A5058275961- Tuberous Sclerosis Complex Research
- PI3K/AKT/mTOR signaling in cancer
- Biomedical Text Mining and Ontologies
- Kruppel-like factors research
- Bioinformatics and Genomic Networks
- Silk-based biomaterials and applications
- Renal and related cancers
- Cancer, Hypoxia, and Metabolism
- Cancer Mechanisms and Therapy
- Genomics and Phylogenetic Studies
- Eosinophilic Disorders and Syndromes
- Cell Adhesion Molecules Research
- Semantic Web and Ontologies
- Vascular Tumors and Angiosarcomas
- NF-κB Signaling Pathways
- Gene expression and cancer classification
- Phytochemicals and Antioxidant Activities
- Histone Deacetylase Inhibitors Research
- Pluripotent Stem Cells Research
- Peptidase Inhibition and Analysis
- Pancreatic and Hepatic Oncology Research
- CRISPR and Genetic Engineering
- Mast cells and histamine
- Tea Polyphenols and Effects
- Vasculitis and related conditions
Kyushu University
2021-2024
Jackson Laboratory
2005-2021
National Cerebral and Cardiovascular Center
2017
Osaka University
2003-2008
Osaka International University
2008
Brigham and Women's Hospital
1998-2007
Harvard University
2002-2005
Harvard University Press
2003
Kanazawa University
2003
The Ohio State University
1990-1993
Although aerobic glycolysis (the Warburg effect) is a hallmark of cancer, key questions, including when, how, and why cancer cells become highly glycolytic, remain less clear. For largely unknown regulatory mechanism, rate-limiting glycolytic enzyme pyruvate kinase M2 (PKM2) isoform exclusively expressed in embryonic, proliferating, tumor cells, plays an essential role metabolism growth. Because the receptor tyrosine kinase/PI3K/AKT/mammalian target rapamycin (RTK/PI3K/AKT/mTOR) signaling...
Tuberous sclerosis (TSC) is a familial tumor syndrome due to mutations in TSC1 or TSC2, which progression malignancy rare. Primary Tsc2(-/-) murine embryo fibroblast cultures display early senescence with overexpression of p21CIP1/WAF1 that rescued by loss TP53. Tsc2(-/-)TP53(-/-) cells, as well tumors from Tsc2(+/-) mice, an mTOR-activation signature constitutive activation S6K, reverted treatment rapamycin. Rapamycin also reverts growth advantage cells. Tsc1/Tsc2 does not bind directly...
Tuberous sclerosis (TSC) is a familial tumor syndrome due to mutations in TSC1 or TSC2, which progression malignancy rare. Primary Tsc2–/– murine embryo fibroblast cultures display early senescence with overexpression of p21CIP1/WAF1 that rescued by loss TP53. Tsc2–/–TP53–/– cells, as well tumors from Tsc2+/– mice, an mTOR-activation signature constitutive activation S6K, reverted treatment rapamycin. Rapamycin also reverts growth advantage cells. Tsc1/Tsc2 does not bind directly mTOR,...
Tuberous sclerosis (TSC) is a hamartoma syndrome caused by mutations in TSC1 or TSC2 which cerebral cortical tubers and seizures are major clinical issues. We have engineered mice most neurons lose Tsc1 expression during embryonic development. These mutant display several neurological abnormalities beginning at postnatal day 5 with subsequent failure to thrive median survival of 35 d. The also electrographic both spontaneously physical stimulation, some end fatal tonic phase. Many...
The Mouse Genome Database (MGD; http://www.informatics.jax.org) is the community model organism knowledgebase for laboratory mouse, a widely used animal comparative studies of genetic and genomic basis human health disease. MGD authoritative source biological reference data related to mouse genes, gene functions, phenotypes models primary official gene, allele, strain nomenclature based on guidelines set by International Committee Standardized Nomenclature Mice. MGD's biocuration scientists...
Abstract Mouse Genome Informatics (MGI) is a federation of expertly curated information resources designed to support experimental and computational investigations into genetic genomic aspects human biology disease using the laboratory mouse as model system. The Database (MGD) Gene Expression (GXD) are core MGI databases that share data system architecture. serves central community resource integrated about genome features, variation, expression, gene function, phenotype, models acquired...
Tuberous sclerosis (TSC) is an autosomal dominant genetic disorder in which benign hamartomas develop multiple organs, caused by mutations either TSC1 or TSC2. We developed a murine model of Tsc2 disease using gene targeting approach. Tsc2-null embryos die at embryonic days 9.5-12.5 from hepatic hypoplasia. heterozygotes display 100% incidence bilateral renal cystadenomas, 50% liver hemangiomas, and 32% lung adenomas 15 months age. Progression to carcinoma, fatal bleeding the extremity...
