The Experts below are selected from a list of 141 Experts worldwide ranked by ideXlab platform
Nobuo Suzuki - One of the best experts on this subject based on the ideXlab platform.
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Protease activation following UV irradiation is linked to hypomutability in human cells selected for resistance to combination of UV and Antipain
Mutation Research, 1998Co-Authors: Eriko Isogai, Hideo Yamamori, Hideko Suzuki, Sumio Ishijima, Tomoko Sonoda, Kazuko Kita, Ritsuko Hasegawa, Yoshiaki Takakubo, Nobuo SuzukiAbstract:Abstract In order to examine the relationship between activation of an Antipain-sensitive protease and suppression of mutability in UV (UVC)-irradiated human cells, a human cell variant with the high protease activity induced by UV was established and characterized for its susceptibility to UV-induced mutagenecity. Cells of a hypermutable cell strain, RSa, were mutagenized with ethyl methanesulfonate and irradiated with 10 J/m2 UV, followed by exposure to 20 mM Antipain for 34 h. Whereas the combined treatment was totally lethal to RSa cells not treated with ethyl methanesulfonate, one surviving clone was isolated from the mutagenized cells and designated UVAP-1. When fibrinolytic protease activity was measured from extracts of the cell, it was found that the protease activity was elevated promptly after UV irradiation, reaching the maximum at 10 min post-irradiation. This protease activity was inhibited by Antipain. After UV irradiation the phenotypic mutation frequencies of UVAP-1 cells were much lower than those of the parent RSa cells, as evaluated by the generation of clones resistant to ouabain-killing. Furthermore, mutation at the K-ras codon 12 in genomic DNA was detected in RSa cells but not in UVAP-1 cells. Thus, the protease activation was correlated with the decreased levels of UV-mutagenicity in UVAP-1 cells, supporting the possible involvement of the Antipain-sensitive protease activity in the regulation of cellular mutability following UV irradiation.
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UV-induced mutations affecting codon 12 of the K-ras gene are suppressed by interferon-α in human RSa cells
Mutation research, 1997Co-Authors: Nobuo Suzuki, Hideo Yamamori, Toshiharu Ishizuka, Hideko Suzuki, Hidetoshi InoAbstract:Abstract K- ras gene sequences mutant at codon 12 were recovered following differential dot-blot hybridization of genomic DNA from human RSa cells up to 12 days after the cells had been irradiated with far-UV (principally 254 nm). By contrast, no mutant codon 12 sequences were recovered from cells which had been treated with 50 IU/ml human interferon (HuIFN)-α for 24 h prior to their UV exposure. HuIFN-α treatment in combination with anti-HuIFN-α antibody did not lead to the loss of mutant sequences. However, culture of interferon-pretreated cells with medium containing the protease inhibitor Antipain (0.01 mM) for 6 h immediately after UV irradiation led to the recovery of mutant codon 12 sequences. Thus, while treatment with HuIFN-α appeared to prevent any UV-induced mutations affecting codon 12 of the K- ras gene from being recovered, the putative Antipain-sensitive protease responsible for this suppressive affect appeared to be significantly affected by the protease inhibitor Antipain.
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Involvement of Antipain-sensitive protease activity in the interferon-β-induced UV-refractoriness of Cockayne syndrome fibroblasts
Mutation Research, 1996Co-Authors: K Sugita, Nobuo Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
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Correlated susceptibility between interferon-beta and UV in human cell lines, F-IFr and RSa.
