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Oncogenic BRAF^V600E induces microglial proliferation through extracellular signal-regulated kinase and neuronal death through c-Jun N-terminal kinase.

ABSTRACT: Activating V600E in v-Raf murine sarcoma viral oncogene homolog B (BRAF) is a common driver mutation in cancers of multiple tissue origins, including melanoma and glioma. BRAF^V600E has also been implicated in neurodegeneration. The present study aims to characterize BRAF^V600E during cell death and proliferation of three major cell types of the central nervous system: neurons, astrocytes, and microglia. Multiple primary cultures (primary cortical mixed culture) and cell lines of glial cells (BV2) and neurons (SH-SY5Y) were employed. BRAF^V600E and BRAF^WT expression was mediated by lentivirus or retrovirus. Blockage of downstream effectors (extracellular signal-regulated kinase 1/2 and JNK1/2) were achieved by siRNA. In astrocytes and microglia, BRA

SUBMITTER: Ye Q

PROVIDER: S-EPMC10075110 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

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Oncogenic BRAF^V600E induces microglial proliferation through extracellular signal-regulated kinase and neuronal death through c-Jun N-terminal kinase.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Oncogenic BRAFV600E induces microglial proliferation through extracellular signal-regulated kinase and neuronal death through c-Jun N-terminal kinase.

OmicsDI is part of the ELIXIR infrastructure

Tweets

Oncogenic BRAF^V600E induces microglial proliferation through extracellular signal-regulated kinase and neuronal death through c-Jun N-terminal kinase.