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

The incidence rate of acute mixed-lineal leukemias, distinguished in a group of patients with acute non-lymphoblastic leukemia, in children and adults was about the same: CALLA 10-20%, T-cell antigens 15-22%, Thy-1 15-17%. The incidence rate of acute lymphoblastic leukemia with myeloid (17-21%) and erythroid (12-13%) antigens did not significantly differ in children and adults. Distinguishing features have been proposed for actual acute mixed-lineal leukemias having markers of mature stages of varying cell line differentiation from cryptic lineal-different-marker leukemias of bi- or polypotent precursor-cell origin.
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PMID:[Acute mixed-cell human leukemia]. 225 55

1. Inbred mouse strains differ markedly in the expression of a kidney brush border metalloendopeptidase, meprin-a. 2. Brush border preparations from mice of the low-meprin-a phenotype (specific activities less than 5% of the high-meprin-a trait) contain a metallo-endopeptidase, meprin-b, that is larger than meprin-a, and which is inactive unless the membrane preparations are treated with trypsin. 3. This cryptic metallo-endopeptidase has been previously postulated to be a stalled precursor of meprin-a. 4. We show here that meprin-b is present in all mice-high and low meprin-a phenotypes--and that this activity is similar in substrate specificity and amount present in the brush border. 5. Meprin-b may therefore be a distinct gene product that is independent of meprin-a phenotype.
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PMID:A cryptic meprin-like proteolytic activity in mouse kidney brush border membranes. 228 66

Ribosomes have been shown to contain a proteolytic activity, characterized as an endopeptidase with serine in the active center. The enzyme has been given the name cathepsin R, following the recommendations of Barrett et al. (in a publication from the Cold Spring Harbor Laboratory, New York) for naming new proteinases. The present paper contains evidence that cathepsin R in rat liver ribosomes is present in a cryptic form. Upon dissociation of ribosomes to subunits (and to minor extent also by 0.5 M KC1 washes), the cryptic proteinase is released. Activation of the released cathepsin R is effected by equilibration with 2 M NaC1/0.05 M sodium acetate, pH 4.8. The molecular weight of free cathepsin R is 25 000-30 000.
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PMID:The ribosomal serine proteinase, cathepsin R. Occurrence in rat-liver ribosomes in a cryptic form. 710 22

Pro-thyrotropin-releasing hormone (proTRH) is the precursor to thyrotropin-releasing hormone (TRH; pGlu-His-Pro-NH2), the hypothalamic releasing factor that stimulates synthesis and release of thyrotropin from the pituitary gland. Five copies of the TRH progenitor sequence (Gln-His-Pro-Gly) and seven cryptic peptides are formed following posttranslational proteolytic cleavage of the 26-kDa rat proTRH precursor. The endopeptidase(s) responsible for the physiological conversion of proTRH to the TRH progenitor form is currently unknown. We examined the in vitro processing of [3H]leucine-labeled or unlabeled proTRH by partially purified recombinant PC1. Recombinant PC1 processed the 26-kDa TRH precursor by initially cleaving the prohormone after the basic amino acid at either position 153 or 159. Based on the use of our well-established antibodies, we propose that the initial cleavage gave rise to the formation of a 15-kDa N-terminal peptide (preproTRH25-152 or pre-proTRH25-158) and a 10-kDa C-terminal peptide (pre-proTRH154-255 or preproTRH160-255). Some initial cleavage occurred after amino acid 108 to generate a 16.5-kDa C-terminal peptide. The 15-kDa N-terminal intermediate was further processed to a 6-kDa peptide (prepro-TRH25-76 or preproTRH25-82) and a 3.8-kDa peptide (preproTRH83-108), whereas the 10-kDa C-terminal intermediate was processed to a 5.4-kDa peptide (prepro-TRH206-255). The optimal pH for these cleavages was 5.5. ZnCl2, EDTA, EGTA, and the omission of Ca2+ inhibited the formation of pYE27 (preproTRH25-50), one of the proTRH N-terminal products, by 48, 82, 72, and 45%, respectively. This study provides evidence, for the first time, that recombinant PC 1 enzyme can process proTRH to its predicted peptide intermediates.
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PMID:Pro-thyrotropin-releasing hormone processing by recombinant PC1. 759 40

