Did you know ? If you order before Friday 14h we deliver 90PCT of the the time next Tuesday, GENTAUR another in time delivery

ATP-sensitive inward rectifier potassium channel 8 (Inward rectifier K( ) channel Kir6.1) (Potassium channel, inwardly rectifying subfamily J member 8) (uKATP-1)

 KCNJ8_HUMAN             Reviewed;         424 AA.
Q15842; O00657;
01-NOV-1997, integrated into UniProtKB/Swiss-Prot.
01-NOV-1996, sequence version 1.
12-SEP-2018, entry version 175.
RecName: Full=ATP-sensitive inward rectifier potassium channel 8;
AltName: Full=Inward rectifier K(+) channel Kir6.1;
AltName: Full=Potassium channel, inwardly rectifying subfamily J member 8;
AltName: Full=uKATP-1;
Name=KCNJ8;
Homo sapiens (Human).
Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi;
Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini;
Catarrhini; Hominidae; Homo.
NCBI_TaxID=9606;
[1]
NUCLEOTIDE SEQUENCE [GENOMIC DNA / MRNA].
TISSUE=Lung, and Placenta;
PubMed=8595887; DOI=10.1006/geno.1995.0018;
Inagaki N., Inazawa J., Seino S.;
"cDNA sequence, gene structure, and chromosomal localization of the
human ATP-sensitive potassium channel, uKATP-1, gene (KCNJ8).";
Genomics 30:102-104(1995).
[2]
NUCLEOTIDE SEQUENCE [LARGE SCALE MRNA].
TISSUE=Brain;
PubMed=15489334; DOI=10.1101/gr.2596504;
The MGC Project Team;
"The status, quality, and expansion of the NIH full-length cDNA
project: the Mammalian Gene Collection (MGC).";
Genome Res. 14:2121-2127(2004).
[3]
TISSUE SPECIFICITY.
PubMed=9573340; DOI=10.1016/S0378-1119(98)00086-9;
Erginel-Unaltuna N., Yang W.P., Blanar M.A.;
"Genomic organization and expression of KCNJ8/Kir6.1, a gene encoding
a subunit of an ATP-sensitive potassium channel.";
Gene 211:71-78(1998).
[4]
REVIEW ON J-WAVE SYNDROMES.
PubMed=20153265; DOI=10.1016/j.hrthm.2009.12.006;
Antzelevitch C., Yan G.X.;
"J wave syndromes.";
Heart Rhythm 7:549-558(2010).
[5]
POSSIBLE INVOLVEMENT IN SUSCEPTIBILITY TO J-WAVE SYNDROMES, VARIANT
LEU-422, AND CHARACTERIZATION OF VARIANT LEU-422.
PubMed=20558321; DOI=10.1016/j.hrthm.2010.06.016;
Medeiros-Domingo A., Tan B.H., Crotti L., Tester D.J., Eckhardt L.,
Cuoretti A., Kroboth S.L., Song C., Zhou Q., Kopp D., Schwartz P.J.,
Makielski J.C., Ackerman M.J.;
"Gain-of-function mutation S422L in the KCNJ8-encoded cardiac K(ATP)
channel Kir6.1 as a pathogenic substrate for J-wave syndromes.";
Heart Rhythm 7:1466-1471(2010).
[6]
POSSIBLE INVOLVEMENT IN HTOCD, VARIANT HTOCD SER-176, AND
CHARACTERIZATION OF VARIANT HTOCD SER-176.
PubMed=24700710; DOI=10.1002/humu.22555;
Cooper P.E., Reutter H., Woelfle J., Engels H., Grange D.K.,
van Haaften G., van Bon B.W., Hoischen A., Nichols C.G.;
"Cantu syndrome resulting from activating mutation in the KCNJ8
gene.";
Hum. Mutat. 35:809-813(2014).
[7]
FUNCTION, CHARACTERIZATION OF VARIANT HTOCD MET-65, AND MUTAGENESIS OF
VAL-65.
PubMed=28842488; DOI=10.1074/jbc.M117.804971;
Cooper P.E., McClenaghan C., Chen X., Stary-Weinzinger A.,
Nichols C.G.;
"Conserved functional consequences of disease-associated mutations in
the slide-helix of Kir6.1 and Kir6.2 subunits of the ATP-sensitive
potassium channel.";
J. Biol. Chem. 292:17387-17398(2017).
[8]
VARIANTS SIDS GLU-332 DEL AND ILE-346, AND CHARACTERIZATION OF
VARIANTS SIDS GLU-332 DEL AND ILE-346.
PubMed=21836131; DOI=10.1161/CIRCGENETICS.111.960195;
Tester D.J., Tan B.H., Medeiros-Domingo A., Song C., Makielski J.C.,
Ackerman M.J.;
"Loss-of-function mutations in the KCNJ8-encoded Kir6.1 KATP channel
and sudden infant death syndrome.";
Circ. Cardiovasc. Genet. 4:510-515(2011).
[9]
VARIANT HTOCD MET-65.
PubMed=24176758; DOI=10.1016/j.ejmg.2013.09.009;
Brownstein C.A., Towne M.C., Luquette L.J., Harris D.J.,
Marinakis N.S., Meinecke P., Kutsche K., Campeau P.M., Yu T.W.,
