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Biomedical subjects

M Yamauchi

Publications and source records attributed to M Yamauchi.

At least 163 records · Page 9Linked to original sources
PubMed1996

Fusion between Jurkat cell and PEO-lipid modified liposome.

Direct fusion between Jurkat cell and a liposome modified with poly(ethylene oxide)-bearing lipid (PEO-lipid) was examined using diphtheria toxin fragment A (DTA) as the probe. Only the DTA-loaded liposome modified with PEO-lipid(n = 32) (n is the number of ethylene oxide units) exerted significant cytotoxicity against Jurkat cells, while liposomes lacking either the PEO-lipid or DTA did not. Liposomes modified by the PEO-lipid with shorter PEO chain(n = 5 or 15) did not show any cytotoxicity, irrespective of their DTA-loading. The cytotoxicity was observed even in the presence of cytochalasin B, an inhibitor of endocytosis. Judging from these results, we concluded that the PEO-lipid(n = 32)-modified liposome directly fused with plasma membrane of Jurkat cell.

Cell Survival↗
PubMed1996

Heterogeneous structure of the polyubiquitin gene UbC of HeLa S3 cells.

The nucleotide sequence of the polyubiquitin gene UbC of HeLa S3 cells and its upstream region was determined and characterized. Recognition sequences for the transcription factors HSF, NF kappa B, AP-1(c-jun), NF-IL6 and Sp1 were found in the upstream control region, a result consistent with the observation of a distinct regulatory response for the UbC gene compared with that of another polyubiquitin gene UbB. Employing a PCR procedure to amplify the entire coding region from genomic DNA, we found a heterogeneity in the repeat number (eight and nine repeats) of the ubiquitin coding units, which resulted from an apparent deletion of either the seventh or the eighth unit in the predominant nine-ubiquitin-unit coding gene. In addition, by comparison with the nucleotide sequence of the UbC gene of human leukocytes previously determined, we found a significant number of nucleotide discrepancies. However, these discrepancies could be substantially reduced by realigning the units so that the first and second ubiquitin units of the sequence determined here are translocated to the boundary between the eighth and the ninth units.

Base Sequence↗
PubMed1996

Identification of a vitamin D3-response element that overlaps a unique inverted TATA box in the rat bone sialoprotein gene.

Bone sialoprotein (BSP), an early marker of osteoblast differentiation, has been implicated in the nucleation of hydroxyapatite during bone formation de novo. Our studies, using the osteoblastic cell line ROS 17/2.8, have revealed that rat BSP gene expression is suppressed by 1,25-dihydroxyvitamin D3[1,25(OH)2D3], which is a powerful regulator of bone formation and resorption. To determine the molecular basis of the transcriptional suppression of BSP gene transcription by 1,25(OH)2D3, we have conducted transient transfection analyses with chimaeric constructs of the rat BSP gene promoter linked to a luciferase reporter gene. 1,25(OH)2D3 suppressed expression in all constructs, including a short construct (pLUC 3; nt -116 to +60) that contained a putative vitamin D3-response element (VDRE; AGGGTTTATAGGTCA; nt -28 to -14) that overlaps a unique inverted TATA (TTTATA) box. Mobility shift assays demonstrated strong binding of recombinant human vitamin D3 receptor protein (hVDR) to the VDRE. Point mutations introduced into each half-site and analysed for 1,25(OH)2D3-mediated suppression of transcription and for hVDR binding either decreased or increased both transcriptional suppression and binding. In comparison with activating VDREs, the rat BSP VDRE bound VDR-VDR homodimers more avidly than VDR-RXR alpha heterodimers (where RXR is retinoid X receptor). These studies have therefore identified a novel 1,25(OH)2D3 suppressor element that overlaps the inverted TATA box in the rat BSP gene and indicate that transcriptional suppression of the rat BSP gene by 1,25(OH)2D3 might involve competition between the VDR and the TATA binding protein (TBP).

Animals↗
PubMed1996

Decreased cytochrome c oxidase activity but unchanged superoxide dismutase and glutathione peroxidase activities in the spinal cords of patients with amyotrophic lateral sclerosis.

