Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunohistological staining patterns of several hundred monoclonal antibodies (Mabs) were studied in normal human kidney tissue. Seven Mabs, 3 hematopoietic (F103.12/CD10, MY7/CD13, 3C4/CD15) and 4 non-hematopoietic (LP34, E29, HEA81, HEA125) revealed a segment-specific or pan-nephron staining. The expression of antigens (Ags) labelled by the 7 selected Mabs was then studied in cryostat sections of a series of 43 renal epithelial tumors (31 renal cell carcinomas, 2 oncocytomas, 10 adenomas) in order to correlate the results with the prevailing hypothesis for the histogenesis of these tumors. The adenomas displayed poor expression of CD10-Ag (proximal nephron marker) compared to carcinomas. The chromophobic type of renal cell carcinoma and the benign oncocytoma did not express CD13-Ag, suggesting a possible histogenetic relationship. More than 95% of all tumors simultaneously expressed a proximal and a distal marker. Our results suggest that CD10-antibody may be of value in the distinction between benign and malignant small-sized renal tumors. We conclude that neoplastic transformation may imply such alterations in the expression of marker-Ags (proximal/distal) that no conclusion can be drawn regarding the tubular segment from which a renal epithelial tumor takes its origin.
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PMID:Expression of segment-specific antigens in the human nephron and in renal epithelial tumors. 246 11

Seventeen patients with acute myeloid leukaemia (AML) whose blasts co-expressed the T-cell associated CD7 antibody were identified among 160 consecutive AML cases. Fourteen had FAB defined AML according to morphocytochemical criteria, whereas three patients were classified as 'MO' on the basis of immunophenotype. The incidence of CD7 positively was particularly significant in the less differentiated subtypes M0 and M1 compared with other FAB groups (P less than 0.001). In all cases the myeloid determinants CD13 and/or CD33 were associated with CD7 expression. Other B-lymphoid (CD10, CD19) or T-lymphoid (CD2, surface and cytoplasmic CD3) markers were analysed and found to be negative. Five out of 15 cases examined were TdT+. Clonal rearrangements of the immunoglobulin heavy chain (IgH) and/or T-cell receptor (TcR) beta chain genes were identified in only three out of 13 cases. Among these, one out of five co-expressing TdT showed IgH rearrangement when analysed at the DNA level. Clinical features at presentation and response to induction therapy did not allow us to consider CD7+ AML patients as a distinct subgroup with prognostic significance. Our data indicate that CD7 expression is a common finding in immature AML, being generally found in the absence of other T-cell features. Rather than suggesting the occurrence of 'mixed leukaemia', such cases confirm a broader spectrum of CD7 reactivity and its possible identification of a particular subset of myeloid progenitors.
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PMID:CD7 positive acute myeloid leukaemia: a subtype associated with cell immaturity. 248 63

Bone marrow and peripheral blood of 25 healthy bone marrow donors from our allogeneic bone marrow transplantation program were assessed for cell subsets bearing T11(CD2), T4(CD4), T8(CD8), B1(CD20) J5(CALLA, CD10), Mo1(CD11b), MY7(CD13). Mo2(CD14), MY9(CD33) and NKH-1 antigens. Bone marrow cell samples were taken for analysis at the start or at the end of the harvesting procedure of aspiration from the iliac crest. All samples were analysed on a flow cytometer at the lymphocyte window as obtained on the two-parameter (L90oLSxFALS) scatter diagram. There were no differences in the lymphocyte subset composition of bone marrow samples taken at the start or at the end of the harvesting procedure. In contrast to the majority of literature data, a high CD4/CD8 ratio was detected in bone marrow samples: it did not differ from that in the peripheral blood. The proportions of CD2 and CD4 T cell markers in the bone marrow correlated with those in the peripheral blood, thus further documenting a substantial bone marrow contamination with peripheral blood cells. A relatively large aspirate volume (4-5 ml) obtained from individual aspiration sites was identified as the only factor possibly accounting for the high-level contamination of bone marrow samples with peripheral blood. This conclusion was corroborated by low T cell proportions and low CD4/CD8 ratios found in the bone marrow washed from bone fragments and in bone marrow samples aspirated at first bone puncture in a volume of 1.0 ml. Taken together, these findings imply that less vigorous suction may decrease the number of T lymphocytes in bone marrow harvested for transplantation purposes.
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PMID:Lymphocyte subsets in normal human bone marrow harvested for routine clinical transplantation. 249 93

