALT1 expression and its implications for the pathology. In this result, MALT1 expression is epigenetically inactivated during tumor progression, suggesting that the detection of MALT1 expression is a useful predictive and prognostic determinant in the clinical management.
Determining binding sites of transcription factor is important for understanding the transcriptional control of target genes. I developed concatenate ChIP that rapidly and cost effectively specifies genomic fragments. Subsequently I investigated GATA3 binding sites and target genes to employed this new method. These data demonstrate that GATA3 binds to regulatory elements and controls target gene expression through physical interaction with core promoter regions.
|