The cause of selective degeneration of motor neurons in the ventral horn of the spinal cord associated with amyotrophic lateral sclerosis (ALS) has still not been elucidated. Recently, so-called oxidative stress has been suggested to be a significant factor in the pathogenesis of this disease. We measured the antioxidant actions of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and cytochrome c oxidase (CO) of the human spinal cord in patients with ALS in comparison with those in control patients. Total SOD activity in spinal cord transections from patients with sporadic ALS was not significantly different from the controls in ventral, lateral, or dorsal regions, although enzymic activity was relatively higher in the ventral compared with the dorsal region. GSH-Px activity in the spinal cord of ALS patients was not very different from that in the control tissue. In contrast, CO activity was significantly reduced in all three regions of the spinal cord in patients with ALS, although the reduction was more marked in the ventral region. These results suggest that reactive oxygen species may attack the mitochondrial respiratory chain, leading eventually to the degeneration of vulnerable motor neurons in the spinal cord, even though no obvious changes in the activity of antioxidant enzymes are detectable.

Adult↗
PubMed1996

Comparative genome mapping of the ataxia-telangiectasia region in mouse, rat, and Syrian hamster.

Chromosomal locations of the Atm (ataxia-telangiectasia (AT)-mutated) and Acat1 (mitochondrial acetoacetyl-CoA thiolase) genes in mouse, rat, and Syrian hamster were determined by direct R-banding FISH. Both genes were colocalized to the C-D band of mouse chromosome 9, the proximal end of q24.1 of rat chromosome 8, and qa4-qa5 of Syrian hamster chromosome 12. The regions in the mouse and rat were homologous to human chromosome 11q. Fine genetic linkage mapping of the mouse AT region was performed using the interspecific backcross mice. Atm, Acat1, and Npat, which is a new gene isolated from the AT region, and 12 flanking microsatellite DNA markers were examined. No recombinations were found among the Atm, Npat, Acat1, and D9Mit6 loci, and these loci were mapped 2.0 cM distal to D9Mit99 and 1.3 cM proximal to D9Mit102. Comparison of the linkage map of mouse chromosome 9 (MMU9) and that of human chromosome 11 (HSA11) indicates that there is a chromosomal rearrangement due to an inversion between Ets1 and Atm-Npat-Acat1 and that the inversion of MMU9 originated from the chromosomal breakage at the boundary between Gria4 and Atm-Npat-Acat1 on HSA11. This type of inversion appeared to be conserved in the three rodent species, mouse, rat, and Syrian hamster, using additional comparative mapping data with the Rck gene.

Acetyl-CoA C-Acetyltransferase↗
PubMed1996

P2u purinoceptor regulation of mucin secretion in SPOC1 cells, a goblet cell line from the airways.

The SPOC1 cell, a novel goblet cell line derived from rat trachea, was tested for its ability to exhibit regulated mucin secretion in response to purinergic (P2) agonists. High-molecular mass glycoconjugates (HMMGs) purified by CsCl-density-gradient centrifugation had a buoyant density of 1.45 g/ml. The purified HMMG material exhibited a single major band with an apparent molecular mass of greater than 1000 kDa in SDS/ polyacrylamide gels stained with silver or blotted and stained with soya-bean agglutinin. [3H]HMMG was resistant to proteoglycan-degrading enzymes, but was susceptible to neuraminidase. The HMMG was approx. 91% carbohydrate by weight, and the glycosides were O-linked. The HMMG amino acid composition was enriched in Ser and Thr (sum 27%). Thus SPOC1-cell HMMG possess the characteristics of mucin. Mucin secretion by SPOC1 cells, grown on permeable supports and perfused luminally, was stimulated by ATP, UTP and adenosine 5'-[gamma-thio]triphosphate (100 microM) 4-5-fold over a baseline of 4 ng/min. The three dose-effect relations were nearly identical (K0.5 approximately 4 microM). SPOC1 cells grown on plastic and rat tracheal epithelial primary cells responded similarly to ATP and/or UTP. SPOC1 cells failed to respond to other purinergic agonists, either luminally or serosally, and consequently seem to possess an apical membrane P2u purinoceptor. SPOC1-cell total RNA was probed for P2u purinoceptor mRNA. Using conserved primers for both reverse transcriptase and PCR, a single band of the predicted size was observed, which had a nucleotide base sequence identical with the rat P2u purinoceptor mRNA. Thus SPOC1 cells secrete mucin under the control of a P2u purinoceptor; they should prove useful in dissecting the associated cellular regulatory pathways.

