[Overexpression of miR-31 regulates TLR4/NF-&#954;B signaling pathway and apoptotic protein in colitis model mice].

Liu, Kai Li; DU, Xin Xin; Zhang, Wen Qin; Wu, Ya Li; Wang, Xi; Wang, Chun Fang; Cui, Xiang Li

[Overexpression of miR-31 regulates TLR4/NF-κB signaling pathway and apoptotic protein in colitis model mice].

Liu, Kai Li; DU, Xin Xin; Zhang, Wen Qin; Wu, Ya Li; Wang, Xi; Wang, Chun Fang; Cui, Xiang Li.

Afiliación

Liu KL; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
DU XX; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
Zhang WQ; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
Wu YL; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
Wang X; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
Wang CF; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.
Cui XL; Department of Cell Physiology, Shanxi Medical University, Taiyuan 030001, China.

Zhongguo Ying Yong Sheng Li Xue Za Zhi ; 36(3): 211-215, 2020 May.

Article en Zh | MEDLINE | ID: mdl-32981274

Asunto(s)

Colitis Ulcerosa; MicroARNs; FN-kappa B; Transducción de Señal; Receptor Toll-Like 4; Animales; Línea Celular; Colitis Ulcerosa/fisiopatología; Colon/fisiopatología; Modelos Animales de Enfermedad; Expresión Génica; Humanos; Ratones; MicroARNs/genética; FN-kappa B/genética; FN-kappa B/metabolismo; Distribución Aleatoria; Transducción de Señal/genética; Receptor Toll-Like 4/genética; Receptor Toll-Like 4/metabolismo

Palabras clave

TLR4/NF-κB signaling pathway; apoptosis; dextran sulfate sodium (DSS); human colon epithelial cell line HCT 116; miR-31; mouse; ulcerative colitis

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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Transducción de Señal / Colitis Ulcerosa / FN-kappa B / MicroARNs / Receptor Toll-Like 4 Tipo de estudio: Clinical_trials / Prognostic_studies Límite: Animals / Humans Idioma: Zh Revista: Zhongguo Ying Yong Sheng Li Xue Za Zhi Asunto de la revista: FISIOLOGIA Año: 2020 Tipo del documento: Article País de afiliación: China

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