Research Topics
Genomes and Genes
| Makoto NodaSummaryCountry: Japan Publications
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Detail Information
Publications
The reversion-inducing cysteine-rich protein with Kazal motifs (RECK) interacts with membrane type 1 matrix metalloproteinase and CD13/aminopeptidase N and modulates their endocytic pathwaysTakao Miki
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto 606 8501, Japan
J Biol Chem 282:12341-52. 2007..This modulation was correlated with the accelerated internalization and decay of MT1-MMP and CD13. This study unveils the novel function and target molecules of RECK...- RECK: a novel suppressor of malignancy linking oncogenic signaling to extracellular matrix remodelingMakoto Noda
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501, Japan
Cancer Metastasis Rev 22:167-75. 2003.... 
The ß1-integrin-dependent function of RECK in physiologic and tumor angiogenesisTakao Miki
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Japan
Mol Cancer Res 8:665-76. 2010..Therefore, we propose that RECK in tumor vascular endothelial cells can be an interesting target of cancer treatment via abortion of tumor angiogenesis...
Involvement of the Reck tumor suppressor protein in maternal and embryonic vascular remodeling in miceEdiriweera P S Chandana
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo ku, Kyoto 606 8501, Japan
BMC Dev Biol 10:84. 2010..Mice lacking the membrane-anchored metalloproteinase regulator Reck die in utero around embryonic day 10.5 with halted vascular development; however, the mechanisms by which this phenotype arises remain unclear...- RECK modulates Notch signaling during cortical neurogenesis by regulating ADAM10 activityTeruyuki Muraguchi
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto 606 8501, Japan
Nat Neurosci 10:838-45. 2007..These findings indicate that RECK is a physiological inhibitor of ADAM10, an upstream regulator of Notch signaling and a critical modulator of brain development... - The Reck tumor suppressor protein alleviates tissue damage and promotes functional recovery after transient cerebral ischemia in miceHuan Wang
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo ku, Kyoto, Japan
J Neurochem 115:385-98. 2010..Our data implicate Reck in protection of ECM/tissue integrity and promotion of functional recovery in the brain after transient cerebral ischemia... - Localization of the membrane-anchored MMP-regulator RECK at the neuromuscular junctionsSatoshi Kawashima
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo ku, Kyoto, Japan
J Neurochem 104:376-85. 2008.... - Dual effects of the membrane-anchored MMP regulator RECK on chondrogenic differentiation of ATDC5 cellsShunya Kondo
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501, Japan
J Cell Sci 120:849-57. 2007.... - Density- and serum-dependent regulation of the Reck tumor suppressor in mouse embryo fibroblastsMamiko Hatta
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501, Japan
Cell Signal 21:1885-93. 2009..Our study has revealed multiple signaling pathways impinging on Reck in cultured mouse embryo fibroblasts and sets a foundation for future studies to find effective Reck inducers of potential value in cancer therapy... - The membrane-anchored MMP-regulator RECK is a target of myogenic regulatory factorsMichiko Echizenya
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Japan
Oncogene 24:5850-7. 2005..These findings suggest that MyoD down regulates RECK to facilitate myotube formation, whereas MRF4 up regulates RECK to promote other aspects of myogenesis that require extracellular matrix integrity... - Rb Regulates DNA damage response and cellular senescence through E2F-dependent suppression of N-ras isoprenylationAwad Shamma
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto, Japan
Cancer Cell 15:255-69. 2009..Furthermore, Rb heterozygous mice additionally lacking any of Ink4a, Arf, or Suv39h1 generated C cell adenocarcinomas, suggesting that cellular senescence antagonizes Rb-deficient carcinogenesis... - What we learn from transformation suppressor genes: lessons from RECKMakoto Noda
Department of Molecular Oncology and Global COE Program, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501, Japan
Future Oncol 6:1105-16. 2010..In this article we discuss the promise, limitations and recent innovations in this approach, taking one transformation suppressor gene, RECK, as an example... - RECK forms cowbell-shaped dimers and inhibits matrix metalloproteinase-catalyzed cleavage of fibronectinAkira Omura
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Kyoto 606 8501, Japan
J Biol Chem 284:3461-9. 2009..Our data demonstrate the ability of RECK to protect fibronectin from MMP-mediated degradation... - A novel screen using the Reck tumor suppressor gene promoter detects both conventional and metastasis-suppressing anticancer drugsRyuya Murai
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Japan
Oncotarget 1:252-64. 2010..The top-ranking compound, disulfiram, strongly suppressed spontaneous lung-metastasis of human fibrosarcoma cells in nude mice. Our data demonstrate the value of this screen in discovering effective cancer therapeutics... - Recklessness as a hallmark of aggressive cancerMakoto Noda
