Uchiumi T., Hinoshita E., Haga S., Nakamura T., Tanaka T., Toh S., Furukawa M., Kawabe T., Wada M., Kagotani K., Okumura K., Kohno K., Akiyama S., Kuwano M.. The human multidrug resistance protein (MRP) gene encodes a membrane protein involved in the ATP-dependent transport of hydrophobic compounds. We previously isolated a canalicular multispecific organic anion transporter, cMOAT1/MRP2, that belongs to the ATP binding cassette (ABC) superfamily, which is specifically expressed in liver, and cMOAT1/MRP2 is responsible for the defects in hyperbilirubinemia II/Dubin-Johnson syndrome. In this study, we isolated a new cDNA of the ABC superfamily designated cMOAT2/MRP3 that is homologous to human MRP1 and cMOAT1/MRP2: cMOAT2/MRP3 is 56% identical to MRP1 and 45% identical to cMOAT1/MRP2, respectively. Fluorescence in situ hybridization demonstrated the chromosomal locus of this gene on chromosome 17q22. The human cMOAT2 cDNA hybridized to a 6.5-kb mRNA that was mainly expressed in liver and to a ...
1. Bailey, AJ, et al. Abnormal collagen cross-linking in the cartilage of a Diastrophic Dysplasia patient. British Journal of Rheumatology. 1995 June; 34(6): 512-515 2. Cetta, G, et al. Diastrophic Dysplasia sulfate transporter gene is not involved in Pseudodiastrophic Dysplasia. American Journal of Medical Genetics. 1997 Dec; 73(4): 493-494. 3. Domer, Timothy P. Diastrophic Dysplasia. The Orthopedic Department; The Alfred Dupont Center. http://gait.aidi.udel.edu/res695/homepage/pd_ortho/orthhome.htm. Feb 1, 2000. 4. Forese, LL, et al. Severe mid-cervical kyphosis with cord compression in Larsen`s syndrome and Diastrophic Dysplasia: unrelated syndromes with similar radiologic findings and neurosurgical implications. Pediatric Radiology. 1995; 25(2): 136-139. 5. Greenberg Center for Skeletal Dysplasias. http://ww2.med.jhu.edu/Greenberg.Center/ diastrop.htm. Feb 1, 2000. 6. Hastbacka, J, et al. The Diastrophic Dysplasia gene encodes a novel sulfate transporter: positional cloning by time structure ...
TY - JOUR. T1 - Mutations in the canalicular multispecific organic anion transporter (cMOAT) gene, a novel ABC transporter, in patients with hyperbilirubinemia II/Dubin-Johnson syndrome. AU - Wada, Morimasa. AU - Toh, Satoshi. AU - Taniguchi, Ken. AU - Nakamura, Takanori. AU - Uchiumi, Takeshi. AU - Kohno, Kimitoshi. AU - Yoshida, Ichiro. AU - Kimura, Akihiko. AU - Sakisaka, Shotaro. AU - Adachi, Yukihiko. AU - Kuwano, Michihiko. PY - 1998/2. Y1 - 1998/2. N2 - Members of the ATP-binding cassette (ABC) transporter superfamily are mutated to cause diseases that include cystic fibrosis, hyperinsulinemia, adrenoleukodystrophy, Stargardt disease and multidrug resistance. We recently isolated a novel human member of ABC transporter superfamily as the candidate transporter for the glucuronide and glutathione-conjugated antitumor agents, and found it highly homologous to the rat cmoat gene. Consistent with recent findings of defects in the homologous cmoat gene in two rat models of hyperbilirubinemia ...
Achondrogenesis, type IB (ACG1B; MIM 600972) is a lethal condition caused by the diastrophic dysplasia sulfate transporter gene mutations (DTDST/SLC26A2). Affected fetuses are usually in breech position and appear hydropic. The limbs and the trunk are shortened. In contrast to the findings in achondrogenesis, type II (ACG2; MIM 200610), the head is of a normal or near normal size and the fingers and toes are short. The feet and toes are rotated inward, a finding shared with diastrophic dysplasia (DTD; MIM 222600), another disorder caused by DTDST mutations.. Read less ...