Adenosine Triphosphate↗
PubMed1996

Cardioprotective effect of nicorandil in histidine-tryptophan-ketoglurate solution during the cold storage of isolated hearts.

We compared the efficacy of using histidine-tryptophan-ketoglurate (HTK) solution with that of University of Wisconsin (UW) solution for heart preservation in an isolated rat heart preparation. Nicorandil (NCR) exerts its action as an ATP-sensitive potassium channel opener at low extracellular potassium concentrations, and HTK solution has a low potassium concentration. Therefore, we also investigated the efficacy of using HTK solution with NCR following 12-hr preservation. Hearts isolated from male Wistar rats were mounted on a Langendorff apparatus to estimate baseline aortic flow (AF), coronary flow (CF), cardiac out-put (CO), heart rate (HR), systolic pressure (SP), aortic mean pressure, and the rate-pressure product (RPP). The hearts were divided into four groups: group 1, 8-hr storage in UW solution; groups 2 and 3, 8- or 12-hr storage in HTK solution, respectively; and group 4, 12-hr storage in HTK solution with NCR. They were arrested and stored at 4 degrees C in each preservation solution. Following storage, they were reperfused and postpreservative function was measured to assess cardiac functional recovery. Concentrations of creatine phosphokinase, troponin-T, and lactate in the coronary perfusate were measured. Frozen tissue samples from groups 3 and 4 were analyzed for adenylate content and cGMP. The myocardial water content was also measured. The recovery of AF, CF, CO, SP, and RPP in group 2 was significantly improved compared with that in group 1 (P<0.05). The recovery of AF, CF, CO and HR in group 4 was significantly better than that in group 3 (P<0.05). Creatine phosphokinase leakage in group 2 and troponin-T leakage in group 4 were significantly reduced (P<0.05 vs. groups 1 and 3, respectively). Total adenine nucleotides and the adenylate energy charge in group 4 were well sustained (P<0.05 vs. group 3). These results suggest that HTK solution is more effective than UW solution for cardiac preservation, and that NCR provides still better protection.

Adenosine↗
PubMed1996

Cross-linking and the molecular packing of corneal collagen.

We have quantitatively characterized, for the first time, the cross-linking in bovine cornea collagen as a function of age. The major iminium reducible cross-links were dehydro-hydroxylysinonorleucine (deH-HLNL) and dehydro-histidinohydroxymerodesmosine (deH-HHMD). The former rapidly diminished after birth; however, the latter persisted in mature animals at a level of 0.3 - 0.4 moles/mole of collagen. A nonreducible cross-link, histidinohydroxylysinonorleucine (HHL), previously found only in skin, was also found to be a major mature cross-link in cornea. The presence of HHL indicates that cornea fibrils have a molecular packing similar to skin collagen. However, like deH-HHMD, the HHL content in corneal fibrils only reaches a maximum value with time about half that of skin. These data suggest that the corneal fibrils are comprised of discrete filaments that are internally stabilized by HHL and deH-HHMD cross-links. This pattern of intermolecular cross-linking would facilitate the special collagen swelling property required for corneal transparency.

Aging↗
PubMed1996

Hyaluronic acid is increased in the skin and urine in patients with amyotrophic lateral sclerosis.

We performed morphological studies of skin and measured glycosaminoglycans in the urine from patients with sporadic amyotrophic lateral sclerosis (ALS) and control subjects. The wide spaces separating collagen bundles reacted strongly with alcian blue stain in ALS patients and stained more markedly as ALS progressed. Staining with alcian blue was virtually eliminated by Streptomyces hyaluronidase. The urinary excretion of hyaluronic acid (HA) (mg/day) was significantly increased (P < 0.01) in ALS patients compared with that of control subjects, and there was a significant positive correlation between the excreted amount of HA and the duration of illness in advanced ALS patients with a duration of more than 2 years from clinical onset (r = 0.72, P < 0.02). We suggest that sporadic ALS includes a metabolic disorder of HA in which an accumulation of HA in the skin is linked to an increased urinary excretion of HA.

Adult↗
PubMed1996

Influence of continuous positive airway pressure on EMG activities of the cricothyroid and posterior cricoarytenoid muscles of the canine larynx.