Margulies D.M., Agrawal P.B., Beggs A.H.;
"Mutation of KCNJ8 in a patient with Cantu syndrome with unique
vascular abnormalities - support for the role of K(ATP) channels in
this condition.";
Eur. J. Med. Genet. 56:678-682(2013).
-!- FUNCTION: This potassium channel is controlled by G proteins.
Inward rectifier potassium channels are characterized by a greater
tendency to allow potassium to flow into the cell rather than out
of it. Their voltage dependence is regulated by the concentration
of extracellular potassium; as external potassium is raised, the
voltage range of the channel opening shifts to more positive
voltages. The inward rectification is mainly due to the blockage
of outward current by internal magnesium. Can be blocked by
external barium (By similarity). {ECO:0000250|UniProtKB:Q63664,
ECO:0000269|PubMed:28842488}.
-!- SUBCELLULAR LOCATION: Membrane; Multi-pass membrane protein
{ECO:0000305}.
-!- TISSUE SPECIFICITY: Predominantly detected in fetal and adult
heart. {ECO:0000269|PubMed:9573340}.
-!- DISEASE: Note=Defects in KCNJ8 may be associated with
susceptibility to J-wave syndromes, a group of heart disorders
characterized by early repolarization events as indicated by
abnormal J-wave manifestation on electrocardiogram (ECG). The J
point denotes the junction of the QRS complex and the ST segment
on the ECG, marking the end of depolarization and the beginning of
repolarization. An abnormal J wave is a deflection with a dome or
hump morphology immediately following the QRS complex of the
surface ECG. Examples of J-wave disorders are arrhythmias
associated with an early repolarization pattern in the inferior or
mid to lateral precordial leads, Brugada syndrome, some cases of
idiopathic ventricular fibrillation (VF) with an early
repolarization pattern in the inferior, inferolateral or global
leads, as well as arrhythmias associated with hypothermia.
{ECO:0000269|PubMed:20558321}.
-!- DISEASE: Sudden infant death syndrome (SIDS) [MIM:272120]: SIDS is
the sudden death of an infant younger than 1 year that remains
unexplained after a thorough case investigation, including
performance of a complete autopsy, examination of the death scene,
and review of clinical history. Pathophysiologic mechanisms for
SIDS may include respiratory dysfunction, cardiac dysrhythmias,
cardiorespiratory instability, and inborn errors of metabolism,
but definitive pathogenic mechanisms precipitating an infant
sudden death remain elusive. {ECO:0000269|PubMed:21836131}.
Note=Disease susceptibility is associated with variations
affecting the gene represented in this entry.
-!- DISEASE: Hypertrichotic osteochondrodysplasia (HTOCD)
[MIM:239850]: A rare disorder characterized by congenital
hypertrichosis, neonatal macrosomia, a distinct
osteochondrodysplasia, and cardiomegaly. The hypertrichosis leads
to thick scalp hair, which extends onto the forehead, and a
general increase in body hair. In addition, macrocephaly and
coarse facial features, including a broad nasal bridge, epicanthal
folds, a wide mouth, and full lips, can be suggestive of a storage
disorder. About half of affected individuals are macrosomic and
edematous at birth, whereas in childhood they usually have a
muscular appearance with little subcutaneous fat. Thickened
calvarium, narrow thorax, wide ribs, flattened or ovoid vertebral
bodies, coxa valga, osteopenia, enlarged medullary canals, and
metaphyseal widening of long bones have been reported. Cardiac
manifestations such as patent ductus arteriosus, ventricular
hypertrophy, pulmonary hypertension, and pericardial effusions are
present in approximately 80% of cases. Motor development is
usually delayed due to hypotonia. Most patients have a mild speech