The addition of 200 pM monoiodinated human atrial natriuretic factor-(99-126) (125I-hANF) to cultured bovine aortic smooth muscle cells at 37 degrees C resulted in a rapid clearance from the medium (t1/2 approximately 7.5 min). Within 5 min, [125I]iodotyrosine126 (125I-Y), Arg125-[125I]iodotyrosine126 (125I-RY) and Phe124-Arg-[125]iodotyrosine126 (125I-FRY) appeared in the medium. The identities of these degradation products were confirmed by 1) retention time on high performance liquid chromatography (HPLC) relative to standards, 2) products generated by digestion with aminopeptidase M, and 3) the absence of the Met110. Preincubation of the cells with ammonium chloride or chloroquine resulted in a significant increase in the intracellular accumulation of radiolabel, indicative of endocytosis and rapid delivery of 125I-hANF to an acidic intracellular compartment (endosome and/or lysosome). Neither ammonium chloride, chloroquine, nor excess unlabeled hANF blocked the rapid appearance in the medium of 125I-RY or 125I-FRY. Bestatin inhibited the generation of 125I-RY, with a concomitant increase in 125I-FRY, suggesting that the 125I-RY is produced by aminopeptidase action on 125I-FRY. The endopeptidase 24.11 (enkephalinase) inhibitor, SCH 39370, did not inhibit the formation of 125I-FRY. These results provide evidence of a peptidase capable of specifically removing the COOH-terminal tripeptide from 125I-hANF. The COOH-terminal tripeptide, Phe124-Arg-Tyr126, was also isolated from cell digests of hANF by HPLC and its identity confirmed by amino acid analysis. Since it is generally believed that the COOH-terminal tripeptide is critical to many of atrial natriuretic factor-(99-126)'s bioactivities, this enzyme may be involved in the inactivation of atrial natriuretic factor-(99-126) in target tissues.
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PMID:Metabolism of 125I-atrial natriuretic factor by vascular smooth muscle cells. Evidence for a peptidase that specifically removes the COOH-terminal tripeptide. 252 21

A 26-year-old male was admitted to our hospital because of fever and leukocytosis. On admission, a white blood cell count was 28,300/microliters with 46.5% blast cells and 16.0% atypical monocytoid cells, a hemoglobin level 13.7 g/dl, and a platelet count 15.0 X 10(4)/microliters. Bone marrow contained 58.8% of peroxidase-negative blast cells. He was diagnosed as acute lymphoblastic leukemia (ALL L2) according to the FAB classification. Chromosome analysis revealed the marrow cells to contain 45, XY, -7, t(9; 22) (q34; q11). On surface marker analysis, the leukemic cells were positive for both lymphoid (CD10) and myeloid markers (CD13). Two color flow-cytometric analysis showed two distinct populations with CD10 and CD1 3, respectively. Rearrangements of both immunoglobulin heavy chain and T cell receptor beta-chain were observed. The "breakpoint cluster region" on chromosome 22 was not rearranged. On the basis of these findings, we thought this case being acute mixed leukemia. He was refractory to AdVP therapy and BHAC-DMP therapy. He is now under treatment with A-Triple-V therapy.
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PMID:[Philadelphia-positive acute mixed leukemia with monosomy 7]. 255 34

Some of the many cell-surface antigens defined by the CD (cluster differentiation) nomenclature have lately emerged as proteins with well-characterised enzymic activities. One important example is CD10 or CALLA (common acute lymphoblastic leukaemia antigen), which is identical to endopeptidase-24.11, an enzyme with an important role in the hydrolysis of biologically active peptides. CD13 and CD26 are also surface peptidases. These enzymes, which have a wide distribution on the surfaces of various cell types, may have specific roles in the control of growth and differentiation in both haemopoietic and epithelial cell systems.
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PMID:Cell-surface peptidases as modulators of growth and differentiation. 257 Oct 20

A detailed investigation is reported about the biodegradation of poly[Lys(DL-Alam)], m approximately 3, (AK) the common inside area of a branched polypeptide model system developed by our group over the last decade. Enzymatic hydrolysis was carried out by the exopeptidase aminopeptidase M, or the endopeptidase trypsin, or their mixture. Ion-exchange column chromatography, paper electrophoresis and thin-layer chromatography were utilised to achieve separation of metabolites. Breakdown products were identified by the aid of synthetic oligopeptides representing the potential fragments (DL-Ala2, DL-Ala3, Lys(DL-Alam), m = 1-3). The kinetics and the degree of enzymatic degradation were determined. The ratio of peptide/amino acid amounts in the hydrolysate was found to be 1.07 after 24 h treatment with aminopeptidase M, 3.0 with trypsin and 1.3 with aminopeptidase - trypsin mixture. The overall results indicated that the proteolysis of AK by an aminopeptidase M and trypsin mixture proceeds stepwise at multiple sites on the polypeptide chain. The degradation is significantly retarded as compared to that of alpha- or epsilon-polylysine. A mechanism of degradation is suggested based on the experimental results.
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PMID:Biodegradability of synthetic branched polypeptide with poly(L-lysine) backbone. 257 93