OBJECTIVES: We investigated the effect of different levels of continuous positive airway pressure (CPAP) on the cricothyroid (CT; a tensor muscle of the vocal folds) and posterior cricoarytenoid (PCA; sole abductor muscle of the vocal folds) muscles in dogs. DESIGN: Prospective, controlled animal study. SUBJECTS: Nine mongrel dogs of both sexes. SETTING: University research laboratory. INTERVENTIONS: After insertion of a cuffed tracheotomy tube low in the neck the compound EMG responses of the CT and PCA muscles during spontaneous respiration were measured simultaneously under different levels (2, 4, 6, and 8 cmH2O) of positive end-expiratory pressure (PEEP). MEASUREMENTS AND RESULTS: The CT showed a progressive increase in phasic expiratory EMG activity with the application of graded levels of PEEP. Application of PEEP over 4 cmH2O produced significant increases in the phasic CT activity (P < 0.05). In contrast to the CT, the PCA failed to increase phasic inspiratory EMG activity statistically until a 8 cmH2O of PEEP was applied (P < 0.05). The phasic expiratory CT and inspiratory PCA activities were 297.9 +/- 77.6 and 124.5 +/- 22.9, respectively, at the application of 6 cmH2O of PEEP (percentage of control, mean +/- SD). CONCLUSION: This study confirms the difference in sensitivity between adductor and abductor laryngeal muscles, demonstrating that the intrinsic laryngeal muscles do not all behave similarly after the application of CPAP.

Analysis of Variance↗
PubMed1996

Differential effects of propofol, thiamylal and ketamine on the cricothyroid and posterior cricoarytenoid muscles of the canine larynx.

PURPOSE: To measure the electromyographic (EMG) responses of the phasic discharge in the cricothyroid (CT; a tensor muscle of the vocal folds) and the posterior cricoarytenoid (PCA; sole abductor muscle of the vocal folds) following intravenous infusion of propofol 1.0 mg.kg-1.min-1, thiamylal 1.0 mg.kg-1.min-1, or ketamine 0.5 mg.kg-1.min-1 for five minutes. DESIGN: Prospective, nonrandomized, controlled animal study. SETTING: University research laboratory. SUBJECTS: Fifteen mongrel dogs, including three groups of five animals in each group. INTERVENTIONS: Under 0.2-0.3% halothane and oxygen anesthesia with spontaneous ventilation, phasic EMG activities of the CT and PCA muscles were recorded in an identical manner after the administration of each drug. MEASUREMENTS AND MAIN RESULTS: Propofol infusion produced almost equal suppression of EMG activity of the CT and the PCA with time and three minutes after the start of infusion of propofol there was a significant depression of the phasic activities in the both muscles; EMG activity of the CT and the PCA was 33.8 +/- 21.2 and 36.6 +/- 22.9% (% of control, mean +/- SD) respectively P < 0.05). Thiamylal selectively reduced rhythmic discharges in the CT muscle during spontaneous breathing and significant depression of discharge in the CT muscle was observed three minutes after the drug (47.3 +/- 24.9%, P < 0.05). In contrast, both phasic EMG activities of the CT and the PCA were rhythmically active and the differential sensitivity between the CT and the PCA muscles was not observed after ketamine, even after ten minutes of administration. CONCLUSIONS: This study confirms a difference in sensitivity between the CT and the PCA muscles, demonstrating that the intrinsic laryngeal muscles do not behave similarly after the administration of conventional intravenous anaesthetic agents.

Anesthetics, Dissociative↗
PubMed1996

Inhibition of platelet aggregation by endocardial endothelial cells.

We assessed the anti-platelet properties of endocardial endothelial cells (EECs) by measuring platelet aggregation after brief interaction with EECs isolated from the right ventricles of porcine hearts. Platelet aggregation in response to thrombin was significantly inhibited by brief incubation of platelet suspensions over EEC monolayers. Pretreatment of EECs with indomethacin restored platelet reaction but that with L-NAME and hemoglobin (Hb) did not. The PGI2 content of platelet suspensions after interaction with cultured EECs was significantly correlated with the inhibition of platelet aggregation. These results suggest that EECs inhibit platelet aggregation by releasing PGI2.

Animals↗
PubMed1996

Induction of tissue transglutaminase in rat superior cervical sympathetic ganglia following in vitro stimulation of retinoic acid.