International journal of oncology, 1996Co-Authors: Nobuo Suzuki, S Iida, Hideo Yamamori, Toshiharu Ishizuka, Y TakakuboAbstract:The human cell line F-IFr is a variant with an increased resistance to cell proliferation inhibition (CPI) by human interferon (HuLFN)-beta, established from RSa cells with high sensitivity to CPI. The parent RSa cells were recently found to be unusually hypermutable after irradiation with far-ultraviolet light (UV), as assessed by two different methods; estimation of the cloning efficiency of ouabain-resistant (Oua(R)) mutants and detection of K-ras codon 12 mutation in genomic DNA identified by polymerase chain reaction following differential dot blot hybridization. In the present study, F-IFr cells were found to be hypomutable; less than one Oua(R) mutant per 10(4) survival cells after UV (0-12 J/m(2)), in contrast to 0.51-85 Oua(R) mutants per 10(4) survivors in RSa cells, and no detectable K-ras codon 12 mutation at any UV dose tested. However, F-IFr cells, when cultured with medium containing the protease inhibitor Antipain immediately and transiently after UV irradiation displayed hypermutability to almost the same extent as RSa cells by both phenotypic and genetic mutation analyses. The refractoriness of F-IFr cells to HuIFN-beta CPI was also suppressed by culture with medium containing Antipain during HuIFN-beta exposure. Moreover, F-IFr cells irradiated with UV or treated with HuIFN-beta showed elevation of Antipain-sensitive protease activity, but not the irradiated or treated RSa cells. UV- and HuIFN-beta-susceptibility were not modulated by Antipain in RSa cells. These antipodal characteristics between the two cell lines suggested that Antipain-sensitive proteases and/or cellular functions may be involved in increased resistance of F-IFr cells to both Wand HuIFN-beta refractoriness.
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suppression of uv and interferon α refractoriness by Antipain in human ifr cells established from rsa cells sensitive to both stimuli
Journal of Cellular Physiology, 1996Co-Authors: Nobuo SuzukiAbstract:The human cell line IFr is a variant with an increased resistance to cell proliferation inhibition (CPI) by human interferon (HuIFN)-alpha, established from RSa cells with unusually high-sensitivity to CPI. IFr cells were later found to have increased resistance to the cell-killing effects of far-ultraviolet (UV) irradiation. Here, in cell lysates extracted from UV-irradiated IFr cells but not in those from irradiated RSa cells, fibrinolytic protease activity was found to be elevated promptly and transiently after irradiation. Treatment of IFr cells with HuIFN-alpha alone also resulted in the elevation of protease activity, but not that of RSa cells. Both the activity elevated after UV irradiation and after HuIFN-alpha treatment was inhibited to the greatest extent by Antipain in vitro. Moreover, the refractoriness of IFr cells to UV cell-killing and to HuIFN-alpha CPI was suppressed by culturing with medium containing Antipain immediately after UV irradiation or during HuIFN-alpha exposure. In similarly treated RSa cells, there was no modulation of UV- or HuIFN-alpha-susceptibility. These comparative characteristics between the two cell lines suggested that Antipain-sensitive proteases and/or cellular functions may be involved in increased resistance to UV and HuIFN-alpha of IFr cells.
H Niimi - One of the best experts on this subject based on the ideXlab platform.
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Involvement of Antipain-sensitive protease activity in the interferon-beta-induced UV-refractoriness of Cockayne syndrome fibroblasts.
Mutation research, 1996Co-Authors: K Sugita, N Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
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Involvement of Antipain-sensitive protease activity in the interferon-β-induced UV-refractoriness of Cockayne syndrome fibroblasts
Mutation Research, 1996Co-Authors: K Sugita, Nobuo Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
N Suzuki - One of the best experts on this subject based on the ideXlab platform.
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Protease activation following UV irradiation is linked to hypomutability in human cells selected for resistance to combination of UV and Antipain.
