Kanato Yamagata

ORCID: 0000-0001-6183-2511
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Inflammatory mediators and NSAID effects
  • Receptor Mechanisms and Signaling
  • Ion channel regulation and function
  • Eicosanoids and Hypertension Pharmacology
  • Axon Guidance and Neuronal Signaling
  • Retinal Development and Disorders
  • Immune Response and Inflammation
  • Estrogen and related hormone effects
  • Melanoma and MAPK Pathways
  • Neuropeptides and Animal Physiology
  • Neurogenesis and neuroplasticity mechanisms
  • Wnt/β-catenin signaling in development and cancer
  • Neurobiology and Insect Physiology Research
  • PI3K/AKT/mTOR signaling in cancer
  • Memory and Neural Mechanisms
  • Nuclear Receptors and Signaling
  • Tuberous Sclerosis Complex Research
  • Cancer-related gene regulation
  • Cancer, Hypoxia, and Metabolism
  • Genetics and Neurodevelopmental Disorders
  • Mitochondrial Function and Pathology
  • Phagocytosis and Immune Regulation
  • Nicotinic Acetylcholine Receptors Study
  • Cancer Mechanisms and Therapy

Tokyo Metropolitan Institute of Medical Science
2015-2024

Kushiro Rosai Hospital
2021-2024

Ritsumeikan University
2022

Shukutoku University
2008-2017

Fuchu Hospital
2002-2012

Tokyo Institute of Psychiatry
2011

Tokyo Women's Medical University
2009

Nihon University
2004

Kyoto University
2002

Osaka University
1990-2000

Neuronal activity is an essential stimulus for induction of plasticity and normal development the CNS. We have used differential cloning techniques to identify a novel immediate-early gene (IEG) cDNA that rapidly induced in neurons by models adult developmental plasticity. Both mRNA encoded protein are enriched neuronal dendrites. Analysis deduced amino acid sequence indicates region homology with alpha-spectrin, full-length protein, prepared vitro transcription/translation, coprecipitates...

10.1016/0896-6273(95)90299-6 article EN cc-by-nc-nd Neuron 1995-02-01

Pentylenetetrazole (PTZ) is a GABA-A receptor antagonist. An intraperitoneal injection of PTZ into an animal induces acute, severe seizure at high dose, whereas sequential injections subconvulsive dose have been used for the development chemical kindling, epilepsy model. A single low-dose mild without convulsion. However, repetitive decrease threshold to evoke convulsive seizure. Finally, continuous administration tonic-clonic This method simple and widely applicable investigate...

10.3791/56573 article EN Journal of Visualized Experiments 2018-06-12

Fever is triggered by an elevation of prostaglandin E(2) (PGE(2)) in the brain. However, mechanism its remains unanswered. We herein cloned rat glutathione-dependent microsomal E synthase (mPGES), terminal enzyme for PGE(2) biosynthesis, and examined induction brain after intraperitoneal injection pyrogen lipopolysaccharide (LPS). In Northern blot analysis, mPGES mRNA was weakly expressed under normal conditions but markedly induced between 2 4 hr LPS injection. situ hybridization study...

10.1523/jneurosci.21-08-02669.2001 article EN cc-by-nc-sa Journal of Neuroscience 2001-04-15

Neuronal activity results in long term cellular changes that underlie normal brain development and synaptic plasticity. To examine the molecular basis of activity-dependent plasticity, we have used differential cloning techniques to identify genes are rapidly induced neurons by activity. Here describe an inducible novel member Ras family small GTP-binding proteins termed Rheb. rheb mRNA is transiently hippocampal granule cells seizures NMDA-dependent potentiation paradigm. The predicted...

10.1016/s0021-9258(17)34012-7 article EN cc-by Journal of Biological Chemistry 1994-06-01

We previously showed that a febrile dose of lipopolysaccharide (LPS) in rats resulted induction cyclooxygenase-2 (COX-2) mRNA brain blood vessels/leptomeninges and telencephalic neurons. To elucidate the causal link between fever LPS-induced COX-2 mRNA, we experimentally modified one or other these parameters examined their relation. 1) was suppressed by pretreatment with COX-2-specific inhibitor. 2) Levels neurons vessels 2.5 h after LPS administration were even higher inhibitor-pretreated...

10.1152/ajpregu.1997.272.6.r1712 article EN AJP Regulatory Integrative and Comparative Physiology 1997-06-01

Significance Cancer cells reprogram their metabolism in response to growth factor receptor mutations. However, the effect of altered nutrient levels on oncogenic signaling and therapeutic is not well understood. We demonstrate that glucose or acetate, two abundant “fuel” sources brain, promote epidermal vIII (EGFRvIII)-dependent through activation mechanistic target rapamycin complex 2 (mTORC2) by acetylation its core component Rictor. This activity mediated elevated acetyl-CoA. A surprising...