The addition of retinoic acid (RA, 50 nM) to Dulbecco's modifed Eagle's medium containing 1.0 percent bovine serum albumin and 50 mu g/l of gentamicin markedly increased the activity of a Ca(2+) -dependent tissue transglutaminase (TGase) (ca. 3.2-fold), which stabilizes newly formed protein assemblies at the sites of synapses, in isolated rat superior cervical sympathetic ganglia (SCG), which is abundant in synapses, following in vitro aerobic incubation for 3 h at 37 degrees C. An isomer of RA, 13-cis-RA (50 nM), showed the same tendency but rather lesser magnitude (ca. 1.7-fold) in ganglionic TGase activation. Also, retinal (50 nM), a precursor of RA, had a little effect on TGase stimulation (ca. 1.5-fold) in SCG. The RA-induced enhancement of ganglionic TGase activity was completely eliminated in the presence of either actinomycin D (1.0 mu g/ml), a depressant of molecular transcriptional activity, or a potent inhibitor of protein synthesis, cycloheximide (10 mu g/ml). Kinetic analyses show that the stimulation of ganglionic TGase activity evoked by RA addition was associated with only an increase in V max value (ca. 3.3-fold) without change in Km value. Thus, the enzyme protein of TGase might be synthesized de novo in the ganglia in response to RA. The RA-induced activation effect of ganglionic TGase almost disappeared (ca. 1.3-fold) 1 week following denervation, by which time preganglionic cholinergic nerve terminals were degradated. In axotomized SCG, where sympathetic neurons were degenerated and reactive proliferation of glial cells was in progress, the RA-evoked increase in ganglionic TGase activity was attenuated (ca. 1.3-fold). These findings imply that some retinoids, especially RA effectively participate in the cholinergic potentiation of synaptic activity.

Animals↗
PubMed1996

Pyridoxine deficiency affects biomechanical properties of chick tibial bone.

The mechanical integrity of bone is dependent on the bone matrix, which is believed to account for the plastic deformation of the tissue, and the mineral, which is believed to account for the elastic deformation. The validity of this model is shown in this study based on analysis of the bones of vitamin B6-deficient and vitamin B6-replete chick bones. In this model, when B6-deficient and control animals are compared, vitamin B6 deficiency has no effect on the mineral content or composition of cortical bone as measured by ash weight (63 +/- 6 vs. 58 +/- 3); mineral to matrix ratio of the FTIR spectra (4.2 +/- 0.6 vs. 4.5 +/- 0.2), line-broadening analyses of the X-ray diffraction 002 peak (beta 002 = 0.50 +/- 0.1 vs. 0.49 +/- 0.01), or other features of the infrared spectra. In contrast, collagen was significantly more extractable from vitamin B6-deficient chick bones (20 +/- 2% of total hydroxyproline extracted vs. 10 +/- 3% p < or = 0.001). The B6-deficient bones also contained an increased amount of the reducible cross-links DHLNL, dehydro-dihydroxylysinonorleucine, (1.03 +/- 0.07 vs. 0.84 +/- 0.13 p < or = 0.001); and a nonsignificant increase in HLNL, dehydro-hydroxylysinonorleucine, (0.51 +/- 0.03 vs. 0.43 +/- 0.03, p < or = 0.10). There were no significant changes in bone length, bone diameter, or area moment of inertia. In four-point bending, no significant changes in elastic modulus, stiffness, offset yield deflection, or fracture deflection were detected. However, fracture load in the B6-deficient animals was decreased from 203 +/- 35 MPa to 151 +/- 23 MPa, p < or = 0.01, and offset yield load was decreased from 165 +/- 9 MPa to 125 +/- 14 MPa, p < or = 0.05. Since earlier histomorphometric studies had demonstrated that the B6-deficient bones were osteopenic, these data suggest that although proper cortical bone mineralization occurred, the alterations of the collagen resulted in changes to bone mechanical performance.

Animals↗
PubMed1996

AP-1 regulation of the rat bone sialoprotein gene transcription is mediated through a TPA response element within a glucocorticoid response unit in the gene promoter.