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Sakyo ku, Kyoto 606 8501, Japan
Cancer Sci 98:1659-65. 2007..Here we review the recent advances in RECK research and discuss some of the important issues to be addressed in future studies... - Mutations in two matrix metalloproteinase genes, MMP-2 and MT1-MMP, are synthetic lethal in miceJunseo Oh
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501, Japan
Oncogene 23:5041-8. 2004..In the absence of MMP-2 and MT1-MMP, myoblast fusion in vitro is also significantly retarded. These findings suggest functional overlap in mice between the two MMPs with distinct molecular natures... - Identification of Rgl3 as a potential binding partner for Rap-family small G-proteins and profilin IIJiegou Xu
Department of Molecular Oncology, Kyoto University Graduate School of Medicine, Yoshida konoe cho, Sakyo ku, Kyoto 606 8501 Japan
Cell Signal 19:1575-82. 2007..These findings raise the possibility that Rgl3 mediates interaction between Ras/Rap-family proteins and profilin II, an important activator of actin polymerization... - Sept4, a component of presynaptic scaffold and Lewy bodies, is required for the suppression of alpha-synuclein neurotoxicityMasafumi Ihara
Biochemistry and Cell Biology Unit, HMRO, Kyoto University Graduate School of Medicine, Yoshida Konoe, Sakyo, Kyoto 606 8501, Japan
Neuron 53:519-33. 2007..Taken together, these data show that Sept4 may be involved in PD as a dual susceptibility factor, as its insufficiency can diminish dopaminergic neurotransmission and enhance alpha-synuclein neurotoxicity... - Matrix metalloproteinase-2 plays a critical role in the pathogenesis of white matter lesions after chronic cerebral hypoperfusion in rodentsKayoko Nakaji
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
Stroke 37:2816-23. 2006..In the present study, we asked whether MMP-2 is involved in the BBB disruption and the subsequent WM lesions after chronic cerebral hypoperfusion... - RECK expression in pancreatic cancer: its correlation with lower invasiveness and better prognosisToshihiko Masui
Department of Surgery, Kyoto University Graduate School of Medicine, Sakyo, Japan
Clin Cancer Res 9:1779-84. 2003..We also analyzed the correlation between RECK expression and MMP activation... - Transcriptional control of the RECK metastasis/angiogenesis suppressor geneRegina Maki Sasahara
, , CP 26077, , SP, Brazil
Cancer Detect Prev 26:435-43. 2002..Understanding of the mechanisms which control RECK gene transcription may lead to the development of new strategies for cancer prevention and treatment... - The membrane-anchored matrix metalloproteinase (MMP) regulator RECK in combination with MMP-9 serves as an informative prognostic indicator for colorectal cancerTaku Takeuchi
Department of Surgery, Nara Medical University, Kashihara City, Nara, Japan
Clin Cancer Res 10:5572-9. 2004..However, the clinical relevance of these findings remains to be fully documented. Here we examined the expression of RECK and one of its targets, MMP-9, in colorectal cancer tissue... - [The membrane-anchored metalloproteinase inhibitor RECK]Chiaki Takahashi
Tanpakushitsu Kakusan Koso 47:1889-95. 2002 - Expression of a novel matrix metalloproteinase regulator, RECK, and its clinical significance in resected non-small cell lung cancerKazumasa Takenaka
Department of Thoracic Surgery, Faculty of Medicine, Kyoto University, Kyoto, Japan
Eur J Cancer 40:1617-23. 2004..009; Hazard ratio (HR), 0.474 with a 95% Confidence interval (CI) of 0.271-0.830). In conclusion, RECK-status is a significant prognostic factor correlated with tumour angiogenesis in NSCLC patients... - Prognostic significance of reversion-inducing cysteine-rich protein with Kazal motifs expression in resected pathologic stage IIIA N2 non-small-cell lung cancerKazumasa Takenaka
Department of Thoracic Surgery, Faculty of Medicine, Kyoto University, Shogoin-kawahara-cho 54, Sakyo-ku, Kyoto, 606-8507, Japan
Ann Surg Oncol 12:817-24. 2005..031). RECK expression in involved N2 nodes was significantly higher than in primary tumors (P < .001). CONCLUSIONS: RECK status was a novel prognostic factor in pathologic stage IIIA N2 NSCLC... - TGF-beta signaling preserves RECK expression in activated pancreatic stellate cellsHongsik Lee
Department of Internal Medicine, Ansan Korea University Hospital, Ansan, Gyeonggi Do, Korea
J Cell Biochem 104:1065-74. 2008.... - Nras loss induces metastatic conversion of Rb1-deficient neuroendocrine thyroid tumorChiaki Takahashi
Department of Medical Oncology, Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Genet 38:118-23. 2006..These findings suggest that the loss of the proto-oncogene Nras in certain cellular contexts can promote malignant tumor progression... - Tissue inhibitors of metalloproteinase 2 inhibits endothelial cell migration through increased expression of RECKJunseo Oh
National Cancer Institute, Center for Cancer Research, Cell and Cancer Biology Branch, Bethesda, Maryland, USA
Cancer Res 64:9062-9. 2004..Secondly, TIMP-2 can disrupt VEGF signaling required for initiation of hMVEC migration. Third, TIMP-2 can enhance expression of RECK via Rap1 signaling resulting in an indirect, time-dependent inhibition of endothelial cell migration...