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Masazumi Nishimoto

Researcher at Saitama Medical University

Publications -  33
Citations -  1801

Masazumi Nishimoto is an academic researcher from Saitama Medical University. The author has contributed to research in topics: Embryonic stem cell & Gene. The author has an hindex of 16, co-authored 31 publications receiving 1705 citations.

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The Gene for the Embryonic Stem Cell Coactivator UTF1 Carries a Regulatory Element Which Selectively Interacts with a Complex Composed of Oct-3/4 and Sox-2.

TL;DR: The biochemical analyses reveal that the UTF1 regulatory element can, by its one-base difference from the canonical octamer-binding sequence, selectively recruit the complex comprising Oct-3/4 and Sox-2 and preclude the binding of the transcriptionally inactive complex containing Oct-1 or Oct-6, and these properties are dictated by the unique ability of the Oct- 3/4 POU-homeodomain that recognizes a variant of theOctamer motif in the UTF2 regulatory element.
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Identification of Sox-2 regulatory region which is under the control of Oct-3/4-Sox-2 complex.

TL;DR: The regulatory regions of the Sox-2 gene are analyzed and two enhancers which stimulate transcription in ES cells as well as in embryonal carcinoma cells are identified which are able to stimulate transcription through the SRR2 element.
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UTF1, a novel transcriptional coactivator expressed in pluripotent embryonic stem cells and extra-embryonic cells

TL;DR: UTF1 displays many of the hallmark characteristics expected for a tissue‐specific transcriptional coactivator that works in early embryogenesis, and is not a major component of the E1A‐like activity present in pluripotent embryonic cells.
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Oct-3/4 maintains the proliferative embryonic stem cell state via specific binding to a variant octamer sequence in the regulatory region of the UTF1 locus.

TL;DR: A molecular pathway by which Oct-3/4 induces rapid proliferation and tumorigenic properties of ES cells through activation of the UTF1 gene is suggested.
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Consequence of the loss of Sox2 in the developing brain of the mouse

TL;DR: Inactivated Sox2 specifically in the developing brain by using Cre–loxP system found that expression level of Sox3 is elevated in Sox2 null developing brain, probably mitigating the effects of loss of Sox2.