Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems

Cesca, Fabrizia; Yabe, A; Spencer‐Dene, Bradley; Scholz‐Starke, Joachim; Medrihan, Lucian; Maden, Charlotte H.; Gerhardt, Holger; Orriss, Isabel R.; Baldelli, Pietro; AlQatari, Mona; Koltzenburg, M; Adams, Ralf H.; Benfenati, Fabio; Schiavo, Giampietro

doi:10.1038/cdd.2011.141

Cited by 64 publications

(147 citation statements)

References 38 publications

(69 reference statements)

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“…Primary cortical cultures were prepared from mouse C57BL/6J (E17-E18) embryos as previously described (48). All experiments were carried out in accordance with the guidelines established by the European Communities Council (Directive 2010/63/EU of 22 September 2010) and were approved by the Italian Ministry of Health.…”

Section: Methodsmentioning

confidence: 99%

Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor

Paonessa

Criscuolo

Sacchetti

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Optogenetics provides new ways to activate gene transcription; however, no attempts have been made as yet to modulate mammalian transcription factors. We report the light-mediated regulation of the repressor element 1 (RE1)-silencing transcription factor (REST), a master regulator of neural genes. To tune REST activity, we selected two protein domains that impair REST-DNA binding or recruitment of the cofactor mSin3a. Computational modeling guided the fusion of the inhibitory domains to the light-sensitive Avena sativa lightoxygen-voltage-sensing (LOV) 2-phototrophin 1 (AsLOV2). By expressing AsLOV2 chimeras in Neuro2a cells, we achieved light-dependent modulation of REST target genes that was associated with an improved neural differentiation. In primary neurons, light-mediated REST inhibition increased Na + -channel 1.2 and brain-derived neurotrophic factor transcription and boosted Na + currents and neuronal firing. This optogenetic approach allows the coordinated expression of a cluster of genes impinging on neuronal activity, providing a tool for studying neuronal physiology and correcting gene expression changes taking place in brain diseases.

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Section: Methodsmentioning

confidence: 99%

Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor

Paonessa

Criscuolo

Sacchetti

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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“…In the present study, we investigated the role of the scaffold protein Kidins220 in the regulation of neuronal excitability using embryonal hippocampal neurons isolated from the previously described Kidins220 Ϫ/Ϫ full knock-out mice (16). Current-clamp recordings revealed increased excitability in GABAergic and, to a lower extent, in glutamatergic Kidins220 Ϫ/Ϫ neurons.…”

Section: Discussionmentioning

confidence: 99%

“…Generation of Kidins220 Ϫ/Ϫ Mice and Primary Hippocampal Cultures-The generation of the Kidins220 Ϫ/Ϫ strain was described in a previous study (16). All embryos used in this study were obtained from crosses of Kidins220 ϩ/Ϫ mice in the C57BL/6 background.…”

Section: Methodsmentioning

confidence: 99%

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Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels

Cesca

Satapathy

Ferrea

et al. 2015

Journal of Biological Chemistry

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Background: Tight regulation of ion channel activity is essential for neuronal function. Results: The scaffold protein Kidins220 associates with brain voltage-gated sodium channels and modulates their activity. Conclusion: Lack of Kidins220 in mice causes deregulated sodium channel function in inhibitory neurons, ultimately leading to impaired network excitability. Significance: Kidins220 may help maintain the balance between excitation and inhibition in neural networks.

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“…Perturbation of its expression led to aberrant dendrite formation and extension of multiple aberrant axons (Higuero 2010). Transgenic studies showed that Kidins220 -/-embryos displayed early embryonic lethality, and adult Kidins220 +/-mice showed defects in dendritic growth and branching (Wu et al, 2009;Cesca et al, 2012). Other studies have shown that Kidins220 localization at the neuromuscular junction (NMJ) enhances EphA4 signaling, through a-syntrophin regulation, suggesting a role in NMJ postsynaptic organization (Luo et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Kidins220/ARMS is dynamically expressed during Xenopus laevis development

Marracci

Giannini²,

Vitiello³

et al. 2013

Int. J. Dev. Biol.

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Kidins220 (Kinase D interacting substrate of 220 kDa)/ARMS (Ankyrin Repeat-rich Membrane Spanning) is a conserved scaffold protein that acts as a downstream substrate for protein kinase D and mediates multiple receptor signalling pathways. Despite the dissecting of the function of this protein in mammals, using both in vitro and in vivo studies, a detailed characterization of its gene expression during early phases of embryogenesis has not been described yet. Here, we have used Xenopus laevis as a vertebrate model system to analyze the gene expression and the protein localization of Kidins220/ARMS. We found its expression was dynamically regulated during development. Kidins220/ARMS mRNA was expressed from neurula to larval stage in different embryonic regions including the nervous system, eye, branchial arches, heart and somites. Similar to the transcript, the protein was present in multiple embryonic domains including the central nervous system, cranial nerves, motor nerves, intersomitic junctions, retinal ganglion cells, lens, otic vesicle, heart and branchial arches. In particular, in some regions such as the retina and somites, the protein displayed a differential localization pattern in stage 42 embryos when compared to the earlier examined stages. Taken together our results suggest that this multidomain protein is involved in distinct spatio-temporal differentiative events.

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Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems

Cited by 64 publications

References 38 publications

Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor

Regulation of neural gene transcription by optogenetic inhibition of the RE1-silencing transcription factor

Functional Interaction between the Scaffold Protein Kidins220/ARMS and Neuronal Voltage-Gated Na+ Channels

Kidins220/ARMS is dynamically expressed during Xenopus laevis development

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