Редактирование: FOXP2

Forkhead box protein P2 (CAG repeat protein 44) (Trinucleotide repeat-containing gene 10 protein) [CAGH44] [TNRC10]

==Publications==

{{medline-entry
|title=Identification of the neurotransmitter profile of AmFoxP expressing neurons in the honeybee brain using double-label in situ hybridization.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30400853
|abstract=FoxP transcription factors play crucial roles for the development and function of vertebrate brains. In humans the neurally expressed FOXPs, [[FOXP1]], [[FOXP2]], and [[FOXP4]] are implicated in cognition, including language. Neural FoxP expression is specific to particular brain regions but FoxP1, FoxP2 and FoxP4 are not limited to a particular neuron or neurotransmitter type. Motor- or sensory activity can regulate FoxP2 expression, e.g. in the striatal nucleus Area X of songbirds and in the auditory thalamus of mice. The DNA-binding domain of FoxP proteins is highly conserved within metazoa, raising the possibility that cellular functions were preserved across deep evolutionary time. We have previously shown in bee brains that FoxP is expressed in eleven specific neuron populations, seven tightly packed clusters and four loosely arranged groups. The present study examined the co-expression of honeybee FoxP (AmFoxP) with markers for glutamatergic, GABAergic, cholinergic and monoaminergic transmission. We found that AmFoxP could co-occur with any one of those markers. Interestingly, AmFoxP clusters and AmFoxP groups differed with respect to homogeneity of marker co-expression; within a cluster, all neurons co-expressed the same neurotransmitter marker, within a group co-expression varied. We also assessed qualitatively whether age or housing conditions providing different sensory and motor experiences affected the AmFoxP neuron populations, but found no differences. Based on the neurotransmitter homogeneity we conclude that AmFoxP neurons within the clusters might have a common projection and function whereas the AmFoxP groups are more diverse and could be further sub-divided. The obtained information about the neurotransmitters co-expressed in the AmFoxP neuron populations facilitated the search of similar neurons described in the literature. These comparisons revealed e.g. a possible function of AmFoxP neurons in the central complex. Our findings provide opportunities to focus future functional studies on invertebrate FoxP expressing neurons. In a broader context, our data will contribute to the ongoing efforts to discern in which cases relationships between molecular and phenotypic signatures are linked evolutionary.
|mesh-terms=* Aging
* Animals
* Bees
* Brain
* Forkhead Transcription Factors
* In Situ Hybridization
* Insect Proteins
* Neurons
* Neurotransmitter Agents
|keywords=* Acetylcholine
* Deep homology
* FoxP
* FoxP1
* GABA
* Glutamate
* Honeybee
* In situ hybridization
* Monoamine
* Songbird
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219247
}}
{{medline-entry
|title=Human skin keratinocytes can be reprogrammed to express neuronal genes and proteins after a single treatment with decitabine.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/23741634
|abstract=Patient-specific cell replacement therapy is fast becoming the future of medicine, requiring safe, effective methods for reprogramming a patient's own cells. Previously, we showed that a single transient transfection with a plasmid encoding Oct4 was sufficient to reprogram human skin keratinocytes (HSKs), and that this transfection resulted in a decrease in global DNA methylation. In more recent work we showed that decreasing global DNA methylation using the U.S. Food and Drug Administration-approved cancer treatment drug decitabine was sufficient to induce expression of endogenous Oct4. Here we report that a single treatment with decitabine, followed by 5 days in a defined neuronal transformation medium, then 7 days in a neuronal maintenance medium is sufficient to convert HSKs into cells that change their morphology substantially, gain expression of neuronal markers, and lose expression of keratinocyte markers. Within 1 week of treatment the cells express mRNA for β3-tubulin and doublecortin, and at the end of 2 weeks express mRNA for NeuN, [[FOXP2]], and [[NCAM1]]. Additionally, at the end of this protocol, neurofilament-1, nestin, synapsin, [[FOXP2]], and GluR1 proteins are detectable by immunostaining. Thus, we demonstrate a simple method that begins the process for producing cells for cell replacement therapies without using exogenously introduced DNA.

|keywords=* aging
* regeneration
* stem cells
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666219
}}