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T Fujiwara

Publications and source records attributed to T Fujiwara.

At least 415 records · Page 23Linked to original sources

The 2.8 A structure of hydroxylamine oxidoreductase from a nitrifying chemoautotrophic bacterium, Nitrosomonas europaea.

The 2.8 A crystal structure of hydroxylamine oxidoreductase of a nitrifying chemoautotrophic bacterium, Nitrosomonas europaea, is described. Twenty-four haems lie in the centre bottom of the trimeric molecule, localized in four clusters within each monomer. The haem clusters within the trimer are aligned to form a ring that has inlet and outlet sites. The inlet is occupied by a novel haem, P460, and there are two possible outlet sites per monomer formed by paired haems lying within a cavity or cleft on the protein surface. The structure suggests pathways by which electron transfer may occur through the precisely arranged haems and provides a framework for the interpretation of previous and future biochemical and genetic observations.

Amino Acid Sequence↗

The identification of an orally active, nonpeptide bradykinin B2 receptor antagonist, FR173657.

1. An orally active, nonpeptide bradykinin (BK) B2 receptor antagonist, FR173657 (E)-3-(6-acetamido-3-pyridyl)-N-[N-[2-4-dichloro-3-[(2-methyl-8-quinolin yl) oxymethyl]phenyl]-N-methylaminocarbonyl-methyl] acrylamide) has been identified. 2. This compound displaced [3H]-BK binding to B2 receptors present in guinea-pig ileum membranes with an IC50 of 5.6 x 10(-10) M and in rat uterus with an IC50 of 1.5 x 10(-9) M. It did not inhibit different specific radio-ligand binding to other receptor sites. 3. In human lung fibroblast IMR-90 cells, FR173657 displaced [3H]-BK binding to B2 receptors with an IC50 of 2.9 x 10(-9) M and a Ki of 3.6 x 10(-10) M, but did not reduce [3H]-des]Arg10-kallidin binding to B1 receptors. 4. In guinea-pig isolated preparations, FR173657 antagonized BK-induced contractions with an IC50 of 7.9 x 10(-9) M, but did not antagonize acetylcholine or histamine-induced contractions even at a concentration of 10(-6) M. FR173657 caused parallel rightward shifts of the concentration-response curves to BK at concentrations of 10(-9) M and 3.2 x 10(-9) M, and a little depression of the maximal response in addition to the parallel rightward shift of the concentration-response curve at a concentration of 10(-8) M. Analysis of the data yield a pA2 of 9.2 +/- 0.2 (n = 5) and a slope of 1.5 +/- 0.2 (n = 5). 5. In vivo, the oral administration of FR173657 inhibited BK-induced bronchoconstriction dose-dependently in guinea-pigs with an ED50 of 0.075 mg kg-1, but did not inhibit histamine-induced bronchoconstriction even at 1 mg kg-1. FR173657 also inhibited carrageenin-induced paw oedema with an ED50 of 6.8 mg kg-1 2 h after the carrageenin injection in rats. 6. These results show that FR173657 is a potent, selective, and orally active bradykinin B2 receptor antagonist.

Administration, Oral↗

Effects of a nonpeptide bradykinin B2 receptor antagonist, FR167344, on different in vivo animal models of inflammation.

1. The effects of a novel, potent and orally active nonpeptide bradykinin B2 receptor antagonist, FR167344 (N-[N-[3-[(3-bromo-2-methylimidazo[1,2-a]pyridin-8-yl)oxymethyl]-2 ,4-dichlorophenyl]-N-methylaminocarbonylmethyl]-4-(dimethylamin ocarbonyl) cinnamylamide hydrochloride) were tested in three different in vivo models of inflammation. 2. Oral administration of FR167344 inhibited carrageenin-induced paw oedema in rats (carrageenin: 1%, 0.1 ml per animal, intraplantar), with an ID50 of 2.7 mg kg(-1) at 2 h after carrageenin injection (n=10 or 11). 3. Oral administration of the compound also inhibited kaolin-induced writhing (kaolin: 250 mg kg(-1), i.p.) in mice, with ID50 of 2.8 mg kg(-1) in 10 min writhing and 4.2 mg kg(-1) in 15 min writhing (n=19 or 20). 4. Additionally, oral administration of FR167344 inhibited caerulein-induced pancreatic oedema with an ID50 of 13.8 mg kg(-1) as well as increases in amylase and lipase of blood samples with ID50 of 10.3 and 7.4 mg kg(-1), respectively, in rats (n=10). 5. These results show that FR167344 is an orally active, anti-inflammatory and anti-nociceptive agent in carrageenin-induced paw oedema, kaolin-induced writhing and caerulein-induced pancreatitis. FR167344 may have therapeutic potential against inflammatory diseases by oral administration and it may be a useful tool for studying the involvement of B2 receptors in various in vivo models of inflammation.

