Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Behavioral and movement disorders may have antibody responses where mimicry and signal transduction may lead to neuropsychiatric abnormalities. In our study, antibodies in pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS) reacted with the neuronal cell surface and caudate-putamen and induced calcium-calmodulin dependent protein (CaM) kinase II activity in neuronal cells. Depletion of serum IgG abrogated CaM kinase II cell signaling and reactivity of CSF was blocked by streptococcal antigen N-acetyl-beta-d-glucosamine (GlcNAc). Antibodies against GlcNAc in PANDAS sera were inhibited by lysoganglioside G(M1). Results suggest that antibodies from an infection may signal neuronal cells in some behavioral and movement disorders.
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PMID:Antibody-mediated neuronal cell signaling in behavior and movement disorders. 1687 42

In songbirds, an anterior forebrain pathway has been implicated in vocal learning. Within Area X, the striatal-pallidal component of this forebrain pathway, early social tutoring dramatically increases the autophosphorylation of CaMKII (calcium-calmodulin-dependent protein kinase II). Activation of CaMKII often is associated with forms of synaptic plasticity (e.g. LTP) underlying learning and memory, and electrophysiological studies have demonstrated NMDA and dopamine (DA) receptor-dependent LTP among Area X medium spiny neurons [Ding, L., Perkel, D.J., 2002. Dopamine modulates excitability of spiny neurons in the avian Basal Ganglia. J. Neurosci. 22, 5210-5218]. Together, these data suggest that Area X neurons may help to encode a representation of song used for vocal mimicry. To identify which Area X neurons could participate in the CaMKII response to song tutoring, we used immunocytochemistry to assess the colocalization of CaMKII with several other biochemical markers that identify specific neuron classes within Area X. Virtually all (approximately 98%) Area X cells expressing CaMKII also expressed DARPP-32 (dopamine- and adenosine 3'5'-monophosphate-regulated phosphoprotein), a dopamine signaling protein enriched in medium spiny striatal neurons. The implication that medium spiny neurons are primary mediators of the pCaMKII response to tutoring is interesting in view of the established dopaminergic modulation of LTP in this cell type. Additionally, BrdU and DARPP-32 immunocytochemistry were combined to test whether medium spiny neurons are among the neurons generated and incorporated into Area X during song learning. Based upon their expression of DARPP-32, the majority of Area X neurons labeled by BrdU injections given on posthatch days 20-25 are medium spiny neurons.
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PMID:Characterization of CaMKII-expressing neurons within a striatal region implicated in avian vocal learning. 1749 95

The molecular mechanisms underlying migraine pain remain unclear and probably require sustained facilitation in pain-sensing P2X(3) receptors gated by extracellular ATP in nociceptive sensory neurons. The major migraine mediator calcitonin gene-related peptide (CGRP) is known to sensitize P2X(3) receptors to increase impulse flow to brainstem trigeminal nuclei. This process is mediated via changes in the expression and function of P2X(3) receptors initially through enhanced trafficking and, later, perhaps through augmented synthesis of P2X(3) receptors. To clarify the mechanisms responsible for CGRP-evoked long lasting alterations in P2X(3) receptors, we used as a model mouse trigeminal ganglion neurons in culture. CGRP activated Ca(2+)-calmodulin-dependent kinase II, which became localized to the perimembrane region and neuronal processes, a phenomenon already apparent after 30 min and accompanied by a parallel increase in cAMP-response element-binding protein (CREB) phosphorylation and nuclear translocation. These effects triggered increased P2X(3) receptor transcription and were prevented by expressing a dominant negative form of CREB. Increased P2X(3) receptor synthesis was partly mediated by endogenous brain-derived neurotrophic factor (BDNF) because of its block by anti-BDNF antibodies and mimicry by exogenous BDNF. Immunocytochemistry experiments indicated distinct subpopulations of BDNF- or CGRP-sensitive trigeminal neurons with only partial overlap. The present data indicate a novel mechanism for enhancing P2X(3) receptor expression and function in trigeminal sensory neurons by CGRP via CREB phosphorylation. BDNF was an intermediate to extend the sensitizing effect of CGRP also to CGRP-insensitive neurons. This combinatorial action could serve as a powerful process to amplify and prolong pain mediated by P2X(3) receptors.
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PMID:Mechanisms mediating the enhanced gene transcription of P2X3 receptor by calcitonin gene-related peptide in trigeminal sensory neurons. 1846 Apr 69