Abstract Persons affected with tuberous sclerosis complex (TSC) develop a wide range of neurological abnormalities including aberrant neuronal migration and seizures. In an effort to model TSC‐associated central nervous system in mice, we generated two independent lines astrocyte‐specific Tsc1 conditional knockout mice by using the Cre‐LoxP system. Astrocyte‐specific ‐null exhibit electroencephalographically proven seizures after first month age begin die at 3 4 months. show significant...
Abstract Tuberous sclerosis complex (TSC) is a familial tumor disorder for which there no effective medical therapy. Disease‐causing mutations in the TSC1 or TSC2 gene lead to increased mammalian target of rapamycin (mTOR) kinase activity conserved mTOR signaling pathway, regulates nutrient uptake, cell growth, and protein translation. The normal function products form that reduces activity. Thus, inhibition may be useful targeted therapeutic approach. Elevated interferon‐gamma (IFN‐γ)...
Tuberous sclerosis (TSC) is a genetic disorder that results in the development of hamartomatous lesions variety organ systems. Both prevalence disease and often devastating consequences these tumors pose serious health medical care problem. The has been mapped to two distinct loci humans, although genes (<i>TSC1</i> and<i>TSC2</i>) for both have recently cloned, their function remains an enigma. Data presented here demonstrates TSC2 protein can bind selectively modulate transcription...
We have identified the genes whose expressions are augmented in blood cells of patients with systemic lupus erythematosus (SLE) using 'stepwise subtraction' technique along microarray analysis. The expression levels these were assessed by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR) 31 SLE and 30 healthy controls. found that following eight significantly increased patients; interferon (IFN)-alpha-inducible protein 27 (IFI27), IFN-alpha-inducible IFI-15K...
We have comprehensively identified the genes whose expressions are augmented in bone marrow-derived mononuclear cells (BMMC) from patients with Rheumatoid Arthritis (RA) as compared BMMCs Osteoarthritis (OA) patients, and named them AURA after RA. Both stepwise subtractive hybridization microarray analyses were used to identify genes, which confirmed by northern blot analysis and/or reverse transcription polymerase chain reaction (RT–PCR). also assessed their expression levels individual...
Abstract Recurrence following chemotherapy is observed in the majority of patients with pancreatic ductal adenocarcinoma (PDAC). Recent studies suggest that cancer stem cells (CSCs) may be involved PDAC recurrence and metastasis. However, an efficient approach to targeting CSCs remains established. Here we show overexpressing 67-kDa laminin receptor (67LR)-dependent cyclic GMP (cGMP) inducer, epigallocatechin-3- O -gallate (EGCG) a phosphodiesterase 3 (PDE3) inhibitor combination...
TLR signaling is critical to innate immune system regulation; however, aberrant involved in several diseases, including insulin resistance, Alzheimer's disease, and tumor metastasis. Moreover, a recent study found that TLR-4 pathway inhibition might be target for the suppression of chronic inflammatory disorders. In this article, we show green tea polyphenol epigallocatechin-3-O-gallate (EGCG) increases expression Toll interacting protein, strong inhibitor TLR4 signaling, by suppressing...
Several well-characterized extracellular matrix (ECM) components have been localized to the amphibian limb regenerate, but identification and characterization of novel ECM molecules received little attention. Here we describe, using mAb MT1 immunocytochemistry, an molecule expressed during regeneration development. In stumps, reactivity was restricted tendons, myotendinous junctions, granules in basal layers epidermis, periosteum (newts) perichondrium (axolotls). regenerating limbs, distal...
Abstract Lung fibrosis, including idiopathic pulmonary is an intractable disease accompanied by irreversible dysfunction in the respiratory system. Its pathogenesis involves transforming growth factorβ (TGFβ)-induced overproduction of extracellular matrix from fibroblasts; however, limited countermeasures have been established. In this study, we identified osa-miR172d-5p, a plant-derived microRNA (miR), as potent anti-fibrotic miR. silico analysis followed vitro assay based on human lung...
Vasculitis (angiitis) is a systemic autoimmune disease that often causes fatal symptoms. We aimed to isolate cDNA markers would be useful for diagnosing not only vasculitis but also other diseases. For this purpose, we used stepwise subtractive hybridization and microarray analyses comprehensively the genes whose expressions are augmented in peripheral blood mononuclear cells (PBMCs) pooled from patients. Subsequently, quantitative real-time polymerase chain reaction (qRT-PCR) examine mRNA...
ABSTRACT Melanoma, a cancer arising from melanocytes, requires novel treatment strategy because of the ineffectiveness conventional therapies in certain patients. Fustin is flavanonol found young fustic (Cotinus coggygria). However, little known about its antimelanoma effects. Our study demonstrates that fustin suppresses growth B16 melanoma cells. Phalloidin staining cytoskeletal actin revealed induced conformational change structure cells, accompanied by suppressed phosphorylation myosin...