5-ブロモウラシル
WordNet
- the 2nd letter of the Roman alphabet (同)b
- the blood group whose red cells carry the B antigen (同)type_B, group B
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/08/03 03:04:15」(JST)
[Wiki en表示]
5-Bromouracil |
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IUPAC name
5-Bromo-1H-pyrimidine-2,4-dione
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Other names
5-Bromo-2,4-dihydroxypyrimidine
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Identifiers |
Abbreviations |
5-BrU
5-BU |
CAS number |
51-20-7 Y |
PubChem |
5802 |
ChemSpider |
5597 Y |
ChEBI |
CHEBI:20552 Y |
ChEMBL |
CHEMBL144730 Y |
Jmol-3D images |
Image 1 |
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InChI=1S/C4H3BrN2O2/c5-2-1-6-4(9)7-3(2)8/h1H,(H2,6,7,8,9) Y
Key: LQLQRFGHAALLLE-UHFFFAOYSA-N Y
InChI=1/C4H3BrN2O2/c5-2-1-6-4(9)7-3(2)8/h1H,(H2,6,7,8,9)
Key: LQLQRFGHAALLLE-UHFFFAOYAN
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Properties |
Molecular formula |
C4H3BrN2O2 |
Molar mass |
190.983 g/mol |
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa) |
Y (verify) (what is: Y/N?) |
Infobox references |
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5-Bromouracil (or 5-bromo-2,4(1H,3H)-pyrimidinedione or 5-BrU or 5-BU) is a brominated derivative of uracil that acts as an antimetabolite or base analog, substituting for thymine in DNA, and can induce DNA mutation in the same way as 2-aminopurine. It is used mainly as an experimental mutagen, but its deoxyriboside derivative (5-bromo-2-deoxy-uridine) is used to treat neoplasms.
5-BrU exists in three tautomeric forms that have different base pairing properties. The keto form (shown in the infobox) is complementary to adenine, so it can be incorporated into DNA by aligning opposite adenine residues during DNA replication (see below left). Alternatively, the enol (below right) and ion forms are complementary to guanine. This means that 5-BrU can be present in DNA either opposite adenine or guanine.
The three forms frequently interchange so base-pairing properties can become altered at any time. The result of this is that during a subsequent round of replication a different base is aligned opposite the 5-BrU residue. Further rounds of replication 'fix' the change by incorporating a normal nitrogen base into the complementary strand.
Thus 5-BrU induces a point mutation via base substitution. This base pair will change from an A-T to a G-C or from a G-C to an A-T after a number of replication cycles, depending on whether 5-BrU is within the DNA molecule or is an incoming base when it is enolized or ionized.
References
- Griffiths, Anthony J. et al. (2005). Introduction to Genetic Analysis (8th Ed.). W.H. Freeman. ISBN 0-7167-4939-4
UpToDate Contents
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English Journal
- Prevalence of clinical hip abnormalities in haemophilia A and B: an analysis of the UDC database.
- Kelly D, C Zhang Q, M Soucie J, Manco-Johnson M, Dimichele D; Joint Outcome Subcommittee of the Coordinating Committee for the Universal Data Collection Database and the Hemophilia Treatment Center Network Investigators.SourceWeill Cornell Medical College, New York, NY,, USA.
- Haemophilia : the official journal of the World Federation of Hemophilia.Haemophilia.2013 May;19(3):426-31. doi: 10.1111/hae.12073. Epub 2012 Dec 17.
- Clinical hip abnormalities, secondary to recurrent joint and/or muscle bleeding in persons with haemophilia, have not been well characterized and have the potential for significant morbidity. We aimed to examine the prevalence of clinical hip abnormalities in the US haemophilia population and to exp
- PMID 23252621
- Evaluation of transfusion-related complications along with estimation of inhibitors in patients with hemophilia: A pilot study from a single center.
