相关实验视频

Updated: Jan 14, 2026

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage

Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C UV-C Damage

Published on: February 15, 2020

通过SLC23A2 - 亚斯科布酸相互作用的氧化压力介导的亡,有助于裂唇的发展

Bin Yin^1,2, Yi Chen Xu¹, Yong Lu¹

¹Nanjing Stomatological Hospital Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.

Frontiers in pediatrics

|October 20, 2025

概括

基因SLC23A2与非综合征性裂唇仅 (NSCLO) 有显著的关联. 它与活性氧物种 (ROS) 和酸 (AA) 的相互作用通过影响氧化应激和亡来影响唇部发育.

科学领域:

遗传学是一个遗传学.
发展生物学发展生物学
分子生物学分子生物学

背景情况:

只有非综合征裂唇 (NSCLO) 是一种常见的先天性疾病.
此前没有报告SLC23A2基因在裂唇发育中的作用.
基因与环境的相互作用对于理解CL/P病因至关重要.

研究的目的:

调查SLC23A2和NSCLO之间的关联.
探索SLC23A2,反应性氧物种 (ROS) 和酸 (AA) 在唇部发育中的相互作用.
阐明SLC23A2在裂唇形成中的作用背后的分子机制.

主要方法:

全基因组关联研究 (GWAS) 对SNP在SLC23A2.2.中的数据分析.
在体外研究使用人类口腔上皮细胞系 (GMSM-K) 来评估氧化应激和亡.
在使用斑马鱼模型的体内研究.
用RNA测序来探索分子机制.

主要成果:

在SLC23A2中,有10个SNP与NSCLO显著相关.
击败SLC23A2增加了ROS和亡,并通过PI3K-Akt通路减少了COL9A3的表达.
亚酸 (AA) 补充剂在具有功能SLC23A2的细胞中减轻了ROS和亡,但在SLC23A2敲击细胞或斑马鱼中没有.

结论:

SLC23A2与NSCLO有显著的相关性.
SLC23A2,外源性ROS和AA之间的相互作用在唇部和面发育中起作用.
这种相互作用影响ROS和细胞亡的细胞水平,影响发育过程.

关键词:

灭症 (apoptosis) 是一种死亡的过程.协会分析协会分析分析基因与环境的相互作用只有非综合症的裂口唇.有活性氧物种的反应性氧物种.

更多相关视频

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures

Author Spotlight: Improved Lipofuscin Models and Quantification of Outer Segment Phagocytosis Capacity in Highly Polarized Human Retinal Pigment Epithelial Cultures

Published on: April 14, 2023

相关概念视频

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...