Neutrophil KLF2 regulates inflammasome-dependent neonatal mortality from endotoxemia.

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Tác giả: E Ricky Chan, Sarah Cioffi, George R Dubyak, Alex Y Huang, Mukesh K Jain, Yuexin Li, Devashis Mukherjee, Lalitha Nayak, Sriram Satyavolu, Asha Thomas, Katherine Wen

Ngôn ngữ: eng

Ký hiệu phân loại: 629.1344 Aerospace engineering

Thông tin xuất bản: United States : bioRxiv : the preprint server for biology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 673698

UNLABELLED: Preterm neonates die at a significantly higher rate from sepsis than full-term neonates, attributable to their dysregulated immune response. In addition to tissue destruction caused directly by bacterial invasion, an overwhelming cytokine response by the immune cells to bacterial antigens also results in collateral damage. Sepsis leads to decreased gene expression of a critical transcription factor, Krüppel-like factor-2 (KLF2), a tonic repressor of myeloid cell activation. Using a murine model of myeloid- SUMMARY SENTENCE: KLF2 regulates the developmental response to endotoxin in neonatal mice through the NLRP3 inflammasome signaling pathway.
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