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1.
RSC Adv ; 12(13): 7757-7761, 2022 Mar 08.
Artículo en Inglés | MEDLINE | ID: mdl-35424746

RESUMEN

We present a PNA microprobe sensing platform to detect trinucleotide repeat mutation by electrochemical impedance spectroscopy. The microprobe platform discriminated Huntington's disease-associated CAG repeats in cell-derived total RNA with S/N 1 : 3. This sensitive, label-free, and PCR-free detection strategy may be employed in the future to develop biosensing platforms for the detection of a plethora of repeat expansion disorders.

2.
Nat Commun ; 7: 10388, 2016 Jan 21.
Artículo en Inglés | MEDLINE | ID: mdl-26790951

RESUMEN

The molecular mechanisms underlying the ability of axons to regenerate after injury remain poorly understood. Here we show that in Caenorhabditis elegans, axotomy induces ectopic expression of serotonin (5-HT) in axotomized non-serotonergic neurons via HIF-1, a hypoxia-inducible transcription factor, and that 5-HT subsequently promotes axon regeneration by autocrine signalling through the SER-7 5-HT receptor. Furthermore, we identify the rhgf-1 and rga-5 genes, encoding homologues of RhoGEF and RhoGAP, respectively, as regulators of axon regeneration. We demonstrate that one pathway initiated by SER-7 acts upstream of the C. elegans RhoA homolog RHO-1 in neuron regeneration, which functions via G12α and RHGF-1. In this pathway, RHO-1 inhibits diacylglycerol kinase, resulting in an increase in diacylglycerol. SER-7 also promotes axon regeneration by activating the cyclic AMP (cAMP) signalling pathway. Thus, HIF-1-mediated activation of 5-HT signalling promotes axon regeneration by activating both the RhoA and cAMP pathways.


Asunto(s)
Axones/fisiología , Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans/metabolismo , Regeneración Nerviosa , Enfermedades Neurodegenerativas/metabolismo , Serotonina/metabolismo , Factores de Transcripción/metabolismo , Animales , Axotomía , Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/genética , AMP Cíclico/metabolismo , Modelos Animales de Enfermedad , Femenino , Humanos , Masculino , Enfermedades Neurodegenerativas/genética , Enfermedades Neurodegenerativas/fisiopatología , Neuronas/metabolismo , Transducción de Señal , Factores de Transcripción/genética
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