1996 Fiscal Year Final Research Report Summary
Expression of the Id helix-loop-helix proteins in human myeloid and lymphoid cells
| Project/Area Number |
07670899
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Teikyo University |
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Principal Investigator |
ISHIGURO Akira Teikyo university, School of Medicine, Department of Pediatrics, Assistant Professor, 医学部, 講師 (90222984)
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| Co-Investigator(Kenkyū-buntansha) |
INABA Yuji Teikyo university, School of Medicine, Department of Pediatrics, Medical Staff, 医学部, 助手 (70266310)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Id / helix-loop-helix protein / transcription factor / differentiation / mycloid leukemia / lymphocytes / human T-cell leukemia virus |
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| Research Abstract |
Id proteins are helix-loop-helix transcriptional factors that lack the basic DNA binding domain. The Id proteins have been generally reported to function as an inhibitor of cell differentiation. We examined the expression of mRNAs encoding human Id1, Id2 and Id3 by Northern hybridization in human mycloid and lymphoid cells. Mycloid leukemia cells with monoblastic and crythroid characteristics expressed Id2 mRNA.The levels of Id2 mRNA markedly increased with induction of differentiation of the mycloid blasts toward both granulocytes and macrophages. Increascs in Id2 mRNA expression were found in more differentiated blasts in fresh AML samples. In normal mycloid cells, Id2 mRNA was expressed cultured macrophages from bone marrow, and in mature granulocytes and monocytes from peripheral blood. Only small numbers of mycloid cells expressed mRNAs for Id1 (K562 crythroid mycloid cells) and Id3 (U-937 and THP-1 monoblastic cells). In contrast, cells from B-and T-cell lines expressed Id2 and/or Id3 mRNAs. Human T-cell leukemia virus-transformed cells prominently expressed only Id2 mRNA.Upon PHA-stimulation of blood normal lymphocytes, Id2 expression decreased and Id3 mRNA levels were up-regulated. These results show that Id2 protein may contribute to mycloid differentiation, and both Id2 and Id3 proteins may be involved in a pathway that controls lymphoid activation.
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