Shin JH, Weitzdoerfer R, Fountoulakis M, Lubec G.
Expression of cystathionine beta-synthase, pyridoxal kinase, and ES1 protein homolog (mitochondrial precursor) in fetal Down syndrome brain.
Neurochem Int. 2004 Jul;45(1):73-9.
PubMed.
It's of interest that Lubec et al. report increased ES1 protein homolog in the Down's syndrome fetal brain. They report no known function in humans; however, the OMIM entry by Sumazaki et al. finds HES1 encodes a basic helix-loop-helix protein that represses positive basic helix-loop-helix genes such as NEUROG3 (604882) in the animal model. An alternative title for ES1 is HES1.
Does this entry belong here, or is it more likely that the entry appear under HES1, hairy enhancer of split?
If not, then the fact that neurogenin3 may be inhibited in Down's syndrome is of interest.
Further to this, is there evidence that HES1, hairy enhancer of split, is increased in glial restricted precursors in Alzheimer's disease and Down's syndrome?
Wu et al. (1) find that overexpression of HES1 in this cell line can drive an astrocyte cell fate at the expense of oligodendrocyte differentiation.
In view of the increased astrocytic markers and reduced oligodendrocyte makers in AD, might it indicate a problem at this level?
References:
Wu Y, Liu Y, Levine EM, Rao MS.
Hes1 but not Hes5 regulates an astrocyte versus oligodendrocyte fate choice in glial restricted precursors.
Dev Dyn. 2003 Apr;226(4):675-89.
PubMed.
Comments
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It's of interest that Lubec et al. report increased ES1 protein homolog in the Down's syndrome fetal brain. They report no known function in humans; however, the OMIM entry by Sumazaki et al. finds HES1 encodes a basic helix-loop-helix protein that represses positive basic helix-loop-helix genes such as NEUROG3 (604882) in the animal model. An alternative title for ES1 is HES1.
Does this entry belong here, or is it more likely that the entry appear under HES1, hairy enhancer of split?
If not, then the fact that neurogenin3 may be inhibited in Down's syndrome is of interest.
Further to this, is there evidence that HES1, hairy enhancer of split, is increased in glial restricted precursors in Alzheimer's disease and Down's syndrome?
Wu et al. (1) find that overexpression of HES1 in this cell line can drive an astrocyte cell fate at the expense of oligodendrocyte differentiation.
In view of the increased astrocytic markers and reduced oligodendrocyte makers in AD, might it indicate a problem at this level?
References:
Wu Y, Liu Y, Levine EM, Rao MS. Hes1 but not Hes5 regulates an astrocyte versus oligodendrocyte fate choice in glial restricted precursors. Dev Dyn. 2003 Apr;226(4):675-89. PubMed.
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