Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

WEHI-231 is a murine B cell lymphoma that has been used extensively as a model for the immature stage B cell and its functional response to Ag receptor cross-linking as a model for immature B cell tolerance. This cell line expresses sIgM, CD5, and FcR gamma, but lacks the B cell-specific isoform of CD45 (B220). This study demonstrates for the first time that WEHI-231, in contrast to classically defined immature B cells, expresses delta on its surface. Analysis of delta on WEHI-231 revealed structural differences with respect to that on BAL-17 or primary splenic B cells. Although the m.w. of delta on the latter two B cell populations was similar, delta on WEHI-231 manifested a marked increase in its apparent m.w. deduced by SDS-PAGE. This difference was found to be due primarily to differential N-linked glycosylation. Signal transduction through the endogenous sIgD on WEHI-231 was investigated. In contrast to cross-linking of sIgM, cross-linking of the endogenous surface IgD on WEHI-231 was unable to generate a negative growth response in these cells. This inability may be due to uncoupling from normal surface Ig signaling pathways. The signaling properties of the endogenous sIgD on WEHI-231 differ from that on primary B cells and other sIgD-expressing cell lines. Whereas sIgD on splenic B lymphocytes or the mature B cell line BAL-17 is coupled to inositol phospholipid hydrolysis and calcium mobilization, cross-linking of sIgD on WEHI-231 failed to elicit these events, although induced changes in tyrosine phosphorylation were observed. Thus, endogenous expression of surface IgD on WEHI-231 is inconsistent with its representing the classically defined immature stage B cell. The structural and signaling differences associated with delta on these cells suggest the potential for developmentally regulated delta function and model for study of sIgD signal transduction.
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PMID:Endogenous expression of delta on the surface of WEHI-231. Characterization of its expression and signaling properties. 840 28

The aim of this study was to investigate the clinical, pathological and biological features of biphenotypic acute leukemia. The morphology of tumor cells was observed by bone marrow examination; the immunophenotype was assayed by flow cytometry and immunohistochemistry; the chromosomal aberrations were detected by conventional chromosomal analysis and RT-multiplex nested PCR. The results showed that extramedullary skin lesions and myelodysplasia occurred before the onset of overt disease. At the time of diagnosis, this case had more than 30% blasts in bone marrow with meningeal involvement. Large-sized tumor cells predominated morphologically over other cells. Flow cytometry revealed the co-expression of myeloid antigens (cMPO, CD33 and CD117) and T-lymphoid antigens (cCD3, CD5, CD7, dual expression of CD4 and CD8). Immunohistochemical staining showed that CD43 and CD99 were strong positive which define the earliest hematopoietic progenitors. Partial tandem duplication of the MLL gene could be detected with normal cytogenetic method. All above-mentioned results led to the diagnosis of biphenotypic acute leukemia. It is concluded that the biphenotypic acute leukemia is an uncommon type of leukemia which may be preceded by myelodysplastic syndrome and has aggressive clinical and biological behavior. Immunophenotype, cytogenetics and molecular analysis can contribute to early diagnosis of BAL and evaluation of prognosis.
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PMID:[Skin lesions and myelodysplastic syndrome as initial manifestations of biphenotypic acute leukemia]. 1795 70