- Dubey A, Verma A, Elhence P, Agarwal P.SourceDepartment of Transfusion Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
- Asian journal of transfusion science.Asian J Transfus Sci.2013 Jan;7(1):8-10. doi: 10.4103/0973-6247.106714.
- BACKGROUND: Apart from inhibitor development in patients with hemophilia (PWH) the old problems of blood borne viral infections and red cell alloimmunization still persist in PWH from developing countries. This study was planned to detect the presence of inhibitors in our PWH and to determine the pr
- PMID 23559756
- Single higher dose of recombinant activated factor VII in the treatment of hemorrhages in patients with hemophilia complicated by inhibitors.
- Łaguna P, Mital A.SourceDepartment of Pediatrics Hematology and Oncology, Medical University of Warsaw, Warsaw, Poland. pawel.laguna@litewska.edu.pl
- Advances in clinical and experimental medicine : official organ Wroclaw Medical University.Adv Clin Exp Med.2012 Jul-Aug;21(4):519-24.
- The development of inhibitors is the most severe complication of treating hemophilia patients with Factor VIII or IX, and providing effective hemostasis for inhibitor patients is challenging. Patients with high responding inhibitors (titer >5 BU/mL) are usually treated with recombinant activated
- PMID 23240458
Japanese Journal
- 胃癌周術期に第VIII凝固因子インヒビターによる後天性血友病を発症した1例
- 宇高 徹総,山本 澄治,遠藤 出,久保 雅俊,水田 稔,宮谷 克也
- 日本消化器外科学会雑誌 46(10), 717-724, 2013
- … ナージ術を施行した.凝固検査でAPTTが著明に延長しており,第VIII凝固因子活性が11.6%と低下していた.そこで第VIII因子製剤を投与したが,第VIII凝固因子活性が上昇せず,第VIII因子インヒビターが5 BU/mlと出現していた.プレドニゾロンの投与で腹腔内,胸腔内出血は漸減し軽快退院した.第VIII凝固因子インヒビター出現による出血傾向は本症例のような重篤な出血傾向を呈することが多く,本疾 …
- NAID 130004560886
- 斉藤 誠,若狭 健太郎,盛 暁生,入江 達朗,田中 雅則,森岡 正信,家子 正裕
- 臨床血液 53(2), 240-245, 2012
- … 3例とも高齢(79歳,77歳,68歳)の男性で,皮下出血とAPTTの延長,貧血を認めたため,紹介入院となり,第VIII因子活性の低下(0.9~3.1%), 第VIII因子インヒビターの存在(57.1~173BU/ml)により後天性血友病Aと診断した。 …
- NAID 130004501633
- 矢野 宏行,角田 美佐子,大西 哲郎 [他],水野 重芳,鯉渕 仁,木川 好章,鈴木 達也,中野 博司,大庭 建三
- 日本老年医学会雑誌 48(2), 185-189, 2011-03-25
- … ,背部,前胸部にわたり皮下血腫が出現した.内服薬に貧血や凝固異常の副作用はなかった.APTT 83.1 sec,第VIII因子活性1%未満(基準値:78~165%),第VIII因子インヒビター18.5 BU/ml (基準値:1.0% BU/ml 以下)より後天性血友病と診断した.経口ステロイド,第VIII因子製剤の補充による併用療法を行い,出血症状は改善をみせたが,経過中に細菌性肺炎を合併し永眠された.後 …
- NAID 10030469503
Related Links
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- 十数年年以上前から使っていますが型が同じでそのまま使えるのが嬉しいです。この品のみ割ったり、自然に割れたりで5~6個目です。耐久性がわからないので星4にしました
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- 英
- 5-bromouracil, 5BU, 5-BU
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- Mg2+存在下でC3, B, Dが反応してC3bBbとなり、これがC3転換酵素(C3bBb)あるいはC5転換酵素(C3bBb3b)を形成する。これらはP(properdin)と結合して活性化し、それぞれC3、C5を活性化する