Mutation research, 1998Co-Authors: E Isogai, Y Takakubo, Sumio Ishijima, Tomoko Sonoda, Kazuko Kita, Ritsuko Hasegawa, H Suzuki, H Yamamori, N SuzukiAbstract:In order to examine the relationship between activation of an Antipain-sensitive protease and suppression of mutability in UV (UVC)-irradiated human cells, a human cell variant with the high protease activity induced by UV was established and characterized for its susceptibility to UV-induced mutagenicity. Cells of a hypermutable cell strain, RSa, were mutagenized with ethyl methanesulfonate and irradiated with 10 J/m2 UV, followed by exposure to 20 mM Antipain for 34 h. Whereas the combined treatment was totally lethal to RSa cells not treated with ethyl methanesulfonate, one surviving clone was isolated from the mutagenized cells and designated UVAP-1. When fibrinolytic protease activity was measured from extracts of the cell, it was found that the protease activity was elevated promptly after UV irradiation, reaching the maximum at 10 min post-irradiation. This protease activity was inhibited by Antipain. After UV irradiation the phenotypic mutation frequencies of UVAP-1 cells were much lower than those of the parent RSa cells, as evaluated by the generation of clones resistant to ouabain-killing. Furthermore, mutation at the K-ras codon 12 in genomic DNA was detected in RSa cells but not in UVAP-1 cells. Thus, the protease activation was correlated with the decreased levels of UV-mutagenicity in UVAP-1 cells, supporting the possible involvement of the Antipain-sensitive protease activity in the regulation of cellular mutability following UV irradiation.
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Involvement of Antipain-sensitive protease activity in the interferon-beta-induced UV-refractoriness of Cockayne syndrome fibroblasts.
Mutation research, 1996Co-Authors: K Sugita, N Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
K Sugita - One of the best experts on this subject based on the ideXlab platform.
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Involvement of Antipain-sensitive protease activity in the interferon-beta-induced UV-refractoriness of Cockayne syndrome fibroblasts.
Mutation research, 1996Co-Authors: K Sugita, N Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
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Involvement of Antipain-sensitive protease activity in the interferon-β-induced UV-refractoriness of Cockayne syndrome fibroblasts
Mutation Research, 1996Co-Authors: K Sugita, Nobuo Suzuki, H NiimiAbstract:Fibroblast cells obtained from two siblings and a female patient with Cockayne syndrome (CS), when pretreated with human interferon (HuIFN)-beta prior to irradiation with UV light (254 nm wavelength), exhibited transiently induced fibrinolytic protease activity immediately after the irradiation in association with increased refractoriness to UV cell-killing. A protease inhibitor, Antipain, inhibited the induction of protease activity in lysates of the CS fibroblasts from these 3 cases after the combination of HuIFN-beta pretreatment and UV irradiation, whereas elastatinal and 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) inhibited the activity less than Antipain did. Antipain also suppressed the increase in UV-refractoriness of HuIFN-beta-pretreated CS fibroblasts, as revealed by culturing cells for 24 h in medium containing the inhibitor immediately after UV exposure and thereafter evaluating the ability of colony formation by the cells. Thus, an Antipain-sensitive protease may be involved in the UV-refractoriness induced by HuIFN-beta in CS fibroblast strains.
I Horii - One of the best experts on this subject based on the ideXlab platform.
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The role of proteases in stratum corneum: involvement in stratum corneum desquamation
Archives of Dermatological Research, 1994Co-Authors: Y. Suzuki, Junko Nomura, J Koyama, I HoriiAbstract:The effects of protease inhibitors on cell dissociation were studied in vitro in order to examine the involvement of proteases in stratum corneum desquamation. Stratum corneum sheet (peeled from human backs after sunburn) was incubated in a detergent mixture containing 8 mM N,N-dimethyldodecylamine oxide, 2 mM sodium lauryl sulphate and 60 micrograms/ml kanamycin with or without protease inhibitors, and the number of released cells was counted after incubation for 48 h. Cell dissociation was inhibited strongly by Antipain or aprotinin, but not at all by N-[N-(L-3-transcarboxyoxiran-2-carbonyl)-L-leucyl]-agmatin, N-ethylmaleimide or pepstatin, which suggests that only serine proteases are associated with desquamation. Furthermore, leupeptin and chymostatin each reduced cell dissociation about half as effectively as aprotinin or Antipain, while a mixture of leupeptin and chymostatin prevented stratum corneum dissociation as potently as Antipain or aprotinin. In addition, the activity of chymotrypsin-like protease in scaly skin was higher than that in normal skin, as we have previously found for trypsin-like protease. These results suggest that both trypsin-like and chymotrypsin-like serine proteases are involved in stratum corneum desquamation.