Title : CREB inactivation by HDAC1/PP1γ contributes to dopaminergic neurodegeneration in Parkinson's disease.

Pub. Date : 2022 Apr 29

PMID : 35501151






5 Functional Relationships(s)
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1 An MPTP mouse model was used to further elucidate the mechanism underlying CREB dephosphorylation. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine cAMP responsive element binding protein 1 Mus musculus
2 Disrupting CREB/HDAC1 interaction via either overexpression of GAL4 M1, a CREB mutant, or administration of trichostatin A, a pan-HDAC inhibitor, restored the expression levels of phospho-CREB (Ser133) and NURR1, and protected nigral dopaminergic neurons in the MPTP-treated mice brain. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine cAMP responsive element binding protein 1 Mus musculus
3 Disrupting CREB/HDAC1 interaction via either overexpression of GAL4 M1, a CREB mutant, or administration of trichostatin A, a pan-HDAC inhibitor, restored the expression levels of phospho-CREB (Ser133) and NURR1, and protected nigral dopaminergic neurons in the MPTP-treated mice brain. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine cAMP responsive element binding protein 1 Mus musculus
4 Disrupting CREB/HDAC1 interaction via either overexpression of GAL4 M1, a CREB mutant, or administration of trichostatin A, a pan-HDAC inhibitor, restored the expression levels of phospho-CREB (Ser133) and NURR1, and protected nigral dopaminergic neurons in the MPTP-treated mice brain. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine cAMP responsive element binding protein 1 Mus musculus
5 Disrupting CREB/HDAC1 interaction restored CREB activity and protected nigral dopaminergic neurons in the MPTP mouse brains. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine cAMP responsive element binding protein 1 Mus musculus