Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:Q8NB91 (FAB)
 3,573 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The p10 murine leukemia virus (MuLV) protein is a basic single-stranded nucleic acid binding protein encoded by the extreme 3' region of the gag gene of MuLV type C. It contains the Cys-X2-Cys-X4-His-X4-Cys sequence shared by all retroviral gag polyproteins. A similar sequence is found in the gene 32 single-stranded DNA binding protein of bacteriophage T4 and is believed to be the zinc binding region of the protein. Solid phase synthesis of p10 was carried out based on the known primary structure of the native protein, with the exception that the acetamidomethyl (Acm) derivative of cysteine was incorporated at all three cysteine positions. The structure of the synthetic p10 was confirmed by direct amino-acid sequencing, as well as by amino acid analysis and FAB mass spectrometry of endoproteinase Lys-C peptides derived from p10. A Chou and Fasman analysis of the primary sequence predicts that p10 contains 9% beta strand and/or sheet and 36% alpha helix. Circular dichroism experiments carried out on the Acm derivatized peptide gave somewhat different results, in that they suggest that p10 contains approximately 70% random coil, less than 30% beta strand and/or sheet and less than 10% alpha helix. With a Ka of greater than 10(8) M-1 for single-stranded RNA, the synthetic peptide binds as tightly as the p10 protein does when isolated directly from infected HTG-2 cells. The Acm groups can be removed from the synthetic p10 peptide by the use of mercuric acetate, followed by treatment with dithiothreitol to sequester the mercuric ion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthesis of the p10 single-stranded nucleic acid binding protein from murine leukemia virus. 285 55

The chromosome der(1;7)(q10;p10) consists of the short arm of chromosome 7 and the long arm of chromosome 1, and is a common abnormality in treatment-related leukemia and myelodysplastic syndrome. Here we describe a 39-year-old Japanese man with acute myeloblastic leukemia (FAB-M2) exhibiting t(8;21)(q22;q22). He entered complete remission after induction therapy, and intensification therapy including alkylating agents was subsequently continued for 3 years. The patient then developed pancytopenia; bone marrow aspiration revealed myelodysplastic syndrome exhibiting the der (1;7) chromosome. To our knowledge, this is the first reported case of such an abnormality in myelodysplastic syndrome secondary to acute myeloblastic leukemia with the 8;21 translocation.
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PMID:Unbalanced 1;7 translocation in myelodysplastic syndrome following treatment of acute myeloblastic leukemia with an 8;21 translocation. 819 45

A 42-year-old woman with Crow-Fukase syndrome developed acute myeloid leukemia (M6: FAB classification) following treatment with alkylating agents (a total of 2,500 mg of melphalan and 9,800 mg of cyclophosphamide). Chromosome analysis of the bone marrow showed 49,XX,der(1;7)(q10;p10), +8, +19, +21 in therapy-related myelodysplastic syndrome with additional chromosomes 8, and 12 and two additional chromosomes 21 in acute leukemia. Because of the risk of therapy-related leukemia, alkylating agents should be used with caution in the treatment of Crow-Fukase syndrome.
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PMID:Development of secondary leukemia associated with (1;7)(q10;p10) in a patient with Crow-Fukase syndrome. 889 44

A rare association of der(1;7)(q10;p10) with de novo acute erythroblastic leukemia (AML-M6) in a 63-year-old male is reported. While this unbalanced 1;7 translocation, der(1;7), has been reported often in therapy-related myelodysplastic syndrome (t-MDS) or therapy-related acute myeloid leukemia (t-AML), its associations with de novo AML-FAB-M6 have rarely been reported. Although der(1;7) has been reported as a cytogenetic factor for poor prognosis in t-MDS/AML, our patient showed a good response to chemotherapy and obtained complete remission, although longer observation is required to evaluate the prognosis.
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PMID:Derivative (1;7)(q10;p10) in a patient with de novo acute erythroblastic leukemia (AML-M6). 1056 2

Sex chromosomes are infrequently involved in patients with hematologic malignancies. In most instances, the abnormality is either duplication in the q arm or deletion and translocation involving the q13 and q24 regions. We report herein a rare translocation t(X;10)(p10;p10) in a newborn with 2 months and 20 days with acute myeloid leukemia (AML) (FAB, M4). Cytogenetic analysis detected a cell clone with t(X;10)(p10;p10). Thus was confirmed by FISH analysis with whole chromosome painting (WCP) specific for chromosomes X and 10. The patient was treated with chemotherapy, and a complete morphologic and cytogenetic remission was achieved. To our knowledge, our case is the first report of a neonatal AML4 with t(X; 10). The patient had an excellent early response to a salvage AML-type therapy. The prognostic significance of the t(X; 10) in this setting remains unclear. Due to the rarity of this translocation, further cytogenetic and molecular biologic studies are required to elucidate the clinical and molecular significance of this unusual karyotypic finding.
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PMID:Translocation t(X;10)(p10;p10): a rare chromosomal abnormality in a new born female with acute myeloid leukemia. 2144 16