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Induction of erythroid differentiation in murine erythroleukemic cells by short chain aliphatic carbonyl compounds and their corresponding precursors
Author(s) -
Malinin George I.,
Ebert Paul S.
Publication year - 1980
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(80)81101-x
Subject(s) - chemistry , stereochemistry , microbiology and biotechnology , biology
Proerythroblastoid murine erythroleukemic (MEL) cells may be induced to differentiate along the erythroid pathway by avariety of chemical agents [l-5]. The state of erythroid differentiation is recognized unequivocally by increased hemoglobin synthesis and concomitant morphological changes [ 5,6]. While the precise nature or the cellular receptor sites of the erythroid differentiation induction signal remain undetermined [ 1,3], it has been suggested that the cell membrane may be the initiation site [ 1,3] as evidenced by changes of certain cell membrane-related functions [7,8]. We have shown recently that SeOz and H$eOa trigger erythroid differentiation of MEL cells [3] and suggested further, that possible oxidation by SeOz of endogenous membrane carbonyls into dicarbonyls may have initiated erythroid differentiation of MEL cells. If endogenous carbonyls are triggering differentiation, then it may be possible that selected exogenous aliphatic carbonyl compounds may likewise initiate erythroid differentiation of MEL cells. Moreover, any precursor which can be metabolized to its corresponding carbonyl derivative should also act as an inducer or erythroid differentiation.