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Regeneration occurs in the CNS of CAST/Ei mice as a consequence of enhanced Activin signaling

ChEBI2015-05-14 更新2026-07-21 收录

神经再生机制

Activin信号通路

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-55424 数据链接链接失效反馈

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Regeneration occurs in the CNS of CAST/Ei mice as a consequence of enhanced Activin signaling

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创建时间：

2015-05-14

中枢神经再生

Activin信号通路

We screened nine genetically diverse inbred mouse strains for differences in axonal growth of adult dorsal root ganglion (DRG) neurons on CNS myelin. Naïve DRG neurite outgrowth on myelin was very li

NIAID Data Ecosystem140

Sciatic Nerve Injury Triggered Inflammation: Insights into Conditioning-Lesion Induced Axon Regeneration [bulk RNA-seq]

神经再生机制

神经免疫交互

Sciatic nerve crush (SNC) triggers sterile inflammation within the distal nerve and deafferented dorsal root ganglia (DRGs). Granulocytes and pro-inflammatory Ly6Chigh monocytes infiltrate the nerve f

NIAID Data Ecosystem80

Data_Sheet_6_GATA3 Promotes the Neural Progenitor State but Not Neurogenesis in 3D Traumatic Injury Model of Primary Human Cortical Astrocytes.ZIP

胶质细胞重编程

神经再生机制

Astrocytes are abundant cell types in the vertebrate central nervous system and can act as neural stem cells in specialized niches where they constitutively generate new neurons. Outside the stem cell

NIAID Data Ecosystem50

Gene expression profiles in the cultured dorsal root ganglia (DRG) neurons treated with PBS or oncomodulin (ONCM)

神经再生机制

RNA-seq分析

Preconditioning nerve injury drives pro-regenerative perineuronal macrophage activation in dorsal root ganglia (DRG). The present study reports that oncomodulin (ONCM) is produced from the regeneratio

NIAID Data Ecosystem80

miRNA sequencing of primary mouse dorsal root ganglia

神经再生机制

miRNA表达分析

Peripheral nerve regeneration after injury is a complex process involving a large number of transcriptional changes. How these changes impact the regenerative outcome is though, poorly understood. Her

NIAID Data Ecosystem60

Regeneration occurs in the CNS of CAST/Ei mice as a consequence of enhanced Activin signaling

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