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convert into a sulfate
a salt or ester of sulphuric acid (同)sulphate
antibiotic (trade name Kantrex) used to treat severe infections (同)Kantrex

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/01/14 16:18:04」(JST)

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Kanamycin (also known as kanamycin A) is an aminoglycoside bacteriocidal antibiotic, available in oral, intravenous, and intramuscular forms, and used to treat a wide variety of infections. Kanamycin is isolated from the bacterium Streptomyces kanamyceticus^[1] and its most commonly used form is kanamycin sulfate.

Spectrum of activity

Kanamycin has been used to treat infections caused by Gram-negative bacteria including E. coli, Proteus spp., Serratia marcescens, and Klebsiella pneumoniae. The following represents MIC susceptibility data for a few medically significant pathogens:

Escherichia coli - 0.05 μg/ml - >512 μg/ml
Klebsiella pneumoniae - 7.5 μg/ml - 128 μg/ml

^[2]

Mechanism

Kanamycin interacts with the 30S subunit of prokaryotic ribosomes. It induces substantial amounts of mistranslation and indirectly inhibits translocation during protein synthesis.^[3]^[4]

Composition

Kanamycin is a mixture of three main components: kanamycin A, B, and C. Kanamycin A is the major component in kanamycin.^[5] The effects of these components do not appear to be widely studied as individual compounds when used against prokaryotic and eukaryotic cells.

Biosynthesis

While the main product produced by Streptomyces kanamyceticus is kanamycin A, additional products are also produced, including kanamycin B, kanamycin C, kanamycin D and kanamycin X.

The kanamycin biosynthetic pathway can be divided into two parts. The first part is common to several aminoglycoside antibiotics, such as butirosin and neomycin. In it a unique aminocyclitol, 2-deoxystreptamine, is biosynthesized from D-glucopyranose 6-phosphate in four steps. At this point the kanamycin pathway splits into two branches due to the promiscuity of the next enzyme, which can utilize two different glycosyl donors - UDP-N-acetyl-α-D-glucosamine and UDP-α-D-glucose. One of the branches forms kanamycin C and kanamycin B, while the other branch forms kanamycin D and kanamycin X. However, both kanamycin B and kanamycin D can be converted to kanamycin A, so both branches of the pathway converge at kanamycin A.^[6]

Side effects

Serious side effects include tinnitus or loss of hearing, toxicity to kidneys, and allergic reactions to the drug.^[7]

Use in research: kanamycin resistance

Kanamycin is used in molecular biology as a selective agent most commonly to isolate bacteria (e.g., E. coli) which have taken up genes (e.g., of plasmids) coupled to a gene coding for kanamycin resistance (primarily Neomycin phosphotransferase II [NPT II/Neo]). Bacteria that have been transformed with a plasmid containing the kanamycin resistance gene are plated on kanamycin (50-100 ug/ml) containing agar plates or are grown in media containing kanamycin (50-100 ug/ml). Only the bacteria that have successfully taken up the kanamycin resistance gene become resistant and will grow under these conditions. As a powder, kanamycin is white to off-white and is soluble in water (50 mg/ml).

At least one such gene, Atwbc19^[8] is native to a plant species, of comparatively large size and its coded protein acts in a manner which decreases the possibility of horizontal gene transfer from the plant to bacteria; it may be incapable of giving resistance to bacteria even if gene transfer occurs.

The KanMX marker

The selection marker kanMX is a hybrid gene consisting of a bacterial aminoglycoside phosphotransferase (kan^r from transposon Tn903) under control of the strong TEF promoter from Ashbya gossypii.^[9]^[10]

Mammalian cells, yeast, and other eukaryotes acquire resistance to geneticin (= G418, an aminoglycoside antibiotic similar to kanamycin) when transformed with a kanMX marker. In yeast, the kanMX marker avoids the requirement of auxotrophic markers. In addition, the kanMX marker renders E. coli resistant to kanamycin. In shuttle vectors the KanMX cassette is used with an additional bacterial promoter. Several versions of the kanMX cassette are in use, e.g. kanMX1-kanMX6. They primarily differ by additional restriction sites and other small changes around the actual open reading frame.^[9]^[11]

