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Biomedical subjects

K Arai

Publications and source records attributed to K Arai.

At least 325 records · Page 18Linked to original sources
PubMed1996

Determination of synephrine enantiomers in food and conjugated synephrine in urine by high-performance liquid chromatography with electrochemical detection.

Determination of synephrine enantiomers was made with HPLC with electrochemical detection using a chiral ligand-exchange column (Sumichiral OA-6000). The calibration curve for each enantiomer showed good linearity (r = 0.999) at 1.0-500 pmol injected with a detection limit of 1.0 pmol (signal-to-noise ratio (S/N) = 3). Relative standard deviation (RSD) was 1.8% at 50 pmol d-synephrine and 1.6% at 50 pmol l-synephrine. The contents of synephrine enantiomer in food such as Citrus unshiu fruit, orange juice, and marmalade were determined. The present method was also used to determine conjugated synephrine enantiomers in urine following the ingestion of C. unshiu pulp. l-Synephrine in fruit was converted to the conjugated form of synephrine, and l-synephrine underwent chiral inversion to d-synephrine in vivo.

Adult↗
PubMed1996

DnaA- and PriA-dependent primosomes: two distinct replication complexes for replication of Escherichia coli chromosome.

Enzymatic analyses of primosome assembly at chromosomal and plasmid origins as well as that at single-stranded replication origins revealed the presence of two distinct primosomes in Escherichia coli for primer RNA synthesis and duplex unwinding. A DnaA-dependent primosome is assembled at oriC, the chromosomal origin of Escherichia coli, as well as at the A site, a single-stranded DNA hairpin containing a dnaA box sequence within its stem. In contrast, PriA protein recognizes a hairpin, called n'-pas (primosome assembly site), and initiates assembly of the phiX174-type PriA-dependent primosome in conjunction with other prepriming proteins. Genetic analyses of the prepriming proteins required specifically for the latter primosome strongly suggested that it is responsible for RecA-dependent, DnaA/oriC-independent replication of the Escherichia coli chromosome. Furthermore, primosome assembly in replication of various plasmids may also be classified into either DnaA-dependent or PriA-dependent type. We propose that Escherichia coli possesses two distinct, mutually exclusive primosomes which are differentially utilized by the chromosome as well as by the plasmids. PriA protein appears to be conserved in a wide range of prokaryotic species, and we will also discuss possible biological function of the PriA-dependent primosome in the process of responses to DNA damages.

Bacterial Proteins↗
PubMed1996

Abundant expression of erythroid transcription factor P45 NF-E2 mRNA in human peripheral granurocytes.

Transcription factor NF-E2 is crucial for regulation of erythroid-specific gene expression. p45 subunit of NF-E2 contains a basic-leucine zipper domain and dimerizes with the small Maf family protein to form functional NF-E2 complex. While p45 expression was shown to be restricted to erythroid cells, megakaryocytes and mast cells in hematopoietic lineage, we found in this study that p45 mRNA is abundantly transcribed in the granulocyte fraction of human peripheral blood cells. As neutrophils occupy approximately 92% of the cells in granulocyte fraction of human peripheral blood cells. As neutrophils occupy approximately 92% of the cells in this fraction, the cells expressing p45 is most likely to be neutrophils. p45 mRNA is also expressed in HL-60 promyelocytes, albeit the expression level is much lower than that of the granulocyte fraction. HL-60 cells were found to express mafK mRNA, indicating the presence of genuine NF-E2 complex in the cells. Although p45 mRNA is transcribed from two different promoters, aNF-E2 promoter and fNF-E2 promoter, in erythroid and megakaryocytic lineage cells, p45 mRNA is transcribed only from aNF-E2 promoter. The expression of p45 megakaryocytic lineage cells, p45 mRNA is transcribed only from aNF-E2 promoter. The expression of p45 mRNA in the neutrophils declined rapidly after transfer of the cells to in vitro culture and G-CSF could not sustain the expression from the down-regulation, suggesting the E2 may also participate in the regulation of neutrophil-specific gene expression.

Alternative Splicing↗
PubMed1996

Signal transduction in Th clones: target of differential modulation by PGE2 may reside downstream of the PKC-dependent pathway.

