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Kif2a operates as a gatekeeper of nociception in sensory neurons [RNA-seq - 3 months]

ABSTRACT: Kif2a operates as a gatekeeper of nociception in sensory neurons [RNA-seq - 3 months]

PROVIDER: PRJNA924037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23085474.fastq.gz	Fastqsanger.gz
	SRR23085475.fastq.gz	Fastqsanger.gz
	SRR23085476.fastq.gz	Fastqsanger.gz
	SRR23085477.fastq.gz	Fastqsanger.gz
	SRR23085478.fastq.gz	Fastqsanger.gz

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Kif2a operates as a gatekeeper of nociception in sensory neurons [RNA-seq - 6 months]

Project description:Kif2a operates as a gatekeeper of nociception in sensory neurons [RNA-seq - 6 months]

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Kif2a operates as a gatekeeper of nociception in sensory neurons [RNA-seq - 1 month]

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Kif2a operates as a gatekeeper of nociception in sensory neurons

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Wnt signaling recruits KIF2A to the spindle to ensure chromosome congression during mitosis

Project description:Canonical Wnt signaling plays critical roles in development and tissue renewal by regulating β-catenin target genes. Recent evidence showed that β-catenin-independent Wnt signaling is also required for faithful execution of mitosis. This mitotic Wnt signaling functions through Wnt-dependent stabilization of proteins (Wnt/STOP), as well as through components of the LRP6 signalosome. However, the targets and specific functions of mitotic Wnt signaling still remain uncharacterized. Using phosphoproteomics, we identified that Wnt signaling regulates the microtubule depolymerase KIF2A during mitosis. We found that Dishevelled recruits KIF2A via its N-terminal and motor domains, which is further promoted upon LRP6 signalosome formation during mitosis. We show that Wnt signaling modulates KIF2A interaction with PLK1, which is critical for KIF2A localization and the assembly of a bipolar mitotic spindle. Accordingly, Wnt signaling promotes chromosome congression during metaphase by monitoring KIF2A protein levels at the spindle poles both in somatic cells and in pluripotent stem cells. Our findings highlight a novel function of Wnt signaling during cell division, which could have important implications for genome maintenance, notably in stem cells.

2021-11-17 | PXD022724 | Pride

Rac1 impairs retinal axon degeneration via Kif2a in a mouse model of chronic ocular hypertension

Project description:Rac1, a member of the small G protein Rho family, has been implicated in neurodegenerative diseases. However, its role in axon degeneration is not fully understood. Here we found that activation of Rac1 exacerbated axonal transport damage in an experimental glaucoma model. Inhibiting Rac1 activity by genetic or pharmacological methods alleviated the dysfunction of axonal transport and improved the integrity of microtubule by upregulating the expression of β-III tubulin and myelin basic protein. Rac1 interacted with Sirt1, a key molecule of Wallerian degeneration, which regulated the activity of PAK1, a downstream molecule of Rac1. Furthermore, Rac1 modulated Kif motors at the transcriptional level, among which Kif2a, a lysosome-location regulator, was negatively regulated by Rac1. Intravitreal injection of Kif2a siRNA reversed the improvement of Rac1 inhibition-mediated axonal transport through reducing autophagolysosomes. Our results suggest that Rac1/Kif2a accelerates the process of RGC axon degeneration by impairing the autophagic flux in glaucoma, which may be an intriguing therapy target for glaucoma.

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Project description:Morphine and other opioids continue to be commonly utilized as clinical analgesics, despite their numerous adverse side effects, including respiratory depression, addiction, and tolerance. The modulation of µ-opioid receptor (MOR) signaling and subsequent behavioral output is one viable approach to improve opioid therapy. Heat shock protein 90 (Hsp90) is a molecular chaperone protein that has recently been implicated in downstream MOR signaling within the brain in mice. Here we identify a context-dependent impact on MOR signaling in which the inhibition of Hsp90 within the spinal cord promotes morphine induced anti-nociception. We show that intrathecal and not systemic administration of the Hsp90 inhibitors 17-AAG or KU-32 amplifies morphine-induced anti-nociception in both thermal and mechanical pain models. Further, we demonstrate that the inhibition of Hsp90 allows for ERK phosphorylation after opioid treatment. ERK activation was localized within the dorsal horns of the spinal cord, which are heavily populated with primary afferents responsible for nociception. The behavioral effects observed with Hsp90 inhibitors were abolished upon intrathecal U0126 (ERK inhibitor) and cycloheximide (translation inhibitor) treatment, suggesting that downstream ERK phosphorylation and rapid protein translation are responsible for the observed amplification of anti-nociception. Quantitative proteomic analysis identified upregulated RSK with spinal cord Hsp90 inhibition, which we further found was necessary for the observed enhancement of anti-nociception. Taken together, we have uncovered a novel downstream MOR ERK/RSK cascade, localized to the spinal cord and repressed by Hsp90, whose modulation may allow for enhanced efficacy and decreased side effects during opioid therapy.

2020-04-24 | PXD015060 | Pride

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