References

^ Garrod, L.P., et al.: "Antibiotic and Chemotherapy", page 131. Churchill Livingstone, 1981
^ http://antibiotics.toku-e.com/antimicrobial_744_6.html
^ Pestka, S.: "The Use of Inhibitors in Studies on Protein Synthesis", Methods in Enzymology 30, pp.261-282, 1975
^ Misumi, M. & Tanaka, N.: "Mechanism of Inhibition of Translocation by Kanamycin and Viomycin: A Comparative Study with Fusidic Acid, Biochem.Biophys.Res.Commun. 92, pp.647-654, 1980
^ United States. National Institutes of Health. Kanamycin Compound Summary. PubChem. Web. 21 Aug. 2012.
^ "kanamycin biosynthesis pathway in MetaCyc". MetaCyc.org. Retrieved 30 September 2014.
^ Consumer Drug Information: Kanamycin, 2 April 2008, retrieved 2008-05-04
^ "Horizontal Gene Transfer: Plant vs. Bacterial Genes for Antibiotic Resistance Scenario's—What's the Difference?". Isb.vt.edu. Retrieved 2013-06-24.
^ ^a ^b Wach, A.; Brachat, A.; Pöhlmann, R.; Philippsen, P. (1994). "New heterologous modules for classical or PCR-based gene disruptions in Saccharomyces cerevisiae". Yeast (Chichester, England) 10 (13): 1793–1808. doi:10.1002/yea.320101310. PMID 7747518. edit
^ Steiner, S.; Philippsen, P. (1994). "Sequence and promoter analysis of the highly expressed TEF gene of the filamentous fungus Ashbya gossypii". Molecular & general genetics : MGG 242 (3): 263–271. doi:10.1007/BF00280415. PMID 8107673. edit
^ Wach, A. (1996). "PCR-synthesis of marker cassettes with long flanking homology regions for gene disruptions in S. Cerevisiae". Yeast 12 (3): 259–265. doi:10.1002/(SICI)1097-0061(19960315)12:3<259::AID-YEA901>3.0.CO;2-C. PMID 8904338. edit

External links

From kanamycin-evopure.com:
- Technical Information
- Purity Survey
- Toxicity Data
- Working Concentrations
- Kanamycin Impurities

UpToDate Contents

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1. 薬剤耐性結核の診断、治療、および予防 diagnosis treatment and prevention of drug resistant tuberculosis
2. 腸球菌における抗菌薬耐性の機構 mechanisms of antibiotic resistance in enterococci
3. 広範囲薬剤耐性結核の臨床症状、診断、および治療 clinical manifestations diagnosis and treatment of extensively drug resistant tuberculosis
4. 広範囲薬剤耐性結核の疫学 epidemiology of extensively drug resistant tuberculosis
5. 妊娠中の結核 tuberculosis in pregnancy

English Journal

Isolation and molecular characterization of Salmonella enterica serovar Enteritidis from poultry house and clinical samples during 2010.