delay, and a small percentage have learning difficulties or
intellectual disability. {ECO:0000269|PubMed:24176758,
ECO:0000269|PubMed:24700710, ECO:0000269|PubMed:28842488}.
Note=The disease may be caused by mutations affecting distinct
genetic loci, including the gene represented in this entry.
-!- SIMILARITY: Belongs to the inward rectifier-type potassium channel
(TC 1.A.2.1) family. KCNJ8 subfamily. {ECO:0000305}.
-----------------------------------------------------------------------
Copyrighted by the UniProt Consortium, see https://www.uniprot.org/terms
Distributed under the Creative Commons Attribution (CC BY 4.0) License
-----------------------------------------------------------------------
EMBL; D50312; BAA08851.1; -; mRNA.
EMBL; D50315; BAA08852.1; -; Genomic_DNA.
EMBL; BC000544; AAH00544.1; -; mRNA.
CCDS; CCDS8692.1; -.
RefSeq; NP_004973.1; NM_004982.3.
RefSeq; XP_005253415.1; XM_005253358.4.
RefSeq; XP_016874772.1; XM_017019283.1.
RefSeq; XP_016874773.1; XM_017019284.1.
UniGene; Hs.102308; -.
UniGene; Hs.619408; -.
UniGene; Hs.741642; -.
ProteinModelPortal; Q15842; -.
SMR; Q15842; -.
BioGrid; 109966; 33.
ELM; Q15842; -.
IntAct; Q15842; 3.
STRING; 9606.ENSP00000240662; -.
ChEMBL; CHEMBL4770; -.
DrugBank; DB01251; Gliquidone.
DrugBank; DB01289; Glisoxepide.
DrugBank; DB01016; Glyburide.
DrugBank; DB00922; Levosimendan.
DrugBank; DB00914; Phenformin.
DrugBank; DB01154; Thiamylal.
DrugBank; DB01392; Yohimbine.
TCDB; 1.A.2.1.13; the inward rectifier k(+) channel (irk-c) family.
iPTMnet; Q15842; -.
PhosphoSitePlus; Q15842; -.
BioMuta; KCNJ8; -.
DMDM; 2493600; -.
PaxDb; Q15842; -.
PeptideAtlas; Q15842; -.
PRIDE; Q15842; -.
ProteomicsDB; 60787; -.
DNASU; 3764; -.
Ensembl; ENST00000240662; ENSP00000240662; ENSG00000121361.
GeneID; 3764; -.
KEGG; hsa:3764; -.
UCSC; uc001rff.4; human.
CTD; 3764; -.
DisGeNET; 3764; -.
EuPathDB; HostDB:ENSG00000121361.3; -.
GeneCards; KCNJ8; -.
HGNC; HGNC:6269; KCNJ8.
HPA; HPA031066; -.
MalaCards; KCNJ8; -.
MIM; 239850; phenotype.
MIM; 272120; phenotype.
MIM; 600935; gene.
neXtProt; NX_Q15842; -.
OpenTargets; ENSG00000121361; -.
Orphanet; 130; Brugada syndrome.
Orphanet; 1517; Hypertrichotic osteochondrodysplasia, Cantu type.
PharmGKB; PA30050; -.
eggNOG; KOG3827; Eukaryota.
eggNOG; ENOG410XQ62; LUCA.
GeneTree; ENSGT00760000118842; -.
HOGENOM; HOG000237325; -.
HOVERGEN; HBG006178; -.
InParanoid; Q15842; -.
KO; K05001; -.
OMA; AMELQCS; -.
OrthoDB; EOG091G08HC; -.
PhylomeDB; Q15842; -.
TreeFam; TF313676; -.
Reactome; R-HSA-1296025; ATP sensitive Potassium channels.
GeneWiki; KCNJ8; -.
GenomeRNAi; 3764; -.
PRO; PR:Q15842; -.
Proteomes; UP000005640; Chromosome 12.
Bgee; ENSG00000121361; Expressed in 191 organ(s), highest expression level in myocardium.
CleanEx; HS_KCNJ8; -.
ExpressionAtlas; Q15842; baseline and differential.
Genevisible; Q15842; HS.
GO; GO:0008282; C:inward rectifying potassium channel; IEA:Ensembl.
GO; GO:0005739; C:mitochondrion; IEA:Ensembl.
GO; GO:0030016; C:myofibril; IEA:Ensembl.
GO; GO:0005886; C:plasma membrane; TAS:Reactome.
GO; GO:0042383; C:sarcolemma; IEA:Ensembl.
GO; GO:0008076; C:voltage-gated potassium channel complex; TAS:ProtInc.
GO; GO:0005524; F:ATP binding; IEA:Ensembl.
GO; GO:0015272; F:ATP-activated inward rectifier potassium channel activity; IDA:BHF-UCL.
GO; GO:0005242; F:inward rectifier potassium channel activity; TAS:ProtInc.
GO; GO:0017098; F:sulfonylurea receptor binding; IEA:Ensembl.
GO; GO:1902282; F:voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization; IMP:BHF-UCL.
GO; GO:0051607; P:defense response to virus; IEA:Ensembl.
GO; GO:0007507; P:heart development; IEA:Ensembl.
GO; GO:0001822; P:kidney development; IEA:Ensembl.
GO; GO:0098915; P:membrane repolarization during ventricular cardiac muscle cell action potential; IMP:BHF-UCL.
