TNFR1-JNK signaling is the shared pathway of neuroinflammation and neurovascular damage after LPS-sensitized hypoxic-ischemic injury in the immature brain. (Q34990855)

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English	TNFR1-JNK signaling is the shared pathway of neuroinflammation and neurovascular damage after LPS-sensitized hypoxic-ischemic injury in the immature brain.	scientific article

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26 February 2020

TNFR1-JNK signaling is the shared pathway of neuroinflammation and neurovascular damage after LPS-sensitized hypoxic-ischemic injury in the immature brain (English)

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26 February 2020

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Chao-Ching Huang

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26 February 2020

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Lan-Wan Wang

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26 February 2020

Ying-Chao Chang

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26 February 2020

Shyi-Jou Chen

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26 February 2020

Chien-Hang Tseng

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26 February 2020

Yi-Fang Tu

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26 February 2020

Nan-Shih Liao

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26 February 2020

Chien-Jung Ho

8

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26 February 2020

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24 December 2014

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26 February 2020

Journal of Neuroinflammation

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26 February 2020

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26 February 2020

215

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26 February 2020

copyright license

Creative Commons Attribution 4.0 International

1 December 2014

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April 2022 Public Data File from Crossref

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0 references

https://scigraph.springernature.com/pub.10.1186/s12974-014-0215-2

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Hypoxic/ischemic and infectious events have cumulative effects on the risk of cerebral palsy in very-low-birth-weight preterm infants

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JNK signaling is the shared pathway linking neuroinflammation, blood-brain barrier disruption, and oligodendroglial apoptosis in the white matter injury of the immature brain

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Overweight worsens apoptosis, neuroinflammation and blood-brain barrier damage after hypoxic ischemia in neonatal brain through JNK hyperactivation.

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Developmentally regulated changes in c-Jun N-terminal kinase signalling determine the apoptotic response of oligodendrocyte lineage cells

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Intrauterine infection induces programmed cell death in rabbit periventricular white matter

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Identifiers

10.1186/S12974-014-0215-2

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26 February 2020

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26 February 2020

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26 February 2020

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