Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency
Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activat...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Chikasawa, Yushi [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014 |
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| Schlagwörter: |
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| Anmerkung: |
© The Japanese Society of Hematology 2014 |
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| Übergeordnetes Werk: |
Enthalten in: International journal of hematology - Tokyo [u.a.] : Springer, 1995, 100(2014), 4 vom: 27. Juli, Seite 345-352 |
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| Übergeordnetes Werk: |
volume:100 ; year:2014 ; number:4 ; day:27 ; month:07 ; pages:345-352 |
| Links: |
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| DOI / URN: |
10.1007/s12185-014-1643-6 |
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| Katalog-ID: |
SPR025115472 |
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| 100 | 1 | |a Chikasawa, Yushi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
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| 520 | |a Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. | ||
| 650 | 4 | |a Factor X deficiency |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Missense mutation |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Recombinant expression study |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cross-reacting material-reduced deficiency |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Homozygous mutation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Shinozawa, Keiko |4 aut | |
| 700 | 1 | |a Amano, Kagehiro |4 aut | |
| 700 | 1 | |a Ogata, Kyoichi |4 aut | |
| 700 | 1 | |a Hagiwara, Takeshi |4 aut | |
| 700 | 1 | |a Suzuki, Takashi |4 aut | |
| 700 | 1 | |a Inaba, Hiroshi |4 aut | |
| 700 | 1 | |a Fukutake, Katsuyuki |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t International journal of hematology |d Tokyo [u.a.] : Springer, 1995 |g 100(2014), 4 vom: 27. Juli, Seite 345-352 |w (DE-627)324615485 |w (DE-600)2028991-1 |x 1865-3774 |7 nnns |
| 773 | 1 | 8 | |g volume:100 |g year:2014 |g number:4 |g day:27 |g month:07 |g pages:345-352 |
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10.1007/s12185-014-1643-6 doi (DE-627)SPR025115472 (SPR)s12185-014-1643-6-e DE-627 ger DE-627 rakwb eng Chikasawa, Yushi verfasserin aut Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 Shinozawa, Keiko aut Amano, Kagehiro aut Ogata, Kyoichi aut Hagiwara, Takeshi aut Suzuki, Takashi aut Inaba, Hiroshi aut Fukutake, Katsuyuki aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 100(2014), 4 vom: 27. Juli, Seite 345-352 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:100 year:2014 number:4 day:27 month:07 pages:345-352 https://dx.doi.org/10.1007/s12185-014-1643-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 100 2014 4 27 07 345-352 |
| spelling |
10.1007/s12185-014-1643-6 doi (DE-627)SPR025115472 (SPR)s12185-014-1643-6-e DE-627 ger DE-627 rakwb eng Chikasawa, Yushi verfasserin aut Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 Shinozawa, Keiko aut Amano, Kagehiro aut Ogata, Kyoichi aut Hagiwara, Takeshi aut Suzuki, Takashi aut Inaba, Hiroshi aut Fukutake, Katsuyuki aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 100(2014), 4 vom: 27. Juli, Seite 345-352 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:100 year:2014 number:4 day:27 month:07 pages:345-352 https://dx.doi.org/10.1007/s12185-014-1643-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 100 2014 4 27 07 345-352 |
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10.1007/s12185-014-1643-6 doi (DE-627)SPR025115472 (SPR)s12185-014-1643-6-e DE-627 ger DE-627 rakwb eng Chikasawa, Yushi verfasserin aut Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 Shinozawa, Keiko aut Amano, Kagehiro aut Ogata, Kyoichi aut Hagiwara, Takeshi aut Suzuki, Takashi aut Inaba, Hiroshi aut Fukutake, Katsuyuki aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 100(2014), 4 vom: 27. Juli, Seite 345-352 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:100 year:2014 number:4 day:27 month:07 pages:345-352 https://dx.doi.org/10.1007/s12185-014-1643-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 100 2014 4 27 07 345-352 |
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10.1007/s12185-014-1643-6 doi (DE-627)SPR025115472 (SPR)s12185-014-1643-6-e DE-627 ger DE-627 rakwb eng Chikasawa, Yushi verfasserin aut Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 Shinozawa, Keiko aut Amano, Kagehiro aut Ogata, Kyoichi aut Hagiwara, Takeshi aut Suzuki, Takashi aut Inaba, Hiroshi aut Fukutake, Katsuyuki aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 100(2014), 4 vom: 27. Juli, Seite 345-352 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:100 year:2014 number:4 day:27 month:07 pages:345-352 https://dx.doi.org/10.1007/s12185-014-1643-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 100 2014 4 27 07 345-352 |
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10.1007/s12185-014-1643-6 doi (DE-627)SPR025115472 (SPR)s12185-014-1643-6-e DE-627 ger DE-627 rakwb eng Chikasawa, Yushi verfasserin aut Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency 2014 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Japanese Society of Hematology 2014 Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 Shinozawa, Keiko aut Amano, Kagehiro aut Ogata, Kyoichi aut Hagiwara, Takeshi aut Suzuki, Takashi aut Inaba, Hiroshi aut Fukutake, Katsuyuki aut Enthalten in International journal of hematology Tokyo [u.a.] : Springer, 1995 100(2014), 4 vom: 27. Juli, Seite 345-352 (DE-627)324615485 (DE-600)2028991-1 1865-3774 nnns volume:100 year:2014 number:4 day:27 month:07 pages:345-352 https://dx.doi.org/10.1007/s12185-014-1643-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 100 2014 4 27 07 345-352 |
