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Altered brain protein expression profiles are associated with molecular neurological dysfunction in the PKU mouse model.

Imperlini E, Orrù S, Corbo C, Daniele A, Salvatore F - J. Neurochem. (2014)

Bottom Line: Our results indicate that differential expression of these proteins may be associated with the processes underlying PKU brain dysfunction, namely, decreased synaptic plasticity and impaired neurotransmission.We identified a set of proteins whose expression is affected by hyperphenylalaninemia.These findings finally confirm that alteration in synaptic function, in transmission and in energy metabolism underlie brain damage provoked by hyperphenylalaninemias.

View Article: PubMed Central - PubMed

Affiliation: IRCCS SDN-Foundation, Naples, Italy.

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Related in: MedlinePlus

Expression of Glu2/3 and NR1 receptor subunits in PKU mouse brain. (a) Representative western blot analyses of Glu2/3 and NR1 receptor subunits performed on total protein extracts of wild-type (WT), heterozygous (HTZ PKU), and homozygous (HMZ PKU) mouse brains; Gapdh was used as loading control. (b) Densitometric analysis of Glu2/3 and NR1 receptor subunit expression performed on three independent replicates. The y-axis shows the optical density of protein expression. The results are shown as means ± SD.
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fig06: Expression of Glu2/3 and NR1 receptor subunits in PKU mouse brain. (a) Representative western blot analyses of Glu2/3 and NR1 receptor subunits performed on total protein extracts of wild-type (WT), heterozygous (HTZ PKU), and homozygous (HMZ PKU) mouse brains; Gapdh was used as loading control. (b) Densitometric analysis of Glu2/3 and NR1 receptor subunit expression performed on three independent replicates. The y-axis shows the optical density of protein expression. The results are shown as means ± SD.

Mentions: We also evaluated the protein levels of the Glu2/3 α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit and the NMDA receptor subunit NR1 in the control and PKU mouse brain extracts. Western blot and densitometric analyses showed that the expressions of the Glu2/3 and NR1 receptor subunits were significantly up-regulated in PKU mouse brain (Fig. 6a and b).


Altered brain protein expression profiles are associated with molecular neurological dysfunction in the PKU mouse model.

Imperlini E, Orrù S, Corbo C, Daniele A, Salvatore F - J. Neurochem. (2014)

Expression of Glu2/3 and NR1 receptor subunits in PKU mouse brain. (a) Representative western blot analyses of Glu2/3 and NR1 receptor subunits performed on total protein extracts of wild-type (WT), heterozygous (HTZ PKU), and homozygous (HMZ PKU) mouse brains; Gapdh was used as loading control. (b) Densitometric analysis of Glu2/3 and NR1 receptor subunit expression performed on three independent replicates. The y-axis shows the optical density of protein expression. The results are shown as means ± SD.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4286000&req=5

fig06: Expression of Glu2/3 and NR1 receptor subunits in PKU mouse brain. (a) Representative western blot analyses of Glu2/3 and NR1 receptor subunits performed on total protein extracts of wild-type (WT), heterozygous (HTZ PKU), and homozygous (HMZ PKU) mouse brains; Gapdh was used as loading control. (b) Densitometric analysis of Glu2/3 and NR1 receptor subunit expression performed on three independent replicates. The y-axis shows the optical density of protein expression. The results are shown as means ± SD.
Mentions: We also evaluated the protein levels of the Glu2/3 α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit and the NMDA receptor subunit NR1 in the control and PKU mouse brain extracts. Western blot and densitometric analyses showed that the expressions of the Glu2/3 and NR1 receptor subunits were significantly up-regulated in PKU mouse brain (Fig. 6a and b).

Bottom Line: Our results indicate that differential expression of these proteins may be associated with the processes underlying PKU brain dysfunction, namely, decreased synaptic plasticity and impaired neurotransmission.We identified a set of proteins whose expression is affected by hyperphenylalaninemia.These findings finally confirm that alteration in synaptic function, in transmission and in energy metabolism underlie brain damage provoked by hyperphenylalaninemias.

View Article: PubMed Central - PubMed

Affiliation: IRCCS SDN-Foundation, Naples, Italy.

Show MeSH
Related in: MedlinePlus