The nonobese diabetic/severe combined immunodeficient (NOD/SCID) xenotransplantation model is increasingly utilized to study both human lymphohematopoietic stem/progenitor cells and committed cell types. Human B lymphoid cells develop and proliferate in this model. We found high numbers of CD19+CD5+ B lymphoid cells in the bone marrows and spleens of NOD/SCID mice transplanted with human CD34+ stem/progenitor cells. The CD5+ cells accounted for a particularly large percentage of the B lymphoid cells in the spleens of chimeras analyzed three months after transplantation. CD19+CD5+ cells from all the analyzed chimeras coexpressed HLA-DR, surface IgM, CD20, CD38, CD43, and CD45. However, CD19+CD5+ cells were negative for kappa light chain, CD10, CD11a, CD11b, CD15, CD21, CD22, CD23, CD25, CD34, CD35, CD44, CD62L, CD69, and CD71. Cell surface expression of the lambda light chain, surface IgD, CD9, and CD40 antigens was detected in some but not all chimeras. Thus, the CD19+CD5+ cell population detected in our study has the phenotype of previously described CD5+ B lymphoid cells in humans and other species. The origin and role of the B lymphoid cells which express CD5 cell surface glycoprotein are poorly understood. The malignant cells in B lymphoid chronic lymphocytic leukemia express CD5, and the numbers of CD5+ B lymphoid cells are elevated in several autoimmune conditions. The human-NOD/SCID chimera system may provide an in vivo model to investigate the maturation and development of this cryptic human CD5+ B lymphoid cell subpopulation.
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PMID:Human hematopoietic stem/progenitor cells generate CD5+ B lymphoid cells in NOD/SCID mice. 1052 59

TEL gene rearrangement due to the 12;21 chromosome translocation is believed to be the most common molecular genetic abnormality in childhood acute lymphoblastic leukemia (ALL). A study was conducted to investigate the frequency and prognostic significance of TEL/AML-1 fusion gene resulting from a cryptic t(12;21)(p13;q22). Bone marrow samples from 86 patients diagnosed over the past 5 years at Columbus Children's Hospital were analyzed by fluorescence in situ hybridization (FISH) technique for TEL/AML-1 fusion gene, using LSI((R)) DNA probes. The positive cases were analyzed for clinical outcome. Patients in this study received treatment according to Children's Cancer Group (CCG) protocols. Fifteen of the 86 cases (17%) were positive for the fusion gene. All were B-cell lineage and except for one, all were CD10 positive. TEL/AML-1 was not found in any T-cell ALL. The mean overall survival (OS) following diagnosis for the TEL/AML-1-positive group was significantly longer than for the TEL/AML-1-negative group by log-rank = 7.84, P = 0.005. Similarly, the event-free survival (EFS) after remission for the positive group (median 94.5 months) was longer than the negative group (median 57 months) by log-rank = 7.19, P = 0.007. This study confirms that the TEL/AML-1 fusion gene may be the most common genetic event in childhood ALL, occurring in 17% of the patients. It appears restricted to the B-cell lineage. In this study, the presence of a TEL/AML-1 fusion gene was statistically significant in predicting both OS and EFS, indicating a favorable clinical outcome for these patients. Screening for TEL/AML-1 should become routine at diagnosis and a useful biological variable for risk stratification in future clinical trials.
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PMID:TEL/AML-1 fusion gene. its frequency and prognostic significance in childhood acute lymphoblastic leukemia. 1110 14

