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Jianrong Li

Researcher at University of Arizona

Publications -  119
Citations -  7382

Jianrong Li is an academic researcher from University of Arizona. The author has contributed to research in topics: Nitric oxide & Axon. The author has an hindex of 42, co-authored 114 publications receiving 6794 citations. Previous affiliations of Jianrong Li include University of Hawaii & Boston Children's Hospital.

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Demyelination and remyelination in anatomically distinct regions of the corpus callosum following cuprizone intoxication.

TL;DR: While demyelination was limited in the rostral region of corpus callosum, nearly complete demyELination occurred in the caudal callosUM, beginning at approximately -0.5mm from bregma.
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Tumor necrosis factor alpha mediates lipopolysaccharide-induced microglial toxicity to developing oligodendrocytes when astrocytes are present.

TL;DR: The results reveal that TNFα signaling, rather than peroxynitrite, is essential in LPS-triggered preOL death in an environment containing all major glial cell types and underscore the importance of intercellular communication in determining the mechanism underlying inflammatory pre OL death.
Journal Article

Signaling Events Triggered by Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL): Caspase-8 Is Required for TRAIL-induced Apoptosis

TL;DR: The data indicate that caspase-8 is required for TRAIL-induced apoptosis and suggest that cospase-10 may play a minor role, if any, in TRAil-induced euthanasia, while reverse transcription-PCR and sequence analyses have revealed that these caspases-8-deficient Jurkat cell express wild-type casp enzyme-10.
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Caspase blockade induces RIP3-mediated programmed necrosis in Toll-like receptor-activated microglia.

TL;DR: It is reported here that microglia activated through Toll-like receptors (TLRs) undergo RIP1/RIP3-dependent programmed necrosis (necroptosis) when exposed to the pan caspase inhibitor zVAD-fmk and suggests that TLR signaling and programmed cell death pathways are closely linked inmicroglia, which could contribute to neuropathology and neuroinflammation when dysregulated.
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Dual regulatory switch through interactions of Tcf7l2/Tcf4 with stage-specific partners propels oligodendroglial maturation.

TL;DR: This work identifies stage-specific co-regulators Kaiso and Sox10 that sequentially interact with Tcf7l2 to coordinate the switch at the transitions of differentiation initiation and maturation during oligodendrocyte development, and point to a previously unrecognized role of Tcf8l2 in control of cholesterol biosynthesis for CNS myelinogenesis.