J:223752 Cai T, Yang L, Cai W, Guo S, Yu P, Li J, Hu X, Yan M, Shao Q, Jin Y, Sun ZS, Luo ZJ, Dysplastic spondylolysis is caused by mutations in the diastrophic dysplasia sulfate transporter gene. Proc Natl Acad Sci U S A. 2015 Jun 30;112(26):8064-9 ...
Summary is not available for the mouse gene. This summary is for the human ortholog.] The diastrophic dysplasia sulfate transporter is a transmembrane glycoprotein implicated in the pathogenesis of several human chondrodysplasias. It apparently is critical in cartilage for sulfation of proteoglycans and matrix organization. [provided by RefSeq, Jul 2008 ...
Irinotecan, 7-ethyl-10-[4-(1-piperidino)-1-piperidino]-carbonyloxycamptothecin (CPT-11), is a potent anticancer drug that is increasingly used in chemotherapy. A frequent limiting side effect involves gastrointestinal toxicity (diarrhea), which is thought to be related to the biliary excretion of CPT-11 and its metabolites. Accordingly, the biliary excretion mechanisms for both the lactone and carboxylate forms of CPT-11 and its metabolites, SN-38 and its glucuronide (SN38-Glu), were investigated using Sprague-Dawley (SD) rats and Eisai hyperbilirubinemic rats (EHBR), with the latter being mutant rats with a genetic deficiency of the canalicular multispecific organic anion transporter. After i.v. administration of CPT-11, the biliary excretion clearance, defined as the biliary excretion rate normalized to the hepatic concentration, of both the lactone and carboxylate forms of SN38-Glu was much lower in EHBR. The biliary excretion clearance for the carboxylate form of both CPT-11 and SN-38 was ...
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Domain combinations containing the Phoshotransferase/anion transport protein superfamily . Domain architectures illustrate each occurrence of the Phoshotransferase/anion transport protein superfamily.
... , AS12 2611, antibody to AtNRT1, Nitrate/chlorate transporter, protein CHLORINA 1, AtNPF6.3, Q05085, AT1G12110
Nitrate transporter structure paves the way for exciting new areas of work, Representing biochemistry research at Oxford University
Shop High affinity sulfate transporter ELISA Kit, Recombinant Protein and High affinity sulfate transporter Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
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Pri ileu je v dôsledku rôznych príčin narušená fyziologická motilita čriev. Dôvody jeho vzniku sú rôznorodé, patria k nim mechanické prekážky pasáže obsahu, poruchy prenosu.... ...
Disruption of the high-affinity nitrate transporter NRT2.1 activates the priming defence against Pseudomonas syringae, resulting in enhanced resistance. In this study, it is demonstrated that the high-affinity ammonium transporter AMT1.1 is a negative regulator of Arabidopsis defence responses. The T-DNA knockout mutant amt1.1 displays enhanced resistance against Plectosphaerella cucumerina and reduced susceptibility to P. syringae. The impairment of AMT1.1 induces significant metabolic changes in the absence of challenge, suggesting that amt1.1 retains constitutive defence responses. Interestingly, amt1.1 combats pathogens differently depending on the lifestyle of the pathogen. In addition, N starvation enhances the susceptibility of wild type plants and the mutant amt1.1 to P. syringae whereas it has no effect on P. cucumerina resistance. The metabolic changes of amt1.1 against P. syringae are subtler and are restricted to the phenylpropanoid pathway, which correlates with its reduced susceptibility.