Lymphokines produced by non-transformed Th clones, Th1 and Th2, were classified into three groups based on their patterns of expression by different stimuli: Group I, GM-CSF and IL-2, characterized by a strict requirement of activation of both the PKC- and calcium-dependent pathways; Group II, IFN-gamma, IL-3, and IL-4, partially induced by calcium ionophore alone; and Group III, IL-5, IL-6, and IL-10, partially induced by either PMA or calcium ionophore alone. Transfection of constitutively active PKC or p21ras replaced the requirement for PMA in expression of these lymphokines, with the exception of GM-CSF. Production of Group II lymphokines was partially induced by constitutively active calcineurin. Production of Group I and II lymphokines was highly sensitive to cyclosporin A, while Group III lymphokines were relatively resistant. Addition of prostaglandin E2 (PGE2) and overexpression of catalytic subunit of protein kinase A inhibited lymphokine production in Th1 cells, but not in Th2 cells, with the exception of GM-CSF. Production of Group III lymphokines induced by PMA alone was upregulated by PGE2, but that of Group II and III lymphokines induced by calcium ionophore alone was not affected. These results suggest that one of the targets of PGE2 is downstream of the PKC-dependent pathway.

Animals↗
PubMed1996

Demonstration of mother-to-infant transmission of Staphylococcus aureus by pulsed-field gel electrophoresis.

UNLABELLED: We assessed mother-to-infant transmission of Staphylococcus aureus. Anterior nares swabs of 466 pregnant women, vaginal swabs of 305 of these women and anterior nares swabs of 305 6-day-old infants were examined for the presence of S. aureus. The results showed that 7.5% of the vaginal swabs from the pregnant women and 10.1% of the anterior nares swabs from the infants were positive for S. aureus. Six of the 466 pregnant women (1.3%) and 12 of the 305 infants (3.9%) carried methicillin-resistant S. aureus (MRSA) in the anterior nares site, but none of the vaginal specimens were positive for MRSA. Analysis of SmaI digested chromosomal DNA analysis using pulsed-field gel electrophoresis (PFGE) showed that methicillin-sensitive S. aureus (MSSA) strains obtained from four pairs of pregnant women and their infants were completely identical, which strongly suggests [correction of suggesting] mother-to-infant transmission of S. aureus. CONCLUSION: This study elucidated the prevalence of S. aureus carriage among pregnant women and newborn infants. Mother-to-infant infection of S. aureus was demonstrated phenotypically and genetically. PFGE is a useful tool to detect infection routes including mother-to-infant infection.

Bacterial Toxins↗
PubMed1996

Efficient production of IgG human monoclonal antibodies by lymphocytes stimulated by lipopolysaccharide, pokeweed mitogen, and interleukin 4.

Extensive screening of the mitogens lipopolysaccharide (LPS), pokeweed mitogen (PWM), and Staphylococcus aureus Cowan I (SAC I), alone and in combination and with and without interleukin (IL) was performed for in vitro activation of regional lymph node lymphocytes from lung cancer patients for the production of human IgG, IgM, and IgA. As assessed by electrofusion of the lymphocytes following their exposure to these agents with mouse myeloma cells and incubation of the fused hybridoma, a remarkable stimulatory effect was shown by LPS and particularly by LPS plus IL-4, which was substantially greater than that of either SAC I or PWM with or without various IL. Optimization studies indicated that the addition of PWM to LPS and IL-4 in the culture medium further stimulated the human antibody (Ab) production, and that the optimal formulation for stimulation of human IgG production was a culture medium containing 20 micrograms/ml of LPS, 1/500 of PWM, and 100 u/ml of IL-4.

Antibodies, Monoclonal↗
PubMed1996

Therapeutic efficacy of a case of pyruvate dehydrogenase complex deficiency monitored by localized proton magnetic resonance spectroscopy.

We experienced a case of pyruvate dehydrogenase deficiency observed by proton magnetic resonance spectroscopy (1H MRS). This case was diagnosed as West syndrome by characteristic convulsion and the periodic hypsarrhythmia pattern of EEG. At the age of 11 months, the first examination of 1H MRS revealed a high peak of lactate, and the high concentration of lactate and pyruvate was confirmed in sampled cerebrospinal fluid (CSF). Deficiency of pyruvate dehydrogenase complex was finally diagnosed by genetic examination. Dichloroacetate was administered to the patient as therapy. Decrease of lactate in the brain was found by 1H MRS. Lactate and pyruvate in the CSF was also decreased. In accordance with the suspension of dichloroacetate, increase of lactate in the brain was detected and the convulsions reappeared. After readministration of dichloroacetate, the patient was almost symptom free and lactate in the brain and CSF had decreased to the normal extent. We considered that 1H MRS provides useful information for screening metabolic disorders of infants and assessing the efficacy of therapy.