We report a case of primary effusion lymphoma (PEL) in a 75-year-old woman without human immunodeficiency virus or hepatitis C virus, which presented as fever, chest pain, and pericardial effusion. The lymphoma cells were positive for CD20 and CD79a, and were negative for CD3 and CD10. Genomic human herpes virus 8 (HHV-8) and Epstein-Barr virus were not detected in the lymphoma cells. Cytogenetic analysis showed complex abnormalities by the G-banding technique, and spectral karyotyping (SKY) analysis provided more detailed characterization of the chromosomal aberrations, including t(1;22)(q21;q11) and t(14;17)(q32;q23). We did not detect C-MYC gene rearrangement or BCL-2 expression. She was treated successfully with six courses of the CHOP regimen. The present case demonstrated a rare category of PEL that is not associated with HHV-8 or C-MYC gene rearrangement. In addition, SKY analysis disclosed cryptic chromosomal abnormalities involving 1q21 and 17q23.
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PMID:Primary effusion lymphoma of the pericardial cavity carrying t(1;22)(q21;q11) and t(14;17)(q32;q23). 1558 55

Structural rearrangements involving the short arm of chromosome 12 are common in acute lymphoblastic leukemia (ALL) and often involve the TEL locus at 12p13. The balanced t(12;17)(p13;q12) is a rare but recurrent aberration in ALL. Whereas the TEL gene has been postulated as a likely candidate for involvement in the t(12;17), the precise molecular consequences of this translocation have not yet been elucidated. We identified a t(12;17) in 2 of 398 childhood ALL patients karyotyped at presentation in our institute. Both cases had a precursor-B immunophenotype and were CD10 negative and CD33 positive. Fluorescence in situ hybridization excluded involvement of the TEL locus in the t(12;17) and provided no evidence for concomitant cryptic deletion of the 12p commonly deleted region. Comparison of these and previously published cases demonstrates that the translocation predominately occurs in children and young adults with precursor B-ALL and is typically characterized by low CD10 expression and high CD33 expression. Our data support the involvement of a new locus telomeric to TEL in the pathogenesis of t(12;17)-positive ALL.
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PMID:A t(12;17)(p13;q12) identifies a distinct TEL rearrangement-negative subtype of precursor-B acute lymphoblastic leukemia. 1649 May 98

Innate immunity is vital for protection from microbes and is mediated by humoral effectors, such as cytokines, and cellular immune defenses, including phagocytic cells (e.g., macrophages). After internalization by phagocytes, microbes are delivered into a phagosome, a complex intracellular organelle with a well-established and important role in microbial killing. However, the role of this organelle in cytokine responses and microbial sensing is less well defined. In this study, we assess the role of the phagosome in innate immune sensing and demonstrate the critical interdependence of phagocytosis and pattern recognition receptor signaling during response to the Gram-positive bacteria Staphylococcus aureus. We show that phagocytosis is essential to initiate an optimal MyD88-dependent response to Staphylococcus aureus. Prior to TLR-dependent cytokine production, bacteria must be engulfed and delivered into acidic phagosomes where acid-activated host enzymes digest the internalized bacteria to liberate otherwise cryptic bacterial-derived ligands that initiate responses from the vacuole. Importantly, in macrophages in which phagosome acidification is perturbed, the impaired response to S. aureus can be rescued by the addition of lysostaphin, a bacterial endopeptidase active at neutral pH that can substitute for the acid-activated host enzymes. Together, these observations delineate the interdependence of phagocytosis with pattern recognition receptor signaling and suggest that therapeutics to augment functions and signaling from the vacuole may be useful strategies to increase host responses to S. aureus.
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PMID:Phagocytosis and phagosome acidification are required for pathogen processing and MyD88-dependent responses to Staphylococcus aureus. 2048 52

Rearrangements of the mixed lineage leukemia (MLL) gene at 11q23 commonly occur in infants with CALLA negative B lymphoblastic leukemia (B-ALL). Most often, these are detected by conventional karyotyping; however, fluorescent in-situ hybridization (FISH) with the help of a dual-color break-apart probe is used to identify cryptic translocations. When there is an MLL gene translocation, the usual FISH signal pattern is 1 red-1 green-1 yellow fusion signal pattern. We present a case of an infant with CALLA negative precursor B-ALL with a characteristic translocation t(4;11) (q21;q23), however, with an unusual MLL FISH signal pattern.
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PMID:CALLA negative precursor B lymphoblastic leukemia with MLL gene translocation and an unusual FISH signal pattern. 2139 11


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