H Watanabe

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi Roles of aggrecan, a large chondroitin sulfate proteoglycan, in cartilage structure and function
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda MD 20892, USA
    J Biochem 124:687-93. 1998
  2. ncbi Perlecan is essential for cartilage and cephalic development
    E Arikawa-Hirasawa
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA
    Nat Genet 23:354-8. 1999
  3. ncbi Dwarfism and age-associated spinal degeneration of heterozygote cmd mice defective in aggrecan
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892 4370, USA
    Proc Natl Acad Sci U S A 94:6943-7. 1997
  4. ncbi Transcriptional cross-talk between Smad, ERK1/2, and p38 mitogen-activated protein kinase pathways regulates transforming growth factor-beta-induced aggrecan gene expression in chondrogenic ATDC5 cells
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, NIDCR, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 276:14466-73. 2001
  5. ncbi Mouse cartilage matrix deficiency (cmd) caused by a 7 bp deletion in the aggrecan gene
    H Watanabe
    Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892
    Nat Genet 7:154-7. 1994
  6. ncbi Mouse aggrecan, a large cartilage proteoglycan: protein sequence, gene structure and promoter sequence
    H Watanabe
    Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892, USA
    Biochem J 308:433-40. 1995
  7. ncbi Mice lacking link protein develop dwarfism and craniofacial abnormalities
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Genet 21:225-9. 1999
  8. ncbi Disrupted expression of matrix genes in the growth plate of the mouse cartilage matrix deficiency (cmd) mutant
    A W Wai
    Department of Biochemistry, University of Hong Kong, China
    Dev Genet 22:349-58. 1998
  9. ncbi Molecular cloning and expression of cDNA encoding chicken UDP-N-acetyl-D-glucosamine (GlcNAc): GlcNAcbeta 1-6(GlcNAcbeta 1-2)- manalpha 1-R[GlcNAc to man]beta 1,4N-acetylglucosaminyltransferase VI
    Y Sakamoto
    Departments of Biochemistry and Ophthalmology, Osaka University Medical School, 2 2 Yamadaoka, Suita, Osaka 565 0871, Japan
    J Biol Chem 275:36029-34. 2000
  10. ncbi Association of autosomal dominantly inherited corneal dystrophies with BIGH3 gene mutations in Japan
    Y Mashima
    Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan
    Am J Ophthalmol 130:516-7. 2000

Collaborators

  • Y Yamada
  • Tomihisa Takahashi
  • A J Quantock
  • Takaaki Ueno
  • S Yamamoto
  • M Okada
  • Y Tano
  • N Maeda
  • Y Inoue
  • Y Shimomura
  • T Abo
  • S Kinoshita
  • T Iiai
  • K Nishida
  • M Tsujikawa
  • K Hatakeyama
  • M Bannai
  • T Inoue
  • T Torimura
  • M K Mannoor
  • R Yasumizu
  • Y Mashima
  • Y Sakamoto
  • H Arase
  • E Arikawa-Hirasawa
  • K Arase
  • A W Wai
  • T Saito
  • K Yamada
  • S Yamagiwa
  • H Okamoto
  • K Hayano
  • T Uchida
  • T Suda
  • T Abe
  • K Takeda
  • M Kin
  • K Hayashi
  • H Kawamura
  • A Weerasinghe
  • R C Halder
  • A Ariyasinghe
  • M Harada
  • S Reza
  • H Hamada
  • H Kameyama
  • R Harada
  • T Kawaguchi
  • C Tsukada
  • R Avraham
  • H Sekikawa
  • R Kumashiro
  • M Taniguchi
  • T Naito
  • H Ishikawa
  • T Nakamura
  • T Kawamura
  • K Okumura
  • Y Nishiyama
  • Y Hori
  • M Sata
  • M Morshed
  • A Horii
  • M Koba
  • S Ikehara
  • M Yamada
  • N Taniguchi
  • Y Yamamoto
  • K Honke
  • M Kondoh-Tanaka
  • K Takio
  • N Dohmae
  • Y Amoh
  • H Korekane
  • S Miyawaki
  • M Konishi
  • T Taguchi
  • N Nishio
  • K Ohgi
  • M Irie
  • K Saijo
  • A Konno
  • J R Hassell
  • H Takami
  • M Iwama
  • A Sanda
  • L J Ng
  • K S Cheah
  • H Kurahashi
  • Y Nakamura

Detail Information

Publications26

  1. ncbi Roles of aggrecan, a large chondroitin sulfate proteoglycan, in cartilage structure and function
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda MD 20892, USA
    J Biochem 124:687-93. 1998
    ..Further studies on aggrecan will lead to prophylaxis and treatment of joint destructive diseases such as osteoarthrosis and to elucidation of cartilage development, which is essential for skeletal formation...
