The Hormonal Regulation of Purine Biosynthesis: Control of the Inosinic acid Branch Point

Author(s):  
Maria Pizzichini ◽  
Anna Di Stefano ◽  
Giuseppe Pompucci ◽  
Enrico Marinello
1985 ◽  
Vol 19 (7) ◽  
pp. 770-770
Author(s):  
Maria Pizzichini ◽  
Anna Di Stefano ◽  
Giuseppe Pompucci ◽  
Enrico Marinello

Author(s):  
M. Pizzichini ◽  
A. Di Stefano ◽  
G. Bruni ◽  
R. Leoncini ◽  
E. Marinello

1988 ◽  
Vol 24 (1) ◽  
pp. 130-130
Author(s):  
Maria Pizzichini ◽  
Anna Di Stefano ◽  
Germano Resconi ◽  
Enrico Marinello

1968 ◽  
Vol 14 (1) ◽  
pp. 39-44 ◽  
Author(s):  
J. de Repentigny ◽  
L. G. Mathieu ◽  
S. Turgeon ◽  
S. Sonea

Growth inhibition by adenine or adenosine and its reversal by other purines were quantitatively different in the four Staphylococcus aureus strains we have studied. After 11 hours, 0.25 μmole/ml adenine or adenosine reduced growth by 6 and 4%, respectively, in the coagulase-negative SA-13 strain, by 35 and 35% in the tryptophan-dependent Smith strain, by 68 and 98% in a Wood 46 thymineless mutant strain, and by 40 and 37% in the parent Wood 46 strain. Normal growth in the presence of adenine or adenosine was restored in most cases by guanine, guanosine, hypoxanthine, inosine, and inosinic acid. However, for the thymineless mutant strain, guanine and inosine were much less effective in this respect in the presence of adenine, and none of these purines could reverse the inhibitory effect of adenosine. Purine analogs were mostly ineffective in inhibiting or in restoring growth. Our observations indicate that some patterns of purine biosynthesis and utilization in Staphylococcus aureus are different from those already known in other bacterial species. Adenine or adenosine had a greater inhibitory effect on the growth of coagulase-positive strains than on that of the coagulase-negative strain.


1989 ◽  
Vol 21 (05) ◽  
pp. 287-289 ◽  
Author(s):  
M. Pizzichini ◽  
A. Di Stefano ◽  
G. Resconi ◽  
E. Marinello

1972 ◽  
Vol 71 (2_Suppla) ◽  
pp. S346-S368 ◽  
Author(s):  
Roger W. Turkington ◽  
Nobuyuki Kadohama

ABSTRACT Hormonal activation of gene transcription has been studied in a model system, the mouse mammary gland in organ culture. Transcriptive activity is stimulated in mammary stem cells by insulin, and in mammary alveolar cells by prolactin and insulin. Studies on the template requirement for expression of the genes for milk proteins demonstrate that DNA methylation has an obligatory dependence upon DNA synthesis, but is otherwise independent from hormonal regulation of mammary cell differentiation. Incorporation of 5-bromo-2′deoxyuridine into DNA selectively inhibits expression of the genes for specific milk proteins. Undifferentiated mammary cells activate the synthesis of specific acidic nuclear proteins when stimulated by insulin. Several of these induced acidic nuclear proteins are undetectable in unstimulated undifferentiated cells, but appear to be characteristic components of the nuclei of differentiated cells. These results indicate that mammary cell differentiation is associated with a change in acidic nuclear proteins, and they provide evidence to support the concept that acidic nuclear proteins may be involved in the regulation of gene transcription and of mammary cell differentiation.


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