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Enthalten in International journal of hematology 100(2014), 4 vom: 27. Juli, Seite 345-352 volume:100 year:2014 number:4 day:27 month:07 pages:345-352 |
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Chikasawa, Yushi @@aut@@ Shinozawa, Keiko @@aut@@ Amano, Kagehiro @@aut@@ Ogata, Kyoichi @@aut@@ Hagiwara, Takeshi @@aut@@ Suzuki, Takashi @@aut@@ Inaba, Hiroshi @@aut@@ Fukutake, Katsuyuki @@aut@@ |
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A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. 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|
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Chikasawa, Yushi |
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Chikasawa, Yushi misc Factor X deficiency misc Missense mutation misc Recombinant expression study misc Cross-reacting material-reduced deficiency misc Homozygous mutation Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
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1865-3774 |
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Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency Factor X deficiency (dpeaa)DE-He213 Missense mutation (dpeaa)DE-He213 Recombinant expression study (dpeaa)DE-He213 Cross-reacting material-reduced deficiency (dpeaa)DE-He213 Homozygous mutation (dpeaa)DE-He213 |
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misc Factor X deficiency misc Missense mutation misc Recombinant expression study misc Cross-reacting material-reduced deficiency misc Homozygous mutation |
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misc Factor X deficiency misc Missense mutation misc Recombinant expression study misc Cross-reacting material-reduced deficiency misc Homozygous mutation |
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misc Factor X deficiency misc Missense mutation misc Recombinant expression study misc Cross-reacting material-reduced deficiency misc Homozygous mutation |
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Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
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Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
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Chikasawa, Yushi |
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International journal of hematology |
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Chikasawa, Yushi Shinozawa, Keiko Amano, Kagehiro Ogata, Kyoichi Hagiwara, Takeshi Suzuki, Takashi Inaba, Hiroshi Fukutake, Katsuyuki |
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Chikasawa, Yushi |
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10.1007/s12185-014-1643-6 |
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factor x m402t: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
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Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
| abstract |
Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. © The Japanese Society of Hematology 2014 |
| abstractGer |
Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. © The Japanese Society of Hematology 2014 |
| abstract_unstemmed |
Abstract We investigated a mildly hemorrhagic patient with factor X (FX) deficiency to identify the nature of his defect by comprehensive analyses. A 42-year-old Japanese man was admitted to our hospital for uncontrolled gingival hemorrhage. His FX activity based on prothrombin time (PT) and activated partial thromboplastin time (aPTT) and FX antigen were <1, 6.5 and 11 %, respectively. A homozygous M402T missense mutation (c.1205 t>c; p.Met402Thr) was identified in the FX gene (F10) from both the patient and his brother. The mutation was not detected in the F10 of 82 unrelated normal Japanese individuals. We studied the functional consequences of this mutation by expressing mutant FX-M402T protein in HEK293 cells. This analysis revealed that the antigen of the FX-M402T mutants was approximately 26 % that of the wild-type FX in conditioned media. The FX-specific activity of FX-M402T mutants measured by a one-stage clotting assay based upon PT and aPTT, and a chromogenic assay using Russell’s viper venom in the concentrated media was 7.7, 31.7, and 41.2 % of wild type, respectively. The results suggest that the mutation FX-M402T may cause a secretion defect and a molecular abnormality in FX. © The Japanese Society of Hematology 2014 |
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| title_short |
Factor X M402T: a homozygous missense mutation identified as the cause of cross-reacting material-reduced deficiency |
| url |
https://dx.doi.org/10.1007/s12185-014-1643-6 |
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| author2 |
Shinozawa, Keiko Amano, Kagehiro Ogata, Kyoichi Hagiwara, Takeshi Suzuki, Takashi Inaba, Hiroshi Fukutake, Katsuyuki |
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Shinozawa, Keiko Amano, Kagehiro Ogata, Kyoichi Hagiwara, Takeshi Suzuki, Takashi Inaba, Hiroshi Fukutake, Katsuyuki |
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10.1007/s12185-014-1643-6 |
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2024-07-03T13:57:28.251Z |
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| score |
7.400139 |