  2. ncbi Perlecan is essential for cartilage and cephalic development
    E Arikawa-Hirasawa
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA
    Nat Genet 23:354-8. 1999
    ..Our findings suggest that these molecules affect similar signalling pathways...
  3. ncbi Dwarfism and age-associated spinal degeneration of heterozygote cmd mice defective in aggrecan
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892 4370, USA
    Proc Natl Acad Sci U S A 94:6943-7. 1997
    ..Electron microscopy showed a degeneration of disc chondrocytes in the heterozygotes. These findings may facilitate the identification of mutations in humans predisposed to spinal degeneration...
  4. ncbi Transcriptional cross-talk between Smad, ERK1/2, and p38 mitogen-activated protein kinase pathways regulates transforming growth factor-beta-induced aggrecan gene expression in chondrogenic ATDC5 cells
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, NIDCR, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 276:14466-73. 2001
    ....
  5. ncbi Mouse cartilage matrix deficiency (cmd) caused by a 7 bp deletion in the aggrecan gene
    H Watanabe
    Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892
    Nat Genet 7:154-7. 1994
    ..DNA sequencing of the aggrecan gene identified a 7 bp deletion in exon 5 resulting in a severely truncated molecule. The finding of an aggrecan mutation in the cmd mouse confirms the critical role of aggrecan in cartilage formation...
  6. ncbi Mouse aggrecan, a large cartilage proteoglycan: protein sequence, gene structure and promoter sequence
    H Watanabe
    Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892, USA
    Biochem J 308:433-40. 1995
    ..There are stretches of sequences similar to the promoter region of both the type-II collagen and link protein genes. These sequences may be important for cartilage gene expression...
  7. ncbi Mice lacking link protein develop dwarfism and craniofacial abnormalities
    H Watanabe
    Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Genet 21:225-9. 1999
    ..These results indicate that LP is important for the formation of proteoglycan aggregates and normal organization of hypertrophic chondrocytes, and suggest that cartilage matrix has a role in chondrocyte differentiation and maturation...
  8. ncbi Disrupted expression of matrix genes in the growth plate of the mouse cartilage matrix deficiency (cmd) mutant
    A W Wai
    Department of Biochemistry, University of Hong Kong, China
    Dev Genet 22:349-58. 1998
    ..The discordance of gene expression in cmd chondrocytes may be additional factors contributing to the disrupted cellular architecture of the growth plate resulting from the primary absence of aggrecan...
  9. ncbi Molecular cloning and expression of cDNA encoding chicken UDP-N-acetyl-D-glucosamine (GlcNAc): GlcNAcbeta 1-6(GlcNAcbeta 1-2)- manalpha 1-R[GlcNAc to man]beta 1,4N-acetylglucosaminyltransferase VI
    Y Sakamoto
    Departments of Biochemistry and Ophthalmology, Osaka University Medical School, 2 2 Yamadaoka, Suita, Osaka 565 0871, Japan
    J Biol Chem 275:36029-34. 2000
    ..1 kilobases. Reverse transcription-polymerase chain reaction analysis showed that GnT VI mRNA was relatively highly expressed in oviduct, spleen, lung, and colon...