GO; GO:0010107; P:potassium ion import; IBA:GO_Central.
GO; GO:1990573; P:potassium ion import across plasma membrane; IDA:BHF-UCL.
GO; GO:0006813; P:potassium ion transport; TAS:ProtInc.
GO; GO:0034765; P:regulation of ion transmembrane transport; IEA:UniProtKB-KW.
GO; GO:0043330; P:response to exogenous dsRNA; IEA:Ensembl.
GO; GO:0032496; P:response to lipopolysaccharide; IEA:Ensembl.
Gene3D; 2.60.40.1400; -; 2.
InterPro; IPR014756; Ig_E-set.
InterPro; IPR016449; K_chnl_inward-rec_Kir.
InterPro; IPR003278; K_chnl_inward-rec_Kir6.1.
InterPro; IPR013518; K_chnl_inward-rec_Kir_cyto.
PANTHER; PTHR11767; PTHR11767; 1.
PANTHER; PTHR11767:SF11; PTHR11767:SF11; 1.
Pfam; PF01007; IRK; 1.
PIRSF; PIRSF005465; GIRK_kir; 1.
PRINTS; PR01331; KIR61CHANNEL.
PRINTS; PR01320; KIRCHANNEL.
SUPFAM; SSF81296; SSF81296; 1.
1: Evidence at protein level;
Complete proteome; Disease mutation; Ion channel; Ion transport;
Membrane; Phosphoprotein; Polymorphism; Potassium;
Potassium transport; Reference proteome; Transmembrane;
Transmembrane helix; Transport; Voltage-gated channel.
CHAIN 1 424 ATP-sensitive inward rectifier potassium
channel 8.
/FTId=PRO_0000154947.
TOPO_DOM 1 69 Cytoplasmic. {ECO:0000250}.
TRANSMEM 70 94 Helical; Name=M1. {ECO:0000250}.
TOPO_DOM 95 126 Extracellular. {ECO:0000250}.
INTRAMEM 127 138 Helical; Pore-forming; Name=H5.
{ECO:0000250}.
INTRAMEM 139 145 Pore-forming. {ECO:0000250}.
TOPO_DOM 146 154 Extracellular. {ECO:0000250}.
TRANSMEM 155 176 Helical; Name=M2. {ECO:0000250}.
TOPO_DOM 177 424 Cytoplasmic. {ECO:0000250}.
MOTIF 140 145 Selectivity filter. {ECO:0000250}.
SITE 170 170 Role in the control of polyamine-mediated
channel gating and in the blocking by
intracellular magnesium. {ECO:0000250}.
MOD_RES 6 6 Phosphoserine.
{ECO:0000250|UniProtKB:P97794}.
VARIANT 65 65 V -> M (in HTOCD; unknown pathological
significance; displays gain of function;
increased open state stability, reduced
sensitivity to ATP inhibition and
increased channel activity; almost
completely abolishes high affinity
sensitivity to glibenclamide, an
inhibitor of ATP-sensitive potassium
channels; dbSNP:rs606231263).
{ECO:0000269|PubMed:24176758,
ECO:0000269|PubMed:28842488}.
/FTId=VAR_079518.
VARIANT 176 176 C -> S (in HTOCD; unknown pathological
significance; displays gain of function;
displays reduced ATP sensitivity;
dbSNP:rs606231264).
{ECO:0000269|PubMed:24700710}.
/FTId=VAR_075226.
VARIANT 332 332 Missing (in SIDS; the mutant channel
displays reduced potassium currents
compared to wild type).
{ECO:0000269|PubMed:21836131}.
/FTId=VAR_065878.
VARIANT 334 334 V -> A (in dbSNP:rs34811413).
/FTId=VAR_049670.
VARIANT 346 346 V -> I (in SIDS; the mutant channel
displays reduced potassium currents
compared to wild type;
dbSNP:rs147316959).
{ECO:0000269|PubMed:21836131}.
/FTId=VAR_065879.
VARIANT 422 422 S -> L (found in Brugada syndrome and
other J-wave syndromes; unknown
pathological significance; the mutant
channel displays an increase in
glibenclamide-sensitive potassium
currents compared to wild type;
dbSNP:rs72554071).
{ECO:0000269|PubMed:20558321}.
/FTId=VAR_065225.
MUTAGEN 65 65 V->L: No effect on channel activity.
{ECO:0000269|PubMed:28842488}.
SEQUENCE 424 AA; 47968 MW; 973EAA5900C6447C CRC64;
MLARKSIIPE EYVLARIAAE NLRKPRIRDR LPKARFIAKS GACNLAHKNI REQGRFLQDI
FTTLVDLKWR HTLVIFTMSF LCSWLLFAIM WWLVAFAHGD IYAYMEKSGM EKSGLESTVC
VTNVRSFTSA FLFSIEVQVT IGFGGRMMTE ECPLAITVLI LQNIVGLIIN AVMLGCIFMK
TAQAHRRAET LIFSRHAVIA VRNGKLCFMF RVGDLRKSMI ISASVRIQVV KKTTTPEGEV
VPIHQLDIPV DNPIESNNIF LVAPLIICHV IDKRSPLYDI SATDLANQDL EVIVILEGVV
ETTGITTQAR TSYIAEEIQW GHRFVSIVTE EEGVYSVDYS KFGNTVKVAA PRCSARELDE
KPSILIQTLQ KSELSHQNSL RKRNSMRRNN SMRRNNSIRR NNSSLMVPKV QFMTPEGNQN
TSES


