Biomedical Engineering Reference
In-Depth Information
cytosine 154 but no peak of unmethylated cytosine (Fig.
10.5b
). The amplitude of
UV absorbance of the unextended primer for cytosine 154 was around 22, suggest-
ing a weak primer extension effi ciency (probably caused by minor amounts of PCR
product).
10.8
Pharmacological Blocking of DNA Methylation
Many neurobiologists may have strong interests in the biological signifi cance of
control of DNA methylation status in brain function. In order to study this relation-
ship, the pharmacological inhibition of DNA methylation has been utilized. In sev-
eral studies, 5-azacytidine (Fig.
10.6a
), 5-aza-2
-deoxycytidine (Fig.
10.6b
), and
zebularine (Fig.
10.6c
) were directly injected into mammalian brains or honeybee
hemolymph (Miller and Sweatt
2007
; Miller et al.
2008
; Han et al.
2010
; Lockett
et al.
2010
). However, the molecular mechanisms of the action of azacytidines have
′
Fig. 10.6
Chemical structures of DNMT and HDAC inhibitors. (
a
) 5-azacytidine , (
b
) 5-aza-2
-
deoxycytidine, (
c
) zebularine , (
d
) RG108 , (
e
) sodium butyrate, (
f
) valproic acid, (
g
) trichostatin A,
and (
h
) valpromide
′