Administration, Oral↗

Children's smoking habits in an agricultural community in Japan and the importance of a no smoking program integrating family, school and community health.

The object of this study is to establish a model of integration of the health promotion projects which have been planned separately by schools and communities so far in an agricultural area in Japan, to solve the problem of children's smoking. The subjects of the study were 10-15 y old schoolchildren and their parents. The questionnaires were completed by the children themselves at school and also by their parents at home, in July 1995. One fourth of the junior high school boys had ever tried smoking, while most of their parents did not notice that their children were smoking. More than half of the children who had ever tried smoking mainly acquired tobacco from their homes. One tenth of them were prompted to smoke by their fathers or other relatives. To develop a health promotion project for children which includes prevention of smoking, the provision of a health education program and an environment which encourages health are important for children. The project should also be community-based because participation of local inhabitants in the project gives it additional impetus. In order to promote the comprehensive health of children, we emphasize the importance of setting up a healthy district plan based on the health policy of the general community.

Adolescent↗

Effect of immunoglobulin therapy on phagocytosis by polymorphonuclear leucocytes in whole blood of neonates.

There has been some disagreement as to the clinical effect of intravenous immunoglobulin (IVIG) therapy on neonatal bacterial infections. We therefore evaluated the effect of IVIG therapy on neonatal polymorphonuclear leucocyte (PMN) functions by monitoring phagocytosis and hydrogen peroxide (H2O2) production. Subjects were 10 mature neonates who had normal plasma levels (i.e. equal to adult plasma levels) of IgG and nine premature neonates who had lower plasma levels of IgG. Phagocytosis by PMN was measured using flow cytometric analysis of whole blood. Addition of gamma-globulin to the whole blood of mature neonates increased phagocytosis, but not significantly. Higher doses of added gamma-globulin (> 2.0 mg/ml, the concentration was expressed as that in the final reaction volume) decreased phagocytosis to under baseline level. In premature neonates addition of gamma-globulin increased phagocytosis and the significant maximum effect was observed with 0.5 mg/ml of the additional gamma-globulin. Higher doses of additional gamma-globulin (2.5 mg/ml) decreased phagocytosis to baseline level. Phagocytosis in four mature and four premature neonates was compared before and after 1 g/kg of IVIG therapy. Phagocytosis in mature neonates after IVIG therapy did not change compared with the pretreatment level. On the other hand, phagocytosis in premature neonates after IVIG therapy significantly increased compared with its pretreatment level. In both mature and premature neonates H2O2 production following phagocytosis varied in parallel with changes of phagocytosis. The patterns of H2O2 production following phagocytosis were essentially similar to those observed with phagocytosis. The above results are expected to form the basis for a rational indication for IVIG therapy against bacterial infections in neonates with low plasma IgG levels.

Cells, Cultured↗

Molecular properties of the proteasome activator PA28 family proteins and gamma-interferon regulation.

BACKGROUND: Recent cDNA cloning of two homologous proteasome activators, PA28 alpha and PA28 beta, indicated the presence of a structurally related third protein, Ki antigen, but a functional relationship between Ki antigen and the two PA28 proteins is unknown. Accumulating evidence has implicated an important role for PA28 in the major histocompatibility complex (MHC) class I-restricted antigen processing pathway. Recently, an immunomodulatory cytokine gamma-interferon (gamma-IFN) was found to increase greatly the messages for PA28 alpha and PA28 beta, but not Ki antigen, in human cells. RESULTS: Ki antigen was co-immunoprecipitated with the 20S proteasome by anti-proteasome antibody, and associated reversibly with the 20S proteasome, as observed for PA28 alpha and PA28 beta. Therefore, Ki antigen was renamed PA28 gamma. Anti-PA28 gamma antibody, however, did not immunoprecipitate PA28 alpha and PA28 beta. gamma-IFN caused an almost complete loss of the PA28 gamma protein in cells without affecting its mRNA level, whereas the levels of both mRNA and protein for PA28 alpha and PA28 beta were coordinately upregulated by gamma-IFN. Finally we showed that the human chromosomal genes of PA28 alpha and PA28 gamma were located on 14q11.2 and 17q21.32-21.33, respectively. CONCLUSION: PA28 gamma (equivalent to Ki antigen) is a new member of the PA28 family proteins. It exists as a unique homopolymer under non-denaturing conditions. gamma-IFN was found to induce the expression of PA28 alpha and PA28 beta, whereas it caused almost complete loss of the PA28 gamma protein in cells. The reciprocal expression of the PA28 family proteins may imply their involvement in distinct biological processes.