By screening databases of human expressed sequence tags, we have identified three new homologues of MRP1, the gene encoding the multidrug resistance-associated protein, and cMOAT (or MRP2), the canalicular multispecific organic anion transporter gene. We call these new genes MRP3, MRP4, and MRP5. MRP3, like cMOAT, is mainly expressed in the liver. MRP4 is expressed only at very low levels in a few tissues, and MRP5, like MRP1, is expressed in almost every tissue tested. To assess a possible role of these new MRP homologues in multidrug or cisplatin resistance, a large set of resistant cell lines was examined for the (over)expression of MRP1, cMOAT, MRP3, MRP4, and MRP5. We find that even in cells selected for a low level of resistance, several MRP-related genes can be up-regulated simultaneously. However, MRP4 is not overexpressed in any of the cell lines we analyzed; MRP3 and MRP5 are only overexpressed in a few cell lines, and the RNA levels do not seem to correlate with resistance to either ...
The symptoms and physical findings associated with diastrophic dysplasia may be extremely variable, differing in range and severity even among affected family members (kindreds). However, in all individuals with the disorder, there is abnormal development of bones and joints of the body (skeletal and joint dysplasia).. During normal development before birth (embryonic and fetal development) as well as development during early childhood, cartilage in many areas of the body is gradually replaced by bone (ossification). In addition, a layer of cartilage (epiphyseal cartilage [growth plate]) separates the shafts (diaphyses) of long bones (e.g., bones of the arms and legs) from their ends (epiphyses), allowing long bones to grow until the cartilage is no longer present. In those affected by diastrophic dysplasia, however, there is delayed growth before and after birth (prenatal and postnatal growth retardation), the development of the ends of the long bones (epiphyses) is irregular, and the ...
Examination of wild ancestors can identify which traits have been altered by selection as possible targets for genetic improvement. We investigated the whole plant response to low nitrogen (LN), especially below ground, by the wild ancestor of modern maize (Zea mays L.), Balsas teosinte (Zea mays subsp. parviglumis H. H. Iltis & Doebley). Teosinte responded to LN by reducing the shoot N concentration and increasing the root:shoot biomass ratio. The lengths of individual crown roots and the total lateral root length increased, compensated by reduced crown root number. Low N caused a decrease in total root hair (RH) length and increased expression of high affinity nitrate transporters. To facilitate future mapping studies, these results were compared to a modern inbred (W22) used as the parent in a modern maize × teosinte population and extensively employed in maize domestication studies. The adaptations to LN in teosinte and W22 were surprisingly conserved, but the strategies employed were ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
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The human solute carrier 26 (SLC26) family of anion transporters consists of ten members that are found in various organs in the body including the stomach, intestine, kidney, thyroid and ear where they transport anions including bicarbonate, chloride and sulfate, typically in an exchange mode. Mutations in these genes cause a plethora of diseases such as diastrophic dysplasia affecting sulfate uptake into chondrocytes (SLC26A2), congenital chloride-losing diarrhoea (SLC26A3) affecting chloride secretion in the intestine and Pendreds syndrome (SLC26A4) resulting in hearing loss. To understand how these mutations affect the structures of the SLC26 membrane proteins and their ability to function properly, 12 human disease-causing mutants from SLC26A2, SLC26A3 and SLC26A4 were introduced into the equivalent sites of the sulfate transporter anti-sigma factor antagonist (STAS) domain of a bacterial homologue SLC26 protein DauA (YchM). Biophysical analyses including size-exclusion chromatography, ...
The macronutrient nitrogen (N) is an essential component of numerous important compounds, including amino acids, proteins, nucleic acids, chlorophyll, and some plant hormones. This element is a major limiting factor in most agricultural systems. Because the N-utilization efficiency strongly influences crop productivity, a vast amount of N fertilizers is applied to maximize yields. However, it is estimated that more than half of that N is lost from the plant-soil system, with unused N fertilizers severely polluting the environment [1]. Thus, N-uptake efficiency must be increased to improve productivity and reduce pollution.. During periods of N-starvation, various deficiency-responsive genes function to support plant survival by increasing the level of chlorophyll synthesis [2], altering root architecture [3], improving N-assimilation [4], enhancing lignin content [5], and changing the amounts of sugars and sugar phosphates [6]. Nitrate transporter genes (NRTs) are responsible for the ...
