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Hirotaka Osada

Researcher at Laboratory of Molecular Biology

Publications -  44
Citations -  4992

Hirotaka Osada is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Lung cancer & LMO2. The author has an hindex of 27, co-authored 44 publications receiving 4850 citations.

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A Polycistronic MicroRNA Cluster, miR-17-92, Is Overexpressed in Human Lung Cancers and Enhances Cell Proliferation

TL;DR: Findings clearly suggest that marked overexpression of the miR-17-92 cluster with occasional gene amplification may play a role in the development of lung cancers, especially in their most aggressive form, small-cell lung cancer, and that the C13orf25 gene may well be serving as a vehicle in this regard.
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The LIM‐only protein Lmo2 is a bridging molecule assembling an erythroid, DNA‐binding complex which includes the TAL1, E47, GATA‐1 and Ldb1/NLI proteins

TL;DR: It is shown that in erythroid cells Lmo2 forms a novel DNA‐binding complex, with GATA‐1, TAL1 and E2A, and the recently identified LIM‐binding protein Ldb1/NLI, which may play a role in haematopoiesis.
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Somatic in vivo alterations of the JV18-1 gene at 18q21 in human lung cancers

TL;DR: Findings suggest that although JV18-1 and DPC4 may play roles in a limited fraction of lung cancers, another tumor suppressor gene may also exist in this chromosome region.
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The LIM protein RBTN2 and the basic helix-loop-helix protein TAL1 are present in a complex in erythroid cells

TL;DR: It is demonstrated, using anti-RBTN2 and anti-TAL1 antisera, that the LIM protein RBTN2 is not phosphorylated and is complexed with the TAL1 phosphoprotein in the nucleus of erythroid cells, providing a direct link between proteins activated by chromosomal translocations in T-cell acute leukemia.
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Frequent loss of imprinting of the H19 gene is often associated with its overexpression in human lung cancers.

TL;DR: It is shown here that LOI of H19 is also a frequent event in lung cancer development, and correlated with hypomethylation of the promoter region, and overexpression of H 19 is often associated with LOIof H19 in lung cancers retaining both parental alleles.