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Naohiko Seki

Researcher at Chiba University

Publications -  391
Citations -  20245

Naohiko Seki is an academic researcher from Chiba University. The author has contributed to research in topics: microRNA & Cancer. The author has an hindex of 74, co-authored 381 publications receiving 18648 citations. Previous affiliations of Naohiko Seki include Toho University & National Institute of Radiological Sciences.

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Hereditary progressive dystonia with marked diurnal fluctuation caused by mutations in the GTP cyclohydrolase I gene

TL;DR: The identification of four independent mutations of the gene for GTP cyclohydrolase I in patients with HPD, as well as a marked decrease in the enzymes activity in mononuclear blood cells, confirms that the GTP cycling enzyme gene is a causative gene for HPD/DRD.
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Prediction of the coding sequences of unidentified human genes. II. The coding sequences of 40 new genes (KIAA0041-KIAA0080) deduced by analysis of cDNA clones from human cell line KG-1.

TL;DR: In this series of projects regarding the accumulation of sequence information of unidentified human genes, the sequences of 40 full-length cDNA clones of human cell line KG-1 are newly deduced, and the coding sequences of the corresponding genes are predicted.
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miR-145, miR-133a and miR-133b: Tumor-suppressive miRNAs target FSCN1 in esophageal squamous cell carcinoma

TL;DR: The identification of tumor‐suppressive miRNAs,miR‐145, miR‐133a and miR-133b, directly control oncogenic FSCN1 gene, and could provide new insights into potential mechanisms of ESCC carcinogenesis.
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Identification of novel microRNA targets based on microRNA signatures in bladder cancer.

TL;DR: The target search algorithm and gene‐expression profiling in BCs revealed that Keratin7 (KRT7) mRNA was a common target of the downregulated miRNAs, and the mRNA expression levels of KRT7 were significantly higher inBCs than in NBEs.
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Influence of hepatitis B virus genotypes on the progression of chronic type B liver disease

TL;DR: Although the patients with genotype B experience earlier HBe seroconversion, slower progression of liver fibrosis, and slower development of HCC, the life‐long risk of progression to advanced fibrosis and development ofHCC may not differ among genotypes B‐ and C‐related chronic liver disease.