Amino Acid Sequence↗

Ring chromosome 20 and nonconvulsive status epilepticus. A new epileptic syndrome.

Six cases of epilepsy associated with ring chromosome 20 are presented. The study of these cases and 20 cases reported in the literature revealed that they constitute a distinct epileptic syndrome: frequent seizures consisting of a prolonged confusional state, with or without additional motor seizures, and an ictal EEG pattern of long-lasting bilateral paroxysmal high-voltage slow waves with occasional spikes. Neurological examination results were normal, and neuroimaging studies often failed to disclose a brain lesion. The seizures were resistant to antiepileptic drug therapy. Comparison of the electroclinical features of nonconvulsive status epilepticus in six patients with and four patients without ring chromosome 20 revealed that the group with the chromosomal anomaly had more frequent, comparatively brief episodes of confusion associated with a less prominent spike component on the EEG. We propose that epilepsy associated with ring chromosome 20 constitutes a new syndrome that may provide an opportunity to scrutinize a genetic mechanism of epilepsy.

Adolescent↗

Infarct size-reducing effect of ischemic preconditioning is related to alpha1b-adrenoceptors but not to alpha1a-adrenoceptors in rabbits.

In rabbits and rats, both stimulation of alpha-adrenoceptors and ischemic preconditioning (PC) reduce infarct size. Activation of alpha1b-adrenoceptors play an important role in the PC effect on ventricular function in rats. However, the alpha1-adrenoceptors have not been reported to be related to the PC effect in rabbits, because the infarct size-reducing effect of PC is not blocked by the nonselective alpha-adrenoceptor antagonist, phenoxybenzamine (POB) or by the alpha1-adrenoceptor antagonist, BE2254. However, we speculated that alpha1b-adrenoceptors but not alpha1a-adrenoceptors may be related to the infarct size-reducing effect of PC in rabbit hearts. Thus we examined in rabbits whether the alpha1b-adrenoceptor blocker chloroethylclonidine (CEC), the alpha1a-adrenoceptor blocker 5-methylurapidil (5-MU), the selective alpha1-adrenoceptor antagonist bunazosin (BN), and the nonselective apha-adrenoceptor antagonist phenoxybenzamine (POB) can block the PC effect on infarct size. Eighty-eight anesthetized open-chest Japanese white male rabbits were subjected to 30-min coronary occlusion and 48-h reperfusion. In five PC groups, the rabbits were subjected to a single 5-min occlusion and 5-min reperfusion before 30-min sustained ischemia. In the PC groups, those with CEC (3 mg/kg, n = 10), 5-MU (3 mg/kg, n = 10), BN (0.3 mg/kg, n = 10), POB (4 mg/kg, n = 10), or placebo saline (n = 10) were pretreated before PC. In the non-PC groups, those with CEC (3 mg/kg, n = 7), 5-MU (3 mg/kg, n = 7), BN (0.3 mg/kg, n = 7), POB (4 mg/kg, n = 7), or placebo saline (n = 10) were pretreated before 30-min sustained ischemia. After a 48-h reperfusion, the infarct size was measured histologically and expressed as a percentage of the area at risk. PC caused a marked reduction of infarct size as compared with the non-PC control (10 +/- 3% vs. 42 +/- 2%; p < 0.05). The PC effect was completely blocked by CEC (36 +/- 2%) and by BN (42 +/- 4%) but not by 5-MU (14 +/- 1%) or POB (13 +/- 2%). None of the drugs by itself affected the infarct size. Stimulation of alpha1b-adrenoceptors but not of alpha1a-adrenoceptors during PC plays an important role in the PC effect on infarct size. This may explain the previous confusion concerning the PC blocking effect of various alpha1-blockers.

