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| Status |
Public on Sep 15, 2015 |
| Title |
Smad2 and Smad3 binding sites in H345-TbRII cells |
| Organism |
Homo sapiens |
| Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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| Summary |
Transforming growth factor (TGF)-beta induces apoptosis of many types of cancer cells and acts as a tumor suppressor. We found lower expression of TGF-beta type II receptor (TbRII) in most of SCLC cells and tissues than in normal lung epithelial cells and normal lung tissues, respectively. In vitro cell growth and in vivo tumor formation were suppressed by TGF-beta-mediated apoptosis when the wild-type TbRII was overexpressed in SCLC cells. We therefore determined Smad2 and Smad3 (Smad2/3) binding sites in a SCLC cell line H345 stably expressing exogenous TbRII (H345-TbRII) to identify target genes of TGF-beta.
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| Overall design |
Smad2 and Smad3 binding sites in H345-TbRII cells were determined by ChIP-seq (one sample analysis, without replicates).
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| Contributor(s) |
Murai F, Ehata S, Koinuma D, Miyazono K |
| Citation missing |
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| |
| Submission date |
Dec 04, 2014 |
| Last update date |
May 15, 2019 |
| Contact name |
Daizo Koinuma |
| E-mail(s) |
d-koinuma@umin.ac.jp
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| Organization name |
University of Tokyo
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| Department |
Pathology
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| Street address |
Hongo 7-3-1, Bunkyo-ku
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| City |
Tokyo |
| ZIP/Postal code |
113-0033 |
| Country |
Japan |
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| Platforms (1) |
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| Samples (1) |
| GSM1558744 |
Smad2 and Smad3 ChIP-seq of H345-TbRII cells |
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| Relations |
| BioProject |
PRJNA269296 |
| SRA |
SRP050562 |