10.1073/pnas.1511759112 article EN Proceedings of the National Academy of Sciences 2015-07-13
Hideo Hagihara Hirotaka Shoji Satoko Hattori Giovanni Sala Yoshihiro Takamiya and 95 more Mika Tanaka Masafumi Ihara Mihiro Shibutani Izuho Hatada Kei Hori Mikio Hoshino Akito Nakao Yasuo Mori Shigeo Okabe Masayuki Matsushita Anja Urbach Yuta Katayama Akinobu Matsumoto Keiichi I. Nakayama Shota Katori Takuya Sato Takuji Iwasato Haruko Nakamura Yoshio Goshima Matthieu Raveau Tetsuya Tatsukawa Kazuhiro Yamakawa Noriko Takahashi Haruo Kasai Johji Inazawa Ikuo Nobuhisa Tetsushi Kagawa Tetsuya Taga Mohamed Darwish Hirofumi Nishizono Keizo Takao Kiran Sapkota Kazu Nakazawa Tsuyoshi Takagi Haruki Fujisawa Yoshihisa Sugimura Kyosuke Yamanishi Lakshmi Rajagopal Nanette Deneen Hannah Herbert Y. Meltzer Tohru Yamamoto Shuji Wakatsuki Toshiyuki Araki Katsuhiko Tabuchi Tadahiro Numakawa Hiroshi Kunugi Freesia L. Huang Atsuko Hayata‐Takano Hitoshi Hashimoto Kota Tamada Toru Takumi Takaoki Kasahara Tadafumi Kato Isabella A. Graef Gerald R. Crabtree Nozomi Asaoka Hikari Hatakama Shuji Kaneko Takao Kohno Mitsuharu Hattori Yoshio Hoshiba Ryuhei Miyake Kisho Obi-Nagata Akiko Hayashi‐Takagi Léa J. Becker İpek Yalçın Yoko Hagino Hiroko Kotajima‐Murakami Yuki Moriya Kazutaka Ikeda Hyopil Kim Bong‐Kiun Kaang Hikari Otabi Yuta Yoshida Atsushi Toyoda Noboru H. Komiyama Seth G. N. Grant Michiru Ida‐Eto Masaaki Narita Ken‐ichi Matsumoto Emiko Okuda‐Ashitaka Iori Ohmori Tadayuki Shimada Kanato Yamagata Hiroshi Ageta Kunihiro Tsuchida Kaoru Inokuchi Takayuki Sassa Akio Kihara Motoaki Fukasawa Nobuteru Usuda Tayo Katano Teruyuki Tanaka Yoshihiro Yoshihara Michihiro Igarashi

Increased levels of lactate, an end-product glycolysis, have been proposed as a potential surrogate marker for metabolic changes during neuronal excitation. These in lactate can result decreased brain pH, which has implicated patients with various neuropsychiatric disorders. We previously demonstrated that such alterations are commonly observed five mouse models schizophrenia, bipolar disorder, and autism, suggesting shared endophenotype among these disorders rather than mere artifacts due...

10.7554/elife.89376.3 article EN public-domain eLife 2024-03-26

Neural activity results in long term changes that underlie synaptic plasticity. To examine the molecular basis of activity-dependent plasticity, we have used differential cloning techniques to identify genes are rapidly induced brain neurons by activity. Here, a novel cadherin molecule Arcadlin (activity-regulated cadherin-like protein).arcadlin mRNA is and transiently hippocampal granule cells seizures byN-methyl-d-aspartate-dependent potentiation. The extracellular domain most homologous...

10.1074/jbc.274.27.19473 article EN cc-by Journal of Biological Chemistry 1999-07-01

As immediate early genes (IEGs) are thought to play a critical role in mediating stimulus-induced neuronal plasticity, several laboratories have characterized the IEG response induced by cocaine help define changes gene expression that may underlie its long-lasting behavioral effects. Although activation of transcription factor IEGs has been described, little is known about which "effector" IEGs, if any, also induced. In present study, we examined whether administration affects recently...

10.1046/j.1471-4159.1995.64052377.x article EN Journal of Neurochemistry 1995-05-01

Injection of kainic acid (KA) into the brain causes severe seizures with hippocampal neuron loss. KA has been shown to immediately induce cyclooxygenase-2 (COX-2) expression in neurons, indicating that neuronal COX-2 might be involved death. In this study, however, we reveal delayed induction non-neuronal cells after injection plays an important role loss rather than early neurons. We find microinjection hemilateral hippocampus shows a later cells, such as endothelial and astrocytes....

10.1016/j.neures.2006.06.003 article EN cc-by-nc-nd Neuroscience Research 2006-07-12

Programs of gene activation may underlie long-term adaptive cellular responses to extracellular ligands. We have used a differential cDNA cloning strategy identify genes that are strongly induced by excitatory stimuli in the adult rat hippocampus. Here, we report sequence zinc-finger transcription factor, Egr3/Pilot, and characterize its regulated mRNA expression brain. Egr3 is rapidly transiently neurons hippocampus cortex electroconvulsive seizure. levels peak 2 hr after seizure remain...

10.1101/lm.1.2.140 article EN Learning & Memory 1994-01-01

Several studies have suggested that cyclooxygenase-2 (COX-2) plays a role in ischemic neuronal death. Genetic disruption of COX-2 has been shown to reduce susceptibility focal injury and N-methyl-D-aspartate-mediated neurotoxicity. The purpose this study was examine the effects deficiency on vulnerability after transient forebrain ischemia. Marked upregulation immunostaining neurons observed at early stage prominent staining persisted CA1 medial sector CA2 over 3 days immunohistologic...

10.1097/01.wcb.0000100065.36077.4a article EN Journal of Cerebral Blood Flow & Metabolism 2003-12-19

10.3791/56573-v article EN Journal of Visualized Experiments 2018-06-12
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