Complete information for SLCO2A1 gene (Protein Coding), Solute Carrier Organic Anion Transporter Family Member 2A1, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for SLCO1A2 gene (Protein Coding), Solute Carrier Organic Anion Transporter Family Member 1A2, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
SLCO1A2 antibody (solute carrier organic anion transporter family, member 1A2) for ELISA, WB. Anti-SLCO1A2 pAb (GTX87607) is tested in Human samples. 100% Ab-Assurance.
Gene target information for Slco1a1 - solute carrier organic anion transporter family, member 1a1 (house mouse). Find diseases associated with this biological target and compounds tested against it in bioassay experiments.
In this study, we describe transcriptional regulation of the hPDS gene encoding pendrin, a major anion exchanger in the CCD, by UGN, an important modulator of fluid and electrolyte homeostasis. We demonstrate a UGN-induced decrease in both pendrin protein expression (Fig. 2) and pendrin mRNA level (Fig. 3, A and B) in kidneys harvested from mice that were injected with this modulator as well as a UGN-induced reduction in endogenous pendrin mRNA level in renal cells (Fig. 3C). In addition, we demonstrate that UGN decreases hPDS promoter activity in transfected renal cells (Figs. 4 and 5). We show that UGN modulates hPDS promoter activity in large part via a HSE located between nt −1119 and −1115 of the hPDS promoter (Figs. 5 and 6), and we demonstrate that HSF1 likely mediates this UGN-induced modulation (Fig. 7). These findings suggest that pendrin gene expression is subject to HSE/HSF1-mediated transcriptional regulation by UGN.. The renal CCD plays a vital role in acid-base homeostasis and ...
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Antivirotika jsou extrémně pestrou skupinou léčiv, které nejrůznějšími mechanizmy působí proti virovým částicím. Některé narušují replikaci virové DNA, jiné blokují tvorbu virových částic v postižené buňce, další narušují průnik virů do buňky atp ...
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1) We have prepared murine monoclonal antibodies to the membrane domain of the human erythrocyte anion transport protein (band 3). (2) All of these antibodies react with regions of the protein located at the cytoplasmic surface of the red cell. (3) One of the antibodies reacts with an epitope present on a cytoplasmic loop of the protein located between the C-terminus and a point 168 amino acids from the C-terminus. The other antibodies recognize different epitopes on the C-terminal tail of the protein and the sequences likely to be involved in these epitopes are defined. (4) Our results show that the C-terminus of the red-cell anion transport protein is located on the cytoplasmic side of the red-cell membrane. (5) None of the antibodies inhibited sulphate exchange transport when introduced into resealed red-cell membranes; however, the bivalent form of one of the antibodies reduced the inhibitory potency of 4-acetamido-4-isothiocyanatostilbene disulphonate on sulphate exchange transport in ...
Purpose. Biliary organic anion excretion is mediated by an ATP-dependent primary active transporter, a so-called canalicular multispecific organic anion transporter (cMOAT). As there appear to be many canalicular organic anion transports, we examined the effects of various organic anions and bile acid conjugates on the biliary excretion of pravastatin in rats. Methods. [l4C]pravastatin was intravenously injected into rats with bile drainage in the presence and absence of the continuous infusion of organic anions and bile acids, and radioactivity of its biliary excretion was studied. Results. Biliary excretion of [14C]pravastatin was markedly inhibited by sulfobromophthalein-glutathione, taurolithocholate-3-sulfate, ursodeoxycholate-3,7-sulfate, and ursodeoxycholate-3-O-glucuronide. In contrast, dibromosulfophthalein only slightly inhibited biliary pravastatin excretion, and cefpiramide did not affect biliary pravastatin excretion. Conclusions. These findings further support the multiplicity of
Congenital hereditary endothelial dystrophy (CHED) is an inherited disorder of the corneal endothelium characterised by bilateral non-inflammatory corneal clouding ranging from a diffuse haze to a ground-glass appearance. CHED can be inherited in an autosomal dominant (CHED1) or recessive (CHED2) manner. CHED2 usually presents at birth or early infancy. Bilateral corneal clouding can lead to visual impairment often accompanied by nystagmus in CHED2 patients requiring corneal transplantation.1 Mutations in the solute carrier family 4 member 11 (SLC4A11) gene have been identified in most patients with CHED2. With PCR sequencing of the entire coding and putative promoter regions of SLC4A11, there were, however, some clinically confirmed CHED2 patients with undetected SLC4A11 mutations.2 ...