Related products :

Catalog number Product name Quantity
18-003-42620 Potassium channel subfamily K member 3 - Acid-sensitive potassium channel protein TASK-1; TWIK-related acid-sensitive K(+) channel 1; Two pore potassium channel KT3.1 Polyclonal 0.1 mg Protein A
E1049Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 48T
YHB0137Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 96T
YHB0133Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 96T
E1050Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 96T
E1039Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11 per Kir6.2 ELISA Kit 48T
YHB0137Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 48T
E1050Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8 per Kir6.1 ELISA Kit 96T
E1038Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 48T
E1039Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11 per Kir6.2 ELISA Kit 96T
YHB0133Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 48T
E1039Ra Rat ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 96T
E1050Ra Rat ATP-sensitive inward rectifier potassium channel 8,KCNJ8 per Kir6.1 ELISA Kit 48T
E0090Rb Rabbit ATP-sensitive inward rectifier potassium channel 11,KCNJ11 per Kir6.2 ELISA Kit 96T
E1795Hu Human ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 48T
E1326Mo Mouse ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 48T
YHB0427Hu Human ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 96T
E1101Hu Human ATP-sensitive inward rectifier potassium channel 8,KCNJ8 per Kir6.1 ELISA Kit 48T
E1795Hu Human ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 96T
E0090Rb Rabbit ATP-sensitive inward rectifier potassium channel 11,KCNJ11 per Kir6.2 ELISA Kit 48T
YHB0014Rb Rabbit ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 48T
E1327Mo Mouse ATP-sensitive inward rectifier potassium channel 8,KCNJ8 per Kir6.1 ELISA Kit 48T
YHB0431Hu Human ATP-sensitive inward rectifier potassium channel 8,KCNJ8-Kir6.1 ELISA Kit 96T
E1101Hu Human ATP-sensitive inward rectifier potassium channel 8,KCNJ8 per Kir6.1 ELISA Kit 96T
E0089Rb Rabbit ATP-sensitive inward rectifier potassium channel 11,KCNJ11-Kir6.2 ELISA Kit 48T