Brain↗
PubMed1996

Effects of a factor derived from polymorphonuclear leukocytes on the growth and collagen metabolism in normal and scleroderma skin fibroblast cultures.

Effects of a factor (15 kDa) derived from polymorphonuclear leukocytes (PMNs) on the growth and collagen metabolism of normal and scleroderma skin fibroblasts in culture were investigated. Skin fibroblasts from papillary, reticular or whole dermis of 5 patients with scleroderma and 7 normal controls were cultured in the presence or absence of PMN factor. The factor affected skin fibroblasts, (i) to stimulate cell proliferation, (ii) to stimulate collagenase production as observed by its functional activity, but (iii) to suppress collagen production with little effect on collagen types at a stage before the translational level. Scleroderma fibroblasts were less susceptible to the factor than normal fibroblasts in terms of cell proliferation and protein synthesis including collagen. Stimulation of cell proliferation by the factor was higher with reticular cells than papillary cells, while stimulation of collagenase production was inversely high in papillary cells and little stimulation was noted with reticular cells. Suppression of collagen production was also eminent in papillary cells, compared with that in reticular cells. These results suggest that PMNs function at the inflammatory stage in shifting tissue metabolism to a catabolic phase by releasing a factor which stimulates connective tissue cells, and that decreased susceptibility of scleroderma cells and reticular cells to PMN factor may provide for a positive factor in the accumulation of collagen in the reticular dermis of scleroderma skin.

Cell Division↗
PubMed1996

Factors affecting the cytokine production of human T cells stimulated by different modes of activation.

According to the widely accepted classification, human TH cell clones can be divided into two mutually exclusive subsets, TH1 and TH2, based on their profile of cytokine production. The intracellular difference between these clones is not clear. To characterize the biochemical nature of T-cell receptor (TCR)/CD3 complex-mediated signal transduction pathways, we introduced several human TH cell clones of THO- or TH1-like phenotype and analyzed the effects of various drugs and antibodies on cytokine production or proliferation of these clones. The tyrosine kinase inhibitor herbimycin inhibited the production of interferon-gamma (IFN-gamma) by THO-like clone, after stimulation with anti-CD3 monoclonal antibody alpha CD3-mAb) or with phorbol 12-myristate 13-acetate (PMA) and the calcium ionophore A23187. However, whereas herbimycin strongly inhibited the production of IL-4 and IL-5 by alpha CD3 mAb stimulated T cells, it did not affect the production of these cytokines after PMA/A23187 stimulation. Cyclosporin A inhibited the proliferation as well as the production of the cytokines, including that of IL-2, IL-4, IL-5, and IFN-gamma, irrespective of the mode of stimulation. A23187, which synergizes with PMA in the induction of IL-4 and IFN-gamma, inhibited PMA-induced IL-10 production in a dose-dependent manner. Transforming growth factor-beta and anti-IL-2 receptor monoclonal antibody partially inhibited alpha CD3 mAb-mediated T-cell proliferation, but had no effect on the proliferation induced by PMA and A23187. Cyclic adenosine monophosphate (cAMP)-elevating drugs, like prostaglandin E2 and dibutyryl cAMP, inhibited the TCR-mediated cytokine production but shifted the cytokine production profile from a TH0 to a TH2 type after stimulation with PMA and A23187. Finally, we analyzed the induction of activity of two transcription factors, nuclear factor-kappa B (NF-kappa B) and nuclear factor of activated T cells, involved in the regulation of cytokine gene expression, after a different mode of activation. The induction of NF-kappa B (p50/p65 heterodimer) by using alpha CD3-mAb stimulation but not by using PMA/A23187 stimulation was found to be inhibited by using cAMP-elevating drugs.

Antibodies, Monoclonal↗
PubMed1996

Specific versus cooperative regulatory mechanisms of the cytokine genes that are clustered on the same chromosome.

