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Masatoshi Hagiwara

Researcher at Kyoto University

Publications -  286
Citations -  17513

Masatoshi Hagiwara is an academic researcher from Kyoto University. The author has contributed to research in topics: Protein kinase A & RNA splicing. The author has an hindex of 60, co-authored 272 publications receiving 16297 citations. Previous affiliations of Masatoshi Hagiwara include University of Tokyo & Tokyo Medical and Dental University.

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Journal ArticleDOI

Full sequence of neurocalcin, a novel calcium-binding protein abundant in central nervous system.

Katsuo Okazaki, +5 more
- 29 May 1992 - 
TL;DR: The deduced amino acid sequence revealed that neurocalcin is composed of 193 amino acids, has a molecular mass of 22,284 daltons, and contains three putative calcium-binding sites (EF-hand motifs) and may play a visinin- or recoverin-like role in brain.
Journal Article

Gene therapy against an experimental glioma using adeno-associated virus vectors

Hideho Okada, +8 more
- 01 Nov 1996 - 
TL;DR: High titer AAV vector treatment may be safe and effective for in vivo gene therapy of human brain tumors and Cocultures of AAV-tk-IRES-IL2 transduced cells and nontransduces cells proved highly sensitive to GCV indicating the contribution of the bystander effect.
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Identification of a novel nuclear speckle-type protein, SPOP

Yasuo Nagai, +7 more
- 24 Nov 1997 - 
TL;DR: Deletion analysis revealed that both the POZ domain and the evolutionarily conserved region at the amino‐terminus are required for the nuclear speckled accumulation of SPOP.
Journal ArticleDOI

Novel SR-protein-specific kinase, SRPK2, disassembles nuclear speckles.

Noriyo Kuroyanagi, +3 more
- 14 Jan 1998 - 
TL;DR: The results indicate that SRPK family members may regulate the disassembly of the SR proteins in a tissue-specific manner.
Journal ArticleDOI

Inhibition of DYRK1A destabilizes EGFR and reduces EGFR-dependent glioblastoma growth

Natividad Pozo, +10 more
- 03 Jun 2013 - 
TL;DR: It is proposed that the recovery of EGFR stability is a key oncogenic event in a large proportion of gliomas and that pharmacological inhibition of DYRK1A could represent a promising therapeutic intervention for EGFR-dependent GBMs.