Bone sialoprotein (BSP), a protein which has been implicated in the initial mineralization of newly-formed bone, provides an early phenotypic marker for differentiated osteoblasts. BSP expression is induced by glucocorticoids in association with osteoblast differentiation, and a glucocorticoid response element (GRE) overlapping a putative TRE (TPA, 12-O-tetradecanoyl-phorbol 13-acetate, response element) site has been identified in the rat BSP promoter (Ogata et al., 1995). Since AP-1 and the glucocorticoid receptor have a central role in regulating cell proliferation and differentiation, we have studied AP-1 activity, stimulated by 100 ng/ml TPA in normal fetal rat calvarial cells and in transformed rat osteosarcoma cells (ROS 17/2.8). A transient induction of both c-fos and c-jun mRNAs by TPA was observed in both cell populations, together with an associated suppression of BSP mRNA in the fetal rat calvarial cells. Rat BSP promoter constructs, transiently transfected into ROS 17/2.8 cells, were used to show that TPA suppressed transcription of a luciferase construct (-938/+60; pLUC6) that included the GRE/TRE, but not transcription of shorter contructs lacking this element. Notably, suppression of pLUC6 transcription by TPA was abrogated in the presence of the synthetic glucocorticoid, dexamethasone. Gel mobility shift analyses were performed using two double-stranded synthetic oligonucleotides. These encompassed the TRE and either the distal pair of GRE half-sites (-936/ -910; GRE3) or the proximal pair of GRE half-sites (-925/-899; GRE 4) that comprise the GRE/AP-1 element. The assay showed binding of both AP-1 complexes and recombinant c-Jun homodimers. Additionally, either the c-Jun or glucocorticoid receptor could displace its counterpart from the GRE/TRE but not from consensus GRE and TRE oligonucleotides, indicating that the abrogation of AP-1-mediated gene suppression by glucocorticoids could involve competitive binding. These studies, therefore, have identified a glucocorticoid response unit through which c-Fos and c-Jun can suppress the expression of BSP in proliferating pre-osteoblastic cells and through which glucocorticoids can ameliorate the effects of AP-1 and promote osteoblast differentiation and the associated expression of BSP.

Animals↗
PubMed1996

Potentiation of local lignocaine-induced sensory block by calcium channel blockers in rats.

We have studied the effects of three different types of calcium channel blockers (verapamil, diltiazem, and nicardipine) on local lignocaine sensory block. The standardized tail flick test was used to measure the duration and degree of lignocaine-induced conduction block in rats. After obtaining baseline tail flick latencies (mean 3.2 s), two 100-microliter doses of 0.3% lignocaine alone, a combination of verapamil 25, 100 or 200 micrograms, diltiazem 25, 100 or 200 micrograms, or nicardipine 0.5, 1.0 or 2.0 micrograms, and a large dose of calcium channel blockers (verapamil 200 micrograms, diltiazem 200 micrograms or nicardipine 2.0 micrograms) were injected on opposite sites of the tail base and the tail flick test was performed every 5 min for 45 min. A large dose of the calcium channel blockers showed no prolongation of tail flick latencies. Administration of 0.3% lignocaine alone produced a significant increase in tail flick thresholds and the peak effect of the percentage maximum possible effect (% MPE) was demonstrated at 5 min after drug injection (mean % MPE 28.8%; P < 0.01 vs baseline). Co-administration of 0.3% lignocaine and three doses of verapamil produced significant increases in area under the curve (AUC) in a dose-dependent fashion. Mean AUC values for 0.3% lignocaine alone and a combination of verapamil 25, 100 or 200 micrograms were 217.5, 502.5, 529.1 and 1600.3, respectively. Almost similar patterns of augmentation in AUC values were demonstrated after addition of different doses of diltiazem or nicardipine to 0.3% lignocaine. We conclude that the use of mixtures of local anaesthetic and calcium channel blocker potentiated lignocaine sensory block at the level of the peripheral nerves.

Anesthetics, Local↗
PubMed1996

Human UDP-galactose translocator: molecular cloning of a complementary DNA that complements the genetic defect of a mutant cell line deficient in UDP-galactose translocator.

We have cloned a cDNA that codes for a putative human UDP-galactose translocator (UGT) protein. The cDNA contained an open reading frame of 1,179 base pairs encoding a novel protein of 393 amino acids. Introduction of the open reading frame sequence into a UGT-deficient mouse cell line, Had-1, complemented the genetic defect of the mutant, namely the inability to transport UDP-galactose from the cytosol to the Golgi lumen, as judged from the lectin-sensitivity spectrum of the transformant. To our knowledge, this is the first mammalian nucleotide-sugar translocator whose cDNA sequence has been described.

Amino Acid Sequence↗