p(RGD:Cdk5r2)
p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169
p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169
p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169
p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169
p39, but not p35, is selectively upregulated by histone acetylation-mediated transcription, underlying the robust increase of Cdk5 activity during rat and mouse neuronal differentiation. Loss of p39 attenuates Cdk5 activity in neurons and preferentially affects phosphorylation of specific Cdk5 targets, leading to aberrant axonal growth and impaired dendritic spine and synapse formation. PubMed:27807169
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.