Adrenergic alpha-Antagonists↗

bor1-1, an Arabidopsis thaliana mutant that requires a high level of boron.

bor1-1 (high boron requiring), an Arabidopsis thaliana mutant that requires a high level of B, was isolated. When the B concentration in the medium was reduced to 3 microM, the expansion of rosette leaves was severely affected in bor1-1 but not in wild-type plants. In a medium containing 30 microM B the mutant grew normally but showed female sterility, whereas the wild type was able to set seeds. These defects of the bor1-1 mutant were not detected with supplementation of 100 microM B. In vivo concentrations of B in bor1-1 mutants were lower than those of the wild type, especially in the inflorescence stems. Tracer experiments using 10B suggested that the mutant has defects in uptake and/or translocation of B. The mutation was mapped on the lower arm of chromosome 2.

Arabidopsis↗

Epilepsia partialis continua of childhood involving bilateral brain hemispheres.

OBJECTIVES: Epilepsia partialis continua (Kojewnikow's syndrome) can be classified into 2 groups. The 1st group had stable neurological deficit, and the 2nd group had slowly progressive neurological deficit. The latter usually manifests not tetraplegia, but hemiplegia. We describe 3 patients with epilepsia partialis continua, rapid neurological and mental deterioration, resulting in tetraplegia and serious mental deficits within 2 to 3 years from the onset. RESULTS: Their interictal EEGs showed progressive findings of deterioration, which resulted in an inactive pattern or a pattern reminiscent of suppression-burst within several years. Their cranial CTs revealed rapid progressive atrophy of both hemispheres. Various screening tests failed to confirm a metabolic disease, a degenerative disease, or an infectious disease in the central nervous system. CONCLUSION: Frequent status epilepticus might contribute to the bilateral brain involvement and the serious neurological and mental outcomes in young patients with epileptia partialis continua.

Age of Onset↗

X-ray microanalysis and phagocytotic activity of cultured retinal pigment epithelial cells in hypoxia.

PURPOSE: To investigate the influence of the functional and morphological changes induced in retinal pigment epithelial (RPE) cells by retinal ischemia, we evaluated the phagocytotic activity, the concentration of various elements, and ultrastructure in cultured RPE cells in hypoxia. METHODS: The concentrations of oxygen in incubators were adjusted to 20, 10, and 1% by the addition of nitrogen for 72 hr. To observe phagocytotic activity and its relationship to actin filaments, the filaments of RPE cells incubated with fluoresbrite carboxylate YG microspheres were stained with rhodamine phalloidin. Some of the specimens were subjected to X-ray microanalysis by scanning electron microscope after being fixed, freeze-dried, and coated with carbon to investigate the cytoplasmic concentration of elements. A part of the latter specimens was also observed by transmission electron microscope after being embedded in epon and cut into ultrathin sections to see the ultrastructural changes inside cell. RESULTS: Lowering oxygen concentrations from 20% to 1% swelled RPE cells and decreased the number of fluoresbrite carboxylate YG microspheres phagocytized by RPE cells. Phagocytosis of a large amount of latex beads (30 microl) for 24 hr in 1% oxygen caused a disruption of RPE cells. Na, S, and P were detected in RPE cells cultured in 20% oxygen. Reducing the oxygen concentration from 20 to 10 or 1% significantly decreased Na and increased S. Mitochondria were observed in RPE cells in 20 and 10% oxygen, but many vacuoles were observed in the cytoplasm in 1% oxygen. CONCLUSION: Hypoxia as low as 1% oxygen induced malfunction of phagocytosis and the fragility of RPE cells. We could speculate the imbalance of the electrolytes such as Na or a decrease of antioxidants such as glutathione containing S as a reason of disturbance of cell viability.

Actins↗

Cloning and characterization of the fmt gene which affects the methicillin resistance level and autolysis in the presence of triton X-100 in methicillin-resistant Staphylococcus aureus.