Mezal EH, Sabol A, Khan MA, Ali N, Stefanova R, Khan AA.Author information Microbiology Division, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR 72079, USA; University of Arkansas at Little Rock, Little Rock, AR 72205, USA; University of Thi-Qar, Science of College, Biology of Dept., Thi-Qar, Iraq.AbstractA total of 60 Salmonella enterica serovar (ser.) Enteritidis isolates, 28 from poultry houses and 32 from clinical samples, were isolated during 2010. These isolates were subjected to testing and analyzed for antibiotic resistance, virulence genes, plasmids and plasmid replicon types. To assess genetic diversity, pulsed-field gel electrophoresis (PFGE) fingerprinting, using the XbaI restriction enzyme, Multiple-Locus Variable-Number Tandem Repeat Analysis (MLVA) and plasmid profiles were performed. All isolates from poultry, and 10 out of 32 clinical isolates were sensitive to ampicillin, chloramphenicol, gentamicin, kanamycin, nalidixic acid, sulfisoxazole, streptomycin, and tetracycline. Twenty-one of thirty-two clinical isolates were resistant to ampicillin and tetracycline, and one isolate was resistant to nalidixic acid. PFGE typing of sixty ser. Enteritidis isolates by XbaI resulted in 10-12 bands and grouped into six clusters each with similarity from 95% to 81%. The MLVA analysis of sixty isolates gave 18 allele profiles with the majority of isolates displayed in three groups, and two clinical isolates found to be new in the PulseNet national MLVA database. All isolates were positive for 12 or more of the 17 virulence genes mostly found in S. enterica (spvB, spiA, pagC, msgA, invA, sipB, prgH, spaN, orgA, tolC, iroN, sitC, IpfC, sifA, sopB, and pefA) and negative for one gene (cdtB). All isolates carried a typical 58 kb plasmid, type Inc/FIIA. Three poultry isolates and one clinical isolate carried small plasmids with 3.8, 6, 7.6 and 11.5 kb. Ten of the clinical isolates carried plasmids, with sizes 36 and 38 kb, types IncL/M and IncN, and one isolate carried an 81 kb plasmid, type IncI. Southern hybridization of a plasmid with an Inc/FIIA gene probe hybridized one large 58 kb plasmid in all isolates. Several large and small plasmids from poultry isolates were not typed by our PCR-based method. These results confirmed that PFGE fingerprinting has limited discriminatory power for ser. Enteritidis in both poultry and clinical sources. However, the plasmid and MLVA allele profiles were a useful and important epidemiology tool to discriminate outbreak strains of ser. Enteritidis from poultry and clinical samples.
Food microbiology.Food Microbiol.2014 Apr;38:67-74. doi: 10.1016/j.fm.2013.08.003. Epub 2013 Aug 27.
A total of 60 Salmonella enterica serovar (ser.) Enteritidis isolates, 28 from poultry houses and 32 from clinical samples, were isolated during 2010. These isolates were subjected to testing and analyzed for antibiotic resistance, virulence genes, plasmids and plasmid replicon types. To assess gene
PMID 24290628

Three novel homozygous mutations in the GNPTG gene that cause mucolipidosis type III gamma.

Liu S1, Zhang W2, Shi H3, Meng Y3, Qiu Z4.Author information 1Department of Pediatrics, PUMC Hospital, CAMS&PUMC, Beijing 100730, PR China.2Clinical Research Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, PR China.3Department of Medical Genetics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, PR China.4Department of Pediatrics, PUMC Hospital, CAMS&PUMC, Beijing 100730, PR China. Electronic address: zhengqingqiu33@aliyun.com.AbstractBACKGROUND: Mucolipidosis type III gamma (MLIII gamma) is an autosomal recessive disease caused by a mutation in the GNPTG gene, which encodes the γ subunit of the N-acetylglucosamine-1-phosphotransferase (GlcNAc-1-phosphotransferase). This protein plays a key role in the transport of lysosomal hydrolases to the lysosome.
Gene.Gene.2014 Feb 10;535(2):294-8. doi: 10.1016/j.gene.2013.11.010. Epub 2013 Dec 6.
BACKGROUND: Mucolipidosis type III gamma (MLIII gamma) is an autosomal recessive disease caused by a mutation in the GNPTG gene, which encodes the γ subunit of the N-acetylglucosamine-1-phosphotransferase (GlcNAc-1-phosphotransferase). This protein plays a key role in the transport of lysosomal hyd
PMID 24316125

Antibiotic resistances of intestinal lactobacilli isolated from wild boars.