  10. ncbi Association of autosomal dominantly inherited corneal dystrophies with BIGH3 gene mutations in Japan
    Y Mashima
    Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan
    Am J Ophthalmol 130:516-7. 2000
    ..To evaluate the incidence of BIGH3 gene mutations in 164 unrelated Japanese patients with corneal stromal dystrophies with an autosomal dominant trait...
  11. ncbi Resistance to malarial infection is achieved by the cooperation of NK1.1(+) and NK1.1(-) subsets of intermediate TCR cells which are constituents of innate immunity
    M K Mannoor
    Department of Immunology, Niigata University School of Medicine, Niigata, 951 8510, Japan
    Cell Immunol 211:96-104. 2001
    ..These results suggest that both NK1.1(-) and NK1.1(+) subsets of TCR(int) cells (i.e., constituents of innate immunity) are associated with resistance to malaria and that an autoimmune-like state is induced during malarial infection...
  12. ncbi Pathology of ALY mice: congenital immunodeficiency with lymph node and Peyer's patch defects
    R Yasumizu
    First Department of Pathology, Kansai Medical University, Moriguchi City, Osaka, Japan
    Immunobiology 202:213-25. 2000
    ..By contrast, the NK activity is normal. Taken together, the ALY mouse is an invaluable model to elucidate the immunological networks between the lymphoid structures (lymph nodes, Peyer's patches, lymphoid follicles, etc.) and functions...
  13. ncbi Autocrine motility factor enhances hepatoma cell invasion across the basement membrane through activation of beta1 integrins
    T Torimura
    The Second Department of Medicine and Research Center for Innovative Cancer Therapy, Kurume University School of Medicine, Kurume City, Japan
    Hepatology 34:62-71. 2001
    ..Our results indicate that AMF/PHI enhances hepatoma cell invasion through Matrigel in an autocrine manner by stimulating the adhesion, motility, and MMP-2 secretion of these cells through activation of beta1 integrins...
  14. ncbi Abundance of unconventional CD8(+) natural killer T cells in the large intestine
    M Bannai
    Department of Immunology, Niigata University School of Medicine, Niigata, Japan
    Eur J Immunol 31:3361-9. 2001
    ..These findings suggest that the large intestine is a site in which unconventional NKT cells carrying the CD8(+) phenotype (or DN CD4(-)8(-)) are abundant and that these cells are independent of MHC and MHC-like antigens...
  15. ncbi Different recurrence patterns after phototherapeutic keratectomy in the corneal dystrophy resulting from homozygous and heterozygous R124H BIG-H3 mutation
    T Inoue
    Department of Ophthalmology, Osaka University Medical School, Suita, Osaka, Japan
    Am J Ophthalmol 132:255-7. 2001
    ..The recurrence-free interval in homozygous patients was shorter. CONCLUSION: The mutation genotype of BIG-H3 gene determines the recurrence pattern after phototherapeutic keratectomy...
  16. ncbi Developmental arrest of NK1.1+ T cell antigen receptor (TCR)-alpha/beta+ T cells and expansion of NK1.1+ TCR-gamma/delta+ T cell development in CD3 zeta-deficient mice
    H Arase
    Division of Molecular Genetics, Chiba University School of Medicine, Japan
    J Exp Med 182:891-5. 1995
    ..1- TCR+, NK1.1+ TCR-alpha/beta+, and NK1.1+ TCR-gamma/delta+ thymocytes, which cannot be replaced by CD3 eta or FcR gamma chains...
  17. ncbi Ablation of a specific cell population by the replacement of a uniquely expressed gene with a toxin gene
    K Arase
    Department of Molecular Genetics, Chiba University Graduate School of Medicine, 1 8 1 Inohana, Chuo Ku, Chiba 260 8670, Japan
    Proc Natl Acad Sci U S A 96:9264-8. 1999
    ....