In methicillin-resistant Staphylococcus aureus (MRSA) strains, Triton X-100 reduced the oxacillin resistance level, although the degree of reduction varied from strain to strain. To study the responses of MRSA strains to Triton X-100, we isolated a Tn551 insertion mutant of the COL strain that became more susceptible to oxacillin in the presence of 0.02% Triton X-100. The Tn551 insertion of the mutant was transduced back to the parent strain, other MRSA strains (strains KSA8 and NCTC 10443), and methicillin-susceptible strain RN450. All transductants of MRSA strains had reduced levels of resistance to oxacillin in the presence of 0.02% Triton X-100, while those of RN450 did not. Tn551 mutants of KSA8 and NCTC 10443 also had reduced levels of resistance in the absence of 0.02% Triton X-100. The autolysis rates of the transductants in the presence of 0.02% Triton X-100 were significantly increased. Amino acid analysis of peptidoglycan and testing of heat-inactivated cells for their susceptibilities to several bacteriolytic enzymes showed that there were no significant differences between the parents and the respective Tn551 mutants. The Tn551 insertion site mapped at a location different from the previously identified fem and llm sites. Cloning and sequencing showed that Tn551 had inserted at the C-terminal region of a novel gene designated fmt. The putative Fmt protein showed a hydropathy pattern similar to that of S. aureus penicillin-binding proteins and contained two of the three conserved motifs shared by penicillin-binding proteins and beta-lactamases, suggesting that fmt may be involved in cell wall synthesis.

Bacteriolysis↗

Preparation of a monoclonal antibody specific for Entamoeba dispar and its ability to distinguish E. dispar from E. histolytica.

A monoclonal antibody (MAb), MAb ED17 (immunoglobulin G2a [IgG2a]), prepared against trophozoites of Entamoeba dispar SAW1734RclAR cultured monoxenically with Crithidia fasciculata, reacted with 25 of 26 isolates of E. dispar by an indirect fluorescent-antibody test. In contrast, the MAb failed to react with any of 20 isolates of E. histolytica or other enteric protozoan parasites. Western blot (immunoblot) analysis showed that the molecular mass of the E. dispar antigen recognized by the MAb was 160 kDa under reduced conditions. Immunoelectron microscopy revealed that the antigen was mainly located on digested C. fasciculata, but not on undigested organisms. Double staining with a mixture of MAb ED17 and MAb 4G6 (an IgG1 MAb which reacts exclusively with E. histolytica), followed by incubation with a mixture of fluorescein isothiocyanate-labeled anti-mouse IgG2a and tetramethylrhodamine isothiocyanate-labeled anti-mouse IgG1 antibodies, simultaneously identified mixed populations of E. dispar and E. histolytica. This method may prove to be useful for the accurate identification of E. dispar and E. histolytica, even in mixed infections.

Animals↗

epr, which encodes glycylglycine endopeptidase resistance, is homologous to femAB and affects serine content of peptidoglycan cross bridges in Staphylococcus capitis and Staphylococcus aureus.

Staphylococcus capitis EPK1 produces a glycylglycine endopeptidase, ALE-1 (M. Sugai, T. Fujiwara, T. Akiyama, M. Ohara, H. Komatsuzawa, S. Inoue, and H. Suginaka, J. Bacteriol. 179:1193-1202, 1997), which hydrolyzes interpeptide pentaglycine chains of cell wall peptidoglycan of S. aureus. Characterizations of the enzyme activity and cloning of ale-1 revealed that ALE-1 is very similar to prolysostaphin produced by S. simulans bv. staphylolyticus. Strain EPK1 is resistant to lysis by ALE-1 and by lysostaphin. A gene that renders the cells resistant to glycylglycine endopeptidase (epr) was found 322 bp upstream of and in the opposite orientation to ale-1. The deduced amino acid sequence of epr showed similarities to FemA and FemB, which have been characterized as factors essential for methicillin resistance of S. aureus. Inactivation of either femA or femB causes decreased resistance to methicillin, increased resistance to lysostaphin, and decreased glycine content in the interpeptide chains of peptidoglycan. Therefore, femAB is suggested to be involved in the addition of glycine to pentapeptide peptidoglycan precursor. S. aureus with epr on a multicopy plasmid had phenotypes similar to those of femAB mutants except that it did not alter resistance level to methicillin. These results suggest that epr and femAB belong to the protein family involved in adding amino acids to the pentapeptide peptidoglycan precursor and that epr is involved in the addition of serine to the pentapeptide.

Acetylglucosaminidase↗

Purification and molecular characterization of glycylglycine endopeptidase produced by Staphylococcus capitis EPK1.

