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I. Tanaka

Researcher at Kyoto University

Publications -  27
Citations -  940

I. Tanaka is an academic researcher from Kyoto University. The author has contributed to research in topics: Receptor & Northern blot. The author has an hindex of 17, co-authored 27 publications receiving 928 citations.

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Journal Article

Molecular cloning and expression of multiple isoforms of human prostaglandin E receptor EP3 subtype generated by alternative messenger RNA splicing: Multiple second messenger systems and tissue-specific distributions

TL;DR: The present study suggests the presence of the multiple systems of PGE2/EP3 isoforms and leads to the better understanding of its physiological and pathophysiological implications in humans.
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Prostaglandin E receptor subtypes in mouse osteoblastic cell line

TL;DR: The results indicate that EP1, EP4, and probably EP2 are present in MC3T3-E1 cells; EP1 promotes cell growth, and EP2 and EP4 mediate differentiation of the osteoblast.
Journal Article

C-type natriuretic peptide in chronic renal failure and its action in humans.

TL;DR: A role for C-type natriuretic peptide in human renal function is suggested after examining the plasma level of CNP in patients with various cardiovascular diseases, including chronic renal failure (CRF) patients who were under hemodialysis therapy.
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Prostaglandin E2 (PGE2) Autoamplifies its Production Through EP1 Subtype of PGE Receptor in Mouse Osteoblastic MC3T3-E1 Cells

TL;DR: Data indicate that PGHS-2 mRNA induction is mediated through EP1 subtype of PGE receptor in MC3T3-E1 cells, which is considered to be important in elongating the otherwise short-lived PGE2 action in certain physiological conditions such as mechanical stress and fracture healing, as well as the pathological inflammatory bone loss.
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Immunoreactive β-Endorphin and Adrenocorticotropin in Human Cerebrospinal Fluid

TL;DR: CSF beta-EP-LI and ACTH-LI levels determined every 5 min over a period of 80 min in three normal volunteers did not show moment-to-moment variability, suggesting that beta-endorphin and ACTh in human CSF share the common regulatory mechanism in normal and pathologic conditions.