A case of chronic lymphocytic leukemia (CLL) treated with chlorambucil, followed by the development of an acute monoblastic leukemia, is described. Cytofluorometric quantitative immunophenotype was determined during the blastic phase. Whereas small lymphocytes displayed a CD19+; CD24+; CD37+; CD5+ phenotype, the blastic population exhibited, besides CD13, CD14 and CD15 positivity, which is usually noted in such a monoblastic leukemia, definite CD9, CD10, CD22, CD24, CD37, CD5 and CD4 staining. Such results argue against a complete independence between the two clones, although their similarity could not be demonstrated.
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PMID:Acute monocytic leukemia with B cell markers expression following B chronic lymphocytic leukemia. 258 3

We have developed a novel fluorescent histochemical method to localize the enzyme neutral endopeptidase-24.11 (NEP, E.C. 3.4.24.11, enkephalinase) in the rat brain in order to directly compare the relative distributions of the enzyme and its putative peptide substrate, the enkephalins. The method is based on the sequential cleavage of the synthetic peptide substrate, glutaryl-alanyl-alanyl-phenylanyl-4-methoxy-2-naphthylamide, by NEP and exogenous aminopeptidase M to yield free 4-methoxy-2-naphthylamine (MNA). In the presence of nitrosalicylaldehyde, free MNA is captured, yielding an insoluble yellow fluorescent precipitate which marks the site of NEP activity. The specificity of the method was demonstrated using the selective NEP inhibitors thiorphan, phosphoramidon, and JHF26. All NEP staining throughout the brain was abolished using a 50-nM concentration of these inhibitors. The enzyme was richly localized to many regions, including the cerebral cortex, caudate putamen, globus pallidus, hippocampus, substantia nigra, periaqueductal gray, several cranial nerve nuclei, nuclei of the reticular formation of the medulla. In most regions, reaction product was associated with cell bodies of varying size and morphology. In a number of regions, colchicine increased the amount of NEP staining, particularly in cell processes. The regional distribution pattern of the enzyme, however, did not change in response to colchicine and was similar to that of untreated animals. The histochemical localization of NEP was combined with fluorescent immunocytochemical visualization of the enkephalins in order to localize both in the same tissue section. In the globus pallidus, this combined fluorescent technique revealed numerous NEP-positive cell bodies surrounded by fiber pathways displaying intense enkephalin-like immunoreactivity. The source of the NEP in the globus pallidus was studied using the neurotoxic agent, N-methyl-D-aspartate (NMDA). A pronounced decrease in NEP cellular staining was observed within 7 d in response to NMDA, persisted for at least 16 weeks, and correlated with injury of pallidal neurons. There was no apparent change in enkephalin-like immunoreactivity in the globus pallidus in response to NMDA. These data provide evidence that NEP and enkephalin in the globus pallidus derive from different sources. This study supports the hypothesis that NEP localizes to enkephalin-rich regions of the rat brain, and that the enzyme may be involved in the inactivation of synaptically released enkephalins.
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PMID:Histochemical visualization of neutral endopeptidase-24.11 (enkephalinase) activity in rat brain: cellular localization and codistribution with enkephalins in the globus pallidus. 259 7

In this paper is reported a case of acute biphenotypic leukemia who was treated by chemotherapy and pursued its effect by two color flow cytometry. A 33-year-old male patient was admitted due to fever and general fatigue and diagnosed as acute leukemia by hematological findings. Surface markers were investigated to find positive reaction of Leu 12 (CD19), J 5 (CD10), My 7 (CD13) and My 9 (CD33), in which Leu 12 and My 9 were simultaneously expressed on the same blast cells by two color flow cytometry. He was treated with daunorubicin, enocitabine, mercaptopurine, vincristine, and prednisolone to obtain partial remission. Then, he was administered L-asparaginase, doxorubicin, vincristine and prednisolone to reach complete remission. The effect of chemotherapy was investigated by not only bone marrow puncture, but also by two color flow cytometry. From the findings in this case, the two flow cytometry was proved to be a useful tool for not only diagnosis of acute mixed leukemia, aut also the judgement of the effect of treatment.
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PMID:[Acute biphenotypic leukemia followed by two color flow cytometry]. 259 47


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