Irinotecan is a relatively new anticancer agent of interest for both its clinical activity and its complex clinical pharmacology. It is a prodrug, requiring activation by carboxylesterases to SN-38, an inhibitor of topoisomerase I. Recent studies suggest that human carboxylesterase-2 is the primary carboxylesterase involved in the hydrolysis at pharmacological concentrations (1) . Irinotecan is also oxidized by CYP3A43 to the inactive metabolite 7-ethyl-10-[4-N-(5-aminopentanoic acid)-1-piperidino]carbonyloxycamptothecin as well as to 7-ethyl-10-[4-(piperidino)-1-amino]carbonyloxycamptothecin, which can undergo hydrolysis to SN-38 (2, 3, 4) . SN-38 undergoes glucuronidation by UGT1A1 (5) and is possibly oxidized by CYP3A4 as well (6) . Mass balance studies have demonstrated that 64% of the total dose is excreted in the feces, confirming the important role of biliary excretion (7) . Studies suggest that canalicular multispecific organic anion transporter is the major transporter of irinotecan and ...
OsNRT1.1a is a low-affinity nitrate (NO3 ) transporter gene. In this study, another mRNA splicing product, OsNRT1.1b, putatively encoding a protein with six transmembrane domains, was identified based on the rice genomic database and bioinformatics analysis. OsNRT1.1a/OsNRT1.1b expression in Xenopus oocytes showed OsNRT1.1a-expressing oocytes accumulated 15N levels to about half as compared to OsNRT1.1b-expressing oocytes. The electrophysiological recording of OsNRT1.1b-expressing oocytes treated with 0.25mM NO3 confirmed 15N accumulation data. More functional assays were performed to examine the function of OsNRT1.1b in rice. The expression of both OsNRT1.1a and OsNRT1.1b was abundant in roots and downregulated by nitrogen (N) deficiency. The shoot biomass of transgenic rice plants with OsNRT1.1a or OsNRT1.1b overexpression increased under various N supplies under hydroponic conditions compared to wild-type (WT). The OsNRT1.1a overexpression lines showed increased plant N accumulation compared ...
Diastrophic dysplasia (DTD) is a chondrodysplasia causing severe growth retardation, and structural and functional abnormalities of joints. Growth retardation and joint abnormalities are already present in utero, and mean height at birth is 32.5 cm. Extremities are short while the trunk is of normal size, upper arms show ulnar deviation with stiff fingers and a hitchhiker thumb. Hips are stiff and most patients have club foot. A cleft palate is frequent. Growth remains slow, the median adult height for males is 135 cm and 129 cm for females. Changes in the joints often progress with age and corrective surgery becomes necessary.
TY - JOUR. T1 - The extracellular loop of pendrin and prestin modulates their voltage-sensing property. AU - Kuwabara, Makoto F.. AU - Wasano, Koichiro. AU - Takahashi, Satoe. AU - Bodner, Justin. AU - Komori, Tomotaka. AU - Uemura, Sotaro. AU - Zheng, Jing. AU - Shima, Tomohiro. AU - Homma, Kazuaki. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Pendrin and prestin belong to the solute carrier 26 (SLC26) family of anion transporters. Prestin is unique among the SLC26 family members in that it displays voltage-driven motor activity (electromotility) and concurrent gating currents that manifest as nonlinear cell membrane electrical capacitance (nonlinear capacitance (NLC)). Although the anion transport mechanism of the SLC26 proteins has begun to be elucidated, the molecular mechanism of electromotility, which is thought to have evolved from an ancestral ion transport mechanism, still remains largely elusive. Here, we demonstrate that pendrin also exhibits large NLC and that charged residues present in one ...