  18. ncbi Characterization of poly C preferential ribonuclease from chicken liver
    K Hayano
    Department of Microbiology, Hoshi College of Pharmacy, Tokyo
    J Biochem 114:156-62. 1993
    ..Among the B1 site components, Thr45 (RNase A numbering) is conserved, but Phe120 and Ser123 are substituted by Leu and Thr, respectively. Among the B2 site residues, Gln69, Asn71, and Glu111 are substituted by other amino acids...
  19. ncbi Existence of a small population of IL-2R beta hi TCRint cells in SCG and MRL-lpr/lpr mice which produce normal Fas mRNA and Fas molecules from the lpr gene
    S Yamagiwa
    Department of Immunology, Niigata University School of Medicine, Japan
    Eur J Immunol 26:1409-16. 1996
    ..This phenomenon explains the leaky appearance of normal Fas mRNA and Fas molecules in mice carrying the lpr gene. It is suggested that a small population of IL-2R beta hi TCRint cells are resistant to the lpr genetic abnormality...
  20. ncbi Base specificity and primary structure of poly U-preferential ribonuclease from chicken liver
    T Uchida
    Department of Microbiology, Hoshi College of Pharmacy, Tokyo, Japan
    Biosci Biotechnol Biochem 60:1982-8. 1996
    ..melanogaster RNase, respectively, and belongs to the RNase T2 family RNase. Reassessment of the base specificity of RNase CL1 found that it is guanylic acid, then uridylic acid-preferential, and not poly U preferential...
  21. ncbi High sensitivity to hepato-tumorigenesis in hypocatalasemic C3H/C(s)b/Gen mice exposed to low doses of 252Cf fission neutrons and 60Co gamma-rays
    K Yamada
    Department of Cancer Research, Hiroshima University, Japan
    Anticancer Res 17:2041-7. 1997
    ..Therefore, the implication of oxygen radicals in hepato-tumorigenesis was strongly suggested and high sensitivity of C(s)b to low doses of radiation would be useful to investigate the mechanism of radiation tumorigenesis...
  22. ncbi Ovulation defect and its restoration by bone marrow transplantation in osteopetrotic mutant mice of Mitf(mi)/Mitf(mi) genotype
    H Watanabe
    Department of Clinical Molecular Biology, Faculty of Medicine, Kyoto University, Japan
    Biol Reprod 57:1394-400. 1997
    ..05). These results indicate that bone marrow-derived cells, defective in mi/mi mice, are necessary for normal ovulation and delivery; the findings are consistent with the notion that macrophages play major roles in ovulation...
  23. ncbi A kerato-epithelin (betaig-h3) mutation in lattice corneal dystrophy type IIIA
    S Yamamoto
    Am J Hum Genet 62:719-22. 1998
  24. ncbi Granular corneal dystrophy with homozygous mutations in the kerato-epithelin gene
    M Okada
    Department of Ophthalmology, Osaka University Medical School, Suita, Japan
    Am J Ophthalmol 126:169-76. 1998
    ..Three members of the family were affected with a severe placoid type of corneal dystrophy. To determine the relationship between gene mutations and phenotypic variations of the disease, we analyzed the kerato-epithelin gene...
  25. ncbi Two distinct kerato-epithelin mutations in Reis-Bücklers corneal dystrophy
    M Okada
    Department of Ophthalmology, Osaka University Medical School, Japan
    Am J Ophthalmol 126:535-42. 1998
    ..To see whether there was a genetic basis for these phenotypic variations, we analyzed beta ig-h3, the gene that codes for kerato-epithelin and that contains a mutation (Arg555Gln) that causes RBCD...
  26. ncbi CD161+ T (NT) cells exist predominantly in human intestinal epithelium as well as in liver
    T Iiai
    Department of Surgery, Niigata University School of Medicine, 1 757 Asahimachi dori, Niigata City, 951 8510 Japan
    Clin Exp Immunol 129:92-8. 2002
    ..These results suggest that CD161+ T (NT) cells predominantly exist in human intestinal epithelium and may play an important role in local immunity...