The genes for IL-3, IL-4, IL-5, IL-9, IL-13, and granulocyte-macrophage colony-stimulating factor (GM-CSF) are known to be clustered on human chromosome 5q and on mouse chromosome 11. IL-2 and interferon gamma (IFN-gamma) genes are located on separate chromosomes. It is well known that upon stimulation by antigen presentation, TH1 and TH2 subsets of T helper cells start to transcribe distinct sets of cytokine genes. Thus mechanisms should exist that transmit extracellular signals into the nucleus, thereby coordinately turning on transcriptional machinery in cell type-specific manners. Several different mechanisms exist in which specific as well as coordinated expression of cytokines are regulated at the transcriptional level. These include (1) regulation by proximal cis-elements, to which specific transcription factors bind, (2) regulation by distal cis-elements, such as enhancers or locus controlling elements, especially those located several kilobases away from the target gene, and (3) enhancement of transcription by viral trans-activators in a pathologic state. In this article, we review the recent studies on the above issues, with particular emphasis on our own results that support the presence of different modes of control mechanisms. We also discuss the possible approaches to the thorough understanding of the coordinated and specific regulation of cytokines.

Animals↗
PubMed1996

Roles of JAK kinases in human GM-CSF receptor signal transduction.

The receptors for human interleukin-3 (IL-3) and human granulocyte-macrophage colony-stimulating factor (GM-CSF), hIL-3R, hGM-CSFR, respectively, consists of two subunits, alpha and beta, both of which are members of the cytokine receptor superfamily. Phosphorylation of tyrosine residues in the hGMR beta subunit and several cellular proteins is observed after hGM-CSF stimulation. We analyzed the role of tyrosine residues in the hGMR beta subunit and the nature of tyrosine kinase, JAK2, in hGMR signal transduction using several hGMR beta subunit mutants. In addition to the box1 region, a membrane distal region (a.a. 544-589) of the hGMR beta was required for c-fos activation. Only one tyrosine residue (Tyr577) existed within the region 544 to 589, and substitution of Tyr577 to phenylalanine in GMR beta 589 resulted in loss of c-fos activation. In contrast, the same substitution in a wild type receptor did not affect GM-CSF induced activities such as c-fos messenger RNA (mRNA) induction and proliferation, but the substitution abolished Shc phosphorylation. These results suggest that the activation of Shc is not essential for c-fos activation and several tyrosine residues cooperate for c-fos activation. It is well documented that IL-3 or GM-CSF activate JAK2 in BA/F3 cells. The role of JAK2 in IL-3/GM-CSF functions, however, is largely unknown. We examined the role of JAK2 in GM-CSF induced signaling pathways. Dominant negative JAK2 (delta JAK2) lacking the C-terminus kinase domain suppressed IL-3/GM-CSF induced c-fos activation and c-myc activation and proliferation, suggesting that JAK2 was involved in both signaling pathways. Protein tyrosine phosphatase SHP-2 (also called PTP 1D) and Shc were phosphorylated by IL-3/GM-CSF in BA/F3 cells; however, these phosphorylation events were inhibited by the expression of delta JAK2. Taken together, these results indicate the JAK2 is a primary kinase regulating all the known activities of GM-CSF. JAK2 mediates GM-CSF induced c-fos activation through receptor phosphorylation and Shc/PTP 1D activation.

Animals↗
PubMed1996

Mechanisms of primer RNA synthesis and D-loop/R-loop-dependent DNA replication in Escherichia coli.

In DNA replication, DNA chains are generally initiated from small pieces of ribonucleotides attached to DNA templates. These 'primers' are synthesized by various enzymatic mechanisms in Escherichia coli. Studies on primer RNA synthesis on single-stranded DNA templates containing specific 'priming signals' revealed the presence of two distinct modes, ie immobile and mobile priming. The former includes primer RNA synthesis by primase encoded by dnaG and by RNA polymerase containing a sigma 70 subunit. Priming is initiated at a specific site in immobile priming. Novel immobile priming signals were identified from various plasmid replicons, some of which function in initiation of the leading strand synthesis. The latter, on the other hands involves a protein complex, primosome, which contains DnaB, the replicative helicase for E coli chromosomal replication. Utilizing the energy fueled by ATP hydrolysis of DnaB protein, primosomes are able to translocate on a template DNA and primase synthesizes primer RNAs at multiple sites. Two distinct primosomes, DnaA-dependent and PriA-dependent, have been identified, which are differentially utilized for E coli chromosomal replication. Whereas DnaA-dependent primosome supports normal chromosomal replication from oriC, the PriA-dependent primosome functions in oriC-independent chromosomal replication observed in DNA-damaged cells or cells lacking RNaseH activity. In oriC-independent replication, PriA protein may recognize the D- or R-loop structure, respectively, to initiate assembly of a primosome which mediates primer RNA synthesis and replication fork progression.