Diastrophic dysplasia is a rare genetic disorder that interferes with bone development and causes abnormal bone growth and dwarfism (short stature).
Pendrin is a Cl-/HCO3- exchanger expressed in the apical regions of renal intercalated cells. Following pendrin gene ablation, blood pressure falls, in part, from reduced renal NaCl absorption. We asked if pendrin is expressed in vascular tissue and if the lower blood pressure observed in pendrin null mice is accompanied by reduced vascular reactivity. Thus, the contractile responses to KCl and phenylephrine (PE) were examined in isometrically mounted thoracic aortas from wild-type and pendrin null mice. Although pendrin expression was not detected in the aorta, pendrin gene ablation changed contractile protein abundance and increased the maximal contractile response to PE when normalized to cross sectional area (CSA). However, the contractile sensitivity to this agent was unchanged. The increase in contractile force/cross sectional area observed in pendrin null mice was due to reduced cross sectional area of the aorta and not from increased contractile force per vessel. The pendrin-dependent ...
Solute carrier organic anion transporter family member 1A2 is a protein that in humans is encoded by the SLCO1A2 gene.[1][2] This gene encodes a sodium-independent transporter which mediates cellular uptake of organic ions in the liver. Its substrates include bile acids, bromosulphophthalein, and some steroidal compounds. The protein is a member of the SLC21A family of solute carriers. Alternate splicing of this gene results in three transcript variants encoding two different isoforms.[2] ...
TY - JOUR. T1 - NaBC1 is a ubiquitous electrogenic Na+-coupled borate transporter essential for cellular boron homeostasis and cell growth and proliferation. AU - Park, Meeyoung. AU - Li, Qin. AU - Shcheynikov, Nikolay. AU - Zeng, Weizong. AU - Muallem, Shmuel. PY - 2004/11/5. Y1 - 2004/11/5. N2 - Boron is a vital micronutrient in plants and may be essential for animal growth and development. Whereas the role of boron in the life cycle of plants is well documented, nothing is known about boron homeostasis and function in animal cells. NaBC1, the mammalian homolog of AtBor1, is a borate transporter. In the absence of borate, NaBC1 conducts Na+ and OH- (H+), while in the presence of borate, NaBC1 functions as an electrogenic, voltage-regulated, Na+-coupled B(OH)4 - transporter. At low concentrations, borate activated the MAPK pathway to stimulate cell growth and proliferation, and at high concentrations, it was toxic. Accordingly, overexpression of NaBC1 shifted both effects of borate to the left, ...
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InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
V deln kolon da byla postavena v dob od 1. jna 1878 do 27. dubna 1879 na m st star d ev n kolon dy podle projektu v de sk ch architekt Ferdinanda Fellnera a Hermanna Gottlieba Helmera. Proto e litinov d ly byly spojov ny ocelov mi prvky, do lo k naru en stability a na ja e roku 1939 bylo p ikro eno k jej demolici. V roce 1946 byla postavena dal konstrukce od architekta Ladislava Koz ka, kter vydr ela tvrt stolet , ve fotogalerii je uvedena jako prozat mn kolon da. V roce 1975 byla otev ena nov V deln kolon da, d lo architekta J. Otruby. ...
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购买SLC35D1兔多克隆抗体(ab106523),SLC35D1抗体经WB验证,可与人,小鼠,大鼠样本反应。产品出库一年都在质保范围内。中国现货速达。
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SLC39A11兔多克隆抗体(ab83950)可与小鼠, 大鼠, 人样本反应并经WB, ELISA, IHC实验严格验证。所有产品均提供质保服务,中国75%以上现货。