Klose V1, Bayer K2, Kern C2, Goelß F3, Fibi S3, Wegl G3.Author information 1BOKU - University of Natural Resources and Applied Life Sciences, Vienna, Dep. IFA-Tulln, Division Environmental Biotechnology, Konrad Lorenz Straße 20, 3430 Tulln, Austria. Electronic address: viviana.klose@boku.ac.at.2BOKU - University of Natural Resources and Applied Life Sciences, Vienna, Dep. IFA-Tulln, Division Environmental Biotechnology, Konrad Lorenz Straße 20, 3430 Tulln, Austria.3BIOMIN Research Center, Technopark 1, 3430 Tulln, Austria.AbstractAcquired antibiotic resistances have been reported in lactobacilli of various animal and food sources, but there are no data from wild boar. The objective was a preliminary examination of the antibiotic resistance prevalence of intrinsically vancomycin-resistant lactobacilli isolated from wild boar intestines and analysis of the genetic determinants implicated. Out of three wild boars, 121 lactobacilli were recovered and grouped according to their whole cell protein patterns. Initial phenotypic screening revealed that all were susceptible to erythromycin (2μg/ml), but 30 were resistant to tetracycline (32μg/ml). Based on Randomly Amplified Polymorphic DNA-PCR clustering, 64 strains were selected as representative genotypes for identification and minimum inhibitory concentration (MIC) determination. Partial 16S rRNA gene sequencing identified four species: (i) L. mucosae (n=57), (ii) L. reuteri (n=47), (iii) L. fermentum (n=12), and (iv) L. murinus (n=5). Most heterofermentative strains displayed low MICs for ampicillin (AMP), chloramphenicol (CHL), streptomycin (STR), kanamycin (KAN), gentamicin (GEN), erythromycin (ERY), quinupristin/dalfopristin (Q/D), and clindamycin (CLI). Atypical MICs were found mainly in L. mucosae and L. reuteri for TET, KAN, STR, AMP and CHL, but except the TET MICs of L. mucosae mostly at low level. L. murinus strains revealed atypical MICs for aminoglycosides, and/or CHL, AMP, CLI. PCR screening detected tet(W) in 12 and tet(M) in one of heterofermentative strains, as well as the aph(3')-III kanamycin gene in L. murinus. This is the first report showing acquired antibiotic resistance determinants in intestinal lactobacilli of wild boar origin.
Veterinary microbiology.Vet Microbiol.2014 Jan 10;168(1):240-4. doi: 10.1016/j.vetmic.2013.11.014. Epub 2013 Nov 22.
Acquired antibiotic resistances have been reported in lactobacilli of various animal and food sources, but there are no data from wild boar. The objective was a preliminary examination of the antibiotic resistance prevalence of intrinsically vancomycin-resistant lactobacilli isolated from wild boar
PMID 24326231

Japanese Journal

アポトーシス抑制タンパクPTD-FNKを用いた内耳タンパク治療

樫尾明憲
Otology Japan 22(5), 897-904, 2012
内耳障害の予防戦略として、アポトーシス関連タンパクなどを直接導入する内耳タンパク治療は有望であるが、内耳血液関門・蝸牛窓膜をタンパクが透過できないという問題から実現は容易ではなかった。これに対して、我々はタンパクなど高分子を効率的に細胞内へ導入できるProtein Transduction domain (PTD) を付加する技術を導入し、PTDをアポトーシス抑制タンパクBcl-x<SUB& …
NAID 130003373590

薬疹やイレウスを併発し, 経口投与ができず, 塩酸シプロフロキサシンの点滴と硫酸カナマイシン筋注およびプレドニゾロン静注にて改善した大腸結核を合併した広汎空洞型結核の1例

白井正浩,早川啓史,中野泰克 [他],中村祐太郎,藤田薫,須田隆文,千田金吾
結核 81(4), 345-349, 2006-04-15
… Then, he was retreated with ciprofloxacin (CPFX), kanamycin sulfate (KM) and prednisolone (PSL). …
NAID 10017985341

治療に苦慮した多剤耐性肺結核症の1例

鶴谷純司,早田宏,岡三喜男,河野茂
日本呼吸器学会雑誌 = The journal of the Japanese Respiratory Society 38(8), 594-598, 2000-08-10
NAID 10005610622

「カナマイシン」

Kanamycin
Systematic (IUPAC) name
	2-(aminomethyl)- 6-[4,6-diamino-3- [4-amino-3,5-dihydroxy-6-(hydroxymethyl) tetrahydropyran-2-yl]oxy- 2-hydroxy- cyclohexoxy]- tetrahydropyran- 3,4,5-triol
Clinical data
AHFS/Drugs.com	monograph
Pregnancy; category	D;
Legal status	?;
Routes	Oral, intravenous, intramuscular
Pharmacokinetic data
Bioavailability	very low after oral delivery
Metabolism	Unknown
Half-life	2 hours 30 minutes
Excretion	Urine (as unchanged drug)
Identifiers
CAS number	59-01-8
ATC code	A07AA08 J01GB04 S01AA24
PubChem	CID 6032
DrugBank	DB01172
ChemSpider	5810
UNII	RUC37XUP2P
ChEBI	CHEBI:17630
ChEMBL	CHEMBL1384
PDB ligand ID	KAN (PDBe, RCSB PDB)
Chemical data
Formula	C18H36N4O11
Molecular mass	484.499
	SMILES O([C@@H]2[C@@H](O)[C@H](O[C@H]1O[C@H](CN)[C@@H](O)[C@H](O)[C@H]1O)[C@@H](N)C[C@H]2N)[C@H]3O[C@@H]([C@@H](O)[C@H](N)[C@H]3O)CO;
	InChI InChI=1S/C18H36N4O11/c19-2-6-10(25)12(27)13(28)18(30-6)33-16-5(21)1-4(20)15(14(16)29)32-17-11(26)8(22)9(24)7(3-23)31-17/h4-18,23-29H,1-3,19-22H2/t4-,5+,6-,7-,8+,9-,10-,11-,12+,13-,14-,15+,16-,17-,18-/m1/s1 ; Key:SBUJHOSQTJFQJX-NOAMYHISSA-N ;
(what is this?) (verify)