Amino Acid Sequence↗
PubMed1996

Generation of human monoclonal antibodies recognising membranous antigens of the lung adenocarcinoma cell line A549 using an AMeX immunohistostaining method.

Four monoclonal antibodies (MAbs) from hybridoma obtained by in vitro stimulation of regional lymph node lymphocytes from lung cancer patients and electrofusion of the stimulated cells with murine or human-mouse myeloma cells were reactive to lung cancer cells in enzyme-linked immunoabsorbent assay, and to lung cancer tissue in immunohistochemical analysis using acetone-methyl benzoate-xylene (AMeX) fixed tissue and in immunofluorescence analysis. Three of the MAbs (designated ZLG40, 27D57 and 28K29) recognised cell-surface antigens of the lung adenocarcinoma cell line A549 and the remaining one (designated 29D38) recognised nuclear membrane antigens of the same cell line. The three surface-binding MAbs showed a significant complement-dependent cytotoxicity (CDC) to the A549 cells, but the membrane-binding 29D38 showed no CDC to the A549 cells. Western blotting of the extracts of the A549 or PC6 (small-cell lung cancer) cell lines by the four MAbs showed a 28K29 antigen band at M(r) of approximately 600,000 (+/- 2-ME), a ZLG40 antigen band at M(r) 50,000 (+/- 2-ME), and one 29D38 antigen band at M(r) of more than 1,000,000 (-2-ME) and M(r) between 20,000 and 80,000 (+2-ME), but no detectable band for 27D57 antigen.

Adenocarcinoma↗
PubMed1996

Genetic interactions between CDC7 and CDC28: growth inhibition of cdc28-1N by Cdc7 point mutants.

BACKGROUND: Cdc7 kinase of Saccharomyces cerevisiae, a nuclear phosphoprotein, regulates initiation of chromosomal DNA replication. Overexpression of kinase-negative Cdc7 point mutants (T281E, D182N and D163N) arrests the cell cycle of the wild-type Saccharomyces cerevisiae cells at the G1/S boundary. This is caused by titration of a regulatory protein, Dbf4, from the wild-type Cdc7, which leads to inactivation of its kinase activity. RESULTS: We report here that kinase-negative Cdc7 mutants, when overexpressed in cdc28-1N(ts) at a permissive temperature, not only inhibit DNA replication by inactivating the wild-type Cdc7 but may also disturb coordination between DNA replication and cell division. Suppression of growth inhibition under this condition requires co-expression of both Dbf4 and Cdc28, whereas Dbf4 alone can counteract the growth inhibition in the wild-type cells. In cdc28-1N(ts), co-expression of the wild-type Dbf4 rescues only the G1/S defect and results in accumulation of those cells with less than 1C DNA as well as 2C DNA. On the other hand, co-expression of Cdc28 alone leads to increase of those cells arrested at the G1/S boundary, as found typically in the wild-type. We also report that overexpression of T281A, a 'weak' allele of Cdc7, causes growth arrest in cdc28-1N(ts) cells, but not in the CDC28 wild-type cells. This suggests that T281A is inactive in cdc28-1N(ts) and is consistent with the idea that Cdc28 activates Cdc7 by phosphorylation. CONCLUSION: We conclude that two essential serine-threonine kinases, Cdc28 and Cdc7, genetically interact for initiation of the S phase and possibly for G2/M progression and/or S phase checkpoint control.

CDC28 Protein Kinase, S cerevisiae↗
PubMed1996

The clinical significance of changes in genetic heterogeneity of the hypervariable region 1 in chronic hepatitis C with interferon therapy.