A novel staphylolytic enzyme, ALE-1, acting on Staphylococcus aureus, was purified from a Staphylococcus capitis EPK1 culture supernatant. The optimal pH range for staphylolytic activity was 7 to 9. ALE-1 contains one Zn2+ atom per molecule. Analysis of peptidoglycan fragments released by ALE-1 indicated that the enzyme is a glycylglycine endopeptidase. The effects of various modulators were determined, and we found that o-phenanthroline, iodoacetic acid, diethylpyrocarbonate, and Cu2+ reduced the staphylolytic activity of ALE-1. beta-Casein, elastin, and pentaglycine were poor substrates for ALE-1. Molecular cloning data revealed that ALE-1 is composed of 362 amino acid residues and is synthesized as a precursor protein which is cleaved after Ala at position 35, thus producing a mature ALE-1 of 35.6 kDa. The primary structure of mature ALE-1 is very similar to the proenzyme form of lysostaphin. It has the modular design of an N-terminal domain of tandem repeats of a 13-amino-acid sequence fused to the active site containing C-terminal domain. Unlike lysostaphin, ALE-1 does not undergo processing of the N-terminal repeat domain in broth culture. ale-1 is encoded on the plasmid. Protein homology search suggested that ALE-1 and lysostaphin are members of the novel Zn2+ protease family with a homologous 38-amino-acid-long motif, Tyr-X-His-X(11)-Val-X(12/20)-Gly-X(5-6)-His.

Amino Acid Sequence↗

Endothelial gaps: time course of formation and closure in inflamed venules of rats.

In the rat trachea, substance P causes rapid but transient plasma leakage. We sought to determine how closely the number, morphology, and size of endothelial gaps correspond to the time course of this leakage. Endothelial gaps were examined by scanning electron microscopy (EM), by transmission EM, or by light microscopy after silver nitrate staining. Substance P-induced leakage of the particulate tracer Monastral blue peaked at 1 min but decreased with a half-life of 0.3 min. The number of silver-stained gaps also peaked at 1 min then decreased significantly more slowly (half-life 1.9 min) than the leakage. Scanning EM revealed two types of endothelial gaps, designated vertical gaps and oblique slits. Vertical gaps predominated at peak leakage, whereas oblique slits became more common as the leakage diminished. Measurements of the mean diameter of vertical gaps made by light microscopy, scanning EM, and transmission EM were all in the range of 0.36-0.47 micron. Fingerlike endothelial cell processes that appeared during gap formation became shorter as the leakage diminished (mean length: 1.44 microns at 1 min compared with 1.06 microns at 3 min after substance P), suggesting a role in gap closure. We conclude that the plasma leakage occurring immediately after an inflammatory stimulus results from the rapid formation of endothelial gaps. Multiple factors, including alterations in gap morphology, gap closure, and changes in driving force, are likely to participate in the rapid decrease in the leakage.

Animals↗

Isolation and mapping of karyopherin alpha 3 (KPNA3), a human gene that is highly homologous to genes encoding Xenopus importin, yeast SRP1 and human RCH1.

From a human fetal-brain cDNA library, we isolated and characterized a novel gene (KPNA3) encoding a protein highly homologous to certain nuclear transport proteins of Xenopus and human. The complete cDNA clone, designated karyopherin alpha 3, contained an open reading frame of 1,563 nucleotides encoding 521 amino acids. The predicted amino acid sequence showed 48%, 45% and 48% identity with Xenopus importin, yeast SRP1 and human RCH1, respectively. The similarities among these proteins suggest that karyopherin alpha 3 may be involved in the nuclear transport system. Eight repeats of the arm motif were well conserved among these proteins. The N-terminal region of the predicted karyopherin alpha 3 product was highly basic and the C-terminal region was strongly acidic. A 4.3-kb transcript was expressed in all adult human tissues examined by Northern blotting. The cDNA clone was assigned to chromosome band 13q14.3 by fluorescence in situ hybridization.

Amino Acid Sequence↗

Cloning and chromosome assignment to 1q32 of a human cDNA (RAB7L1) encoding a small GTP-binding protein, a member of the RAS superfamily.

A full-length cDNA homologous to RAB7, a member of the RAB-related GTP-binding protein subfamily, was isolated from a human placenta cDNA library. This cDNA, designated RAB7L1, has an open reading frame of 609 nucleotides encoding 203 amino acids. Northern analysis showed that the mRNA is ubiquitously expressed in human tissues, although signal intensities were different among the various organs examined. This gene was located on chromosome band 1q32 by fluorescence in situ hybridization.

Amino Acid Sequence↗