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Pieter Dikkes

Researcher at Harvard University

Publications -  43
Citations -  8802

Pieter Dikkes is an academic researcher from Harvard University. The author has contributed to research in topics: Corticotropin-releasing hormone & Sciatic nerve. The author has an hindex of 31, co-authored 43 publications receiving 8530 citations. Previous affiliations of Pieter Dikkes include Boston Children's Hospital & Tufts University.

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Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration

TL;DR: It is found that p25, a truncated form of p35, accumulates in neurons in the brains of patients with Alzheimer's disease, and this accumulation correlates with an increase in Cdk5 kinase activity.
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p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours

TL;DR: It is shown that mice functionally deficient for all p73 isoforms exhibit profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways, and there is a marked divergence in the physiological functions of the p53 family members.
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Mice Lacking p35, a Neuronal Specific Activator of Cdk5, Display Cortical Lamination Defects, Seizures, and Adult Lethality

TL;DR: It is demonstrated here that p35, the neuronal-specific activator of cyclin-dependent kinase 5, plays a key role in proper neuronal migration and demonstrates that the formation of cortical laminar structure depends on the action of the p35/cdk5 kinase.
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A Critical Role for DNA End-Joining Proteins in Both Lymphogenesis and Neurogenesis

TL;DR: These findings demonstrate that differentiating lymphocytes and neurons strictly require the XRCC4 and DNA ligase IV end-joining proteins and point to the general stage of neuronal development in which these proteins are necessary.
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Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A.

TL;DR: The characterization of a regulatory NMDAR subunit, NR3A, is reported, which is expressed primarily during brain development and suggested to be involved in the development of synaptic elements by modulating N MDAR activity.