Abstract
Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-S-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.
| Original language | English |
|---|---|
| Pages (from-to) | 14-19 |
| Number of pages | 6 |
| Journal | Medical Molecular Morphology |
| Volume | 46 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 16-01-2013 |
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All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
- Molecular Biology
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Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1. / Shimomura, Atsushi; Takasaki, Akihiko; Nomura, Ryuji; Hayashi, Nobuhiro; Senda, Takao.
In: Medical Molecular Morphology, Vol. 46, No. 1, 16.01.2013, p. 14-19.Research output: Contribution to journal › Article
TY - JOUR
T1 - Identification of DNA-dependent protein kinase catalytic subunit as a novel interaction partner of lymphocyte enhancer factor 1
AU - Shimomura, Atsushi
AU - Takasaki, Akihiko
AU - Nomura, Ryuji
AU - Hayashi, Nobuhiro
AU - Senda, Takao
PY - 2013/1/16
Y1 - 2013/1/16
N2 - Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-S-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.
AB - Lymphocyte enhancer factor 1 (LEF1), a member of the LEF/T-cell-specific factor (TCF) family of the high mobility group domain transcription factors, acts downstream in canonical Wnt signaling. Aberrant transactivation of LEF1 contributes to the tumorigenesis of colonic neoplasms, sebaceous skin tumors, and lymphoblastic leukemia. LEF1-associated proteins are crucial for regulating its transcriptional activity. In this study, glutathione-S-transferase pull-down assay and mass spectrometry enabled identification of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a novel interaction partner for LEF1. The interaction between LEF1 and DNA-PKcs was confirmed using in vivo co-immunoprecipitation. Furthermore, double immunofluorescence observations showed that LEF1 and DNA-PKcs colocalized in the nuclei of colon adenocarcinoma cell lines. Identification of the interaction between LEF1 and DNA-PKcs may provide clues for a novel therapy for cancer treatment as well as for understanding LEF1-mediated transcriptional regulation.
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UR - http://www.scopus.com/inward/citedby.url?scp=84875243092&partnerID=8YFLogxK
U2 - 10.1007/s00795-012-0002-z
DO - 10.1007/s00795-012-0002-z
M3 - Article
C2 - 23325550
AN - SCOPUS:84875243092
VL - 46
SP - 14
EP - 19
JO - Medical Molecular Morphology
JF - Medical Molecular Morphology
SN - 1860-1480
IS - 1
ER -