　　[★]

英: kanamycin, KM
ラ: kanamycinum
化: 硫酸カナマイシン kanamycin sulfate、一硫酸カナマイシン kanamycin monosulfate
関

抗菌薬

蛋白合成阻害

アミノグリコシド系抗菌薬

「kanamycin monosulfate」

　　[★]

一硫酸カナマイシン

関: kanamycin、kanamycin sulfate

「bekanamycin sulfate」

　　[★]

硫酸ベカナマイシン

関: bekanamycin

「sulfate」

　　[★]

n.

(官能基やイオンを表して)硫酸、(化合物)硫酸塩、硫酸エステル、硫酸化する

関: H2SO4、inorganic sulfate、sulfate ester、sulfated、sulfation、sulfuric acid、sulfuric acid ester、sulphate、sulphuric acid

「sulfated」

　　[★]

adj.

硫酸化の

関: sulfate、sulfation、sulphate

「sulfa」

　　[★]

スルファ、サルファ

[1] Garrod, L.P., et al.: "Antibiotic and Chemotherapy", page 131. Churchill Livingstone, 1981

[2] ttp://antibiotics.toku-e.com/antimicrobial_744_6.html

[3] Pestka, S.: "The Use of Inhibitors in Studies on Protein Synthesis", Methods in Enzymology 30, pp.261-282, 1975

[4] Misumi, M. & Tanaka, N.: "Mechanism of Inhibition of Translocation by Kanamycin and Viomycin: A Comparative Study with Fusidic Acid, Biochem.Biophys.Res.Commun. 92, pp.647-654, 1980

[5] United States. National Institutes of Health. Kanamycin Compound Summary. PubChem. Web. 21 Aug. 2012.

[6] "kanamycin biosynthesis pathway in MetaCyc". MetaCyc.org. Retrieved 30 September 2014.

[7] Consumer Drug Information: Kanamycin, 2 April 2008, retrieved 2008-05-04

[8] "Horizontal Gene Transfer: Plant vs. Bacterial Genes for Antibiotic Resistance Scenario's—What's the Difference?". Isb.vt.edu. Retrieved 2013-06-24.

[Wach1994-9] Wach, A.; Brachat, A.; Pöhlmann, R.; Philippsen, P. (1994). "New heterologous modules for classical or PCR-based gene disruptions in Saccharomyces cerevisiae". Yeast (Chichester, England) 10 (13): 1793–1808. doi:10.1002/yea.320101310. PMID 7747518. edit

[Steiner1994-10] Steiner, S.; Philippsen, P. (1994). "Sequence and promoter analysis of the highly expressed TEF gene of the filamentous fungus Ashbya gossypii". Molecular & general genetics : MGG 242 (3): 263–271. doi:10.1007/BF00280415. PMID 8107673. edit

[Wach1996-11] Wach, A. (1996). "PCR-synthesis of marker cassettes with long flanking homology regions for gene disruptions in S. Cerevisiae". Yeast 12 (3): 259–265. doi:10.1002/(SICI)1097-0061(19960315)12:3<259::AID-YEA901>3.0.CO;2-C. PMID 8904338. edit

リンク元	「カナマイシン」「kanamycin monosulfate」
拡張検索	「bekanamycin sulfate」
関連記事	「sulfate」「sulfated」「sulfa」

匿名

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案内

案内

kanamycin sulfate