We examined changes in the hypervariable region 1 of the hepatitis C virus (HCV) RNA that occurred with interferon therapy in 33 patients with chronic hepatitis C to assess the clinical significance of this region. The 33 patients had HCV genotype 1b and were classified into three groups based on serum aminotransferase levels during and after therapy with alpha interferon; long-term responders (n = 9), short-term responders (n = 11), and nonresponders (n = 13). Changes in the genetic heterogeneity of the hypervariable region 1 were determined by using nonisotopic polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP). HCV RNA levels were evaluated by reverse transcriptase PCR and branched DNA probe assays. Changes in sequences were determined by cloning and sequencing analysis. Before therapy, the long-term responders had significantly lower degrees of heterogeneity and lower viral levels than nonresponders. There were no significant differences between short-term and nonresponders. With interferon therapy, viral levels and degree of heterogeneity decreased to a greater extent among long-term and short-term responders than among nonresponders. Sequencing analysis showed that the three groups had similar clone numbers initially, but long-term responders had rather homogeneous viral populations, whereas short-term and nonresponders had heterogeneous populations, but that there were no nucleotide sequences or amino acid alignments that were specific for any group before, during, and 6 months after therapy. Approximately half of short-term and nonresponders received a second course of interferon 7 to 10 months after the initial therapy; all showed an identical response to the second course of therapy regardless of interim changes in the heterogeneity of hypervariable region 1. These findings suggest that (1) patients who were nonresponders or short-term responders had mixed viral populations that had differing sensitivities to interferon, (2) the changes in the hypervariable region 1 (HVR 1) did not affect responsiveness to interferon, and (3) the lower heterogeneity in the HVR 1 was associated with a long-term response to interferon only when the viral levels were low.

Chronic Disease↗
PubMed1996

Lysophosphatidic acid and bFGF control different modes in proliferating myoblasts.

Myogenic cells provide excellent in vitro models for studying the cell growth and differentiation. In this study we report that lysophosphatidic acid (LPA), a bioactive phospholipid contained in serum, stimulates the growth and inhibits the differentiation of mouse C2C12 myoblast cells, in a distinct manner from basic fibroblast growth factor (bFGF) whose mitotic and anti-differentiation actions have been well investigated. These actions of LPA were both blocked by pertussis toxin, suggesting the involvement of Gi class of G proteins, whereas bFGF acts through receptor tyrosine kinases. Detailed analysis revealed that LPA and bFGF act differently in regulating the myogenic basic helix-loop-helix (bHLH) proteins, the key players in myogenic differentiation process. LPA stimulates the proliferation of undifferentiated myoblasts allowing the continued expression of MyoD, but in contrast, bFGF does so with the MyoD expression suppressed at the mRNA level. Both compounds maintain the myf-5 expression, and suppress the myogenin expression. In addition, while LPA did not inhibit cell-cell contact-induced differentiation, bFGF strongly inhibited this process. Furthermore, LPA and bFGF act cooperatively in their mitogenic and anti-differentiation abilities. These findings indicate that LPA and bFGF differently stimulate intracellular signaling pathways, resulting in proliferating myoblasts each bearing a distinct expression pattern of myogenic bHLH proteins and distinct differentiation potentials in response to cell-cell contact, and illustrate the biological significance of Gi-mediated and tyrosine kinase-mediated signals.

Animals↗
PubMed1996

Characterization of monoclonal antibodies recognizing human merosin and their use in affinity purification of native merosin.

Two monoclonal antibodies (MAbs) to human placenta laminin (pl-LAM), 1D8 (IgG1) and 6G5 (IgG2b) were generated and shown by ELISA and immunoblot analysis to recognize only native pl-LAM, but not denatured, reduced pl-LAM or mouse EHS laminin. Intact pl-LAM was easily isolated and purified in large scale from human placenta by 1D8-conjugated affinity chromatography. Electrophoretic analysis of the purified pl-LAM revealed the presence of a major 750-kDa component composed of 320-, 220-, and 200-kDa polypeptides and a minor 800-kDa component composed of 320-, 240-, and 220-kDa polypeptides. Neither molecule had a 400-kDa component corresponding to the A chain. It has already been shown that the 320-kDa polypeptide is identical to the M chain of human merosin (Hori et al. J. Biochem. 1994;116:1212-1219). Electron microscopy revealed that isolated merosin was composed of three short arms and one long arm. By immunohistochemistry, MAbs showed positive staining in human adult kidney and liver. These results indicate that these MAbs recognize only native merosin and can be used to study merosin structure and function by rapid purification of native merosin and by immunohistochemical analysis.

Animals↗