 

GENTAUR Belgium BVBA BE0473327336
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45

Fax 0032 16 50 90 45
info@gentaur.com | Gentaur





GENTAUR Ltd.
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
uk@gentaur.com | Gentaur

 

 




GENTAUR France SARL
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50

Fax 01 43 25 01 60
RCS Paris B 484 237 888

SIRET 48423788800017

BNP PARIBAS PARIS PL MAUBERT BIC BNPAFRPPPRG

france@gentaur.com | Gentaur

GENTAUR GmbH
Marienbongard 20
52062 Aachen Deutschland
Support Karolina Elandt
Tel: 0035929830070
Fax: (+49) 241 56 00 47 88

Logistic :0241 40 08 90 86
Bankleitzahl 39050000
IBAN lautet DE8839050000107569353
Handelsregister Aachen HR B 16058
Umsatzsteuer-Identifikationsnummer *** DE 815175831
Steuernummer 201/5961/3925
de@gentaur.com | Gentaur

GENTAUR U.S.A
Genprice Inc, Logistics
547, Yurok Circle
San Jose, CA 95123
CA 95123
Tel (408) 780-0908,
Fax (408) 780-0908,
sales@genprice.com

Genprice Inc, Invoices and accounting
6017 Snell Ave, Ste 357
San Jose, CA 95123




GENTAUR Nederland BV
NL850396268B01 KVK nummer 52327027
Kuiper 1
5521 DG Eersel Nederland
Tel:  0208-080893  Fax: 0497-517897
nl@gentaur.com | Gentaur
IBAN: NL04 RABO 0156 9854 62   SWIFT RABONL2U






GENTAUR Spain
tel:0911876558
spain@gentaur.com | Gentaur






ГЕНТАУЪР БЪЛГАРИЯ
ID # 201 358 931 /BULSTAT
София 1000, ул. "Граф Игнатиев" 53 вх. В, ет. 2
Tel 0035924682280 Fax 0035924808322
e-mail: Sofia@gentaur.com | Gentaur
IBAN: BG11FINV91501014771636
BIC: FINVBGSF

GENTAUR Poland Sp. z o.o.


ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
TEL Gdansk 058 710 33 44 FAX  058 710 33 48              

poland@gentaur.com | Gentaur

Other countries

Österreich +43720880899

Canada Montreal +15149077481

Ceská republika Praha +420246019719

Danmark +4569918806

Finland Helsset +358942419041

Magyarország Budapest +3619980547

Ireland Dublin+35316526556

Luxembourg+35220880274

Norge Oslo+4721031366

Sverige Stockholm+46852503438

Schweiz Züri+41435006251

US New York+17185132983

GENTAUR Italy
SRL IVA IT03841300167
Piazza Giacomo Matteotti, 6
24122 Bergamo Tel 02 36 00 65 93
Fax 02 36 00 65 94
italia@gentaur.com | Gentaur