相关实验视频

Updated: Jun 26, 2025

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

METTL3 调节Ctsk⁺ 血统支持通过刺通过头骨骨质生成

R Xu^1,2, R Sheng^1,3, W Lin^1,3

¹State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, China.

Journal of dental research

|May 16, 2024

概括

甲基转移酶样3 (METTL3) 调节了cathepsin K (CTSK) 阳性干细胞中的N6-methyladenosine (m6A) 修饰,通过调节刺信号通路,影响骨的发育和维护.

科学领域:

分子生物学分子生物学
发展生物学发展生物学
干细胞生物学干细胞生物学

背景情况:

由甲基转移酶类3 (METTL3) 调节的N6-甲基氨酸 (m⁶A) 修饰对于干细胞命运至关重要.
骨发育依赖于头骨和cathepsin K (CTSK) 阳性骨干细胞 (CSC).
在发育过程中,m⁶A在调节CTSK+系细胞中的作用尚不清楚.

研究的目的:

为了研究METTL3-介导的m6在骨发育和维护过程中CTSK+血统细胞的修饰的功能.
阐明METTL3通过哪些分子机制影响骨骨的形成.

主要方法:

新生儿和成年小鼠中CTSK+系细胞中Mettl3的耗尽.
对骨骨结构,矿化和骨细胞形态的分析.
甲基化RNA免疫沉降测序 (MeRIP-seq) 和RNA测序 (RNA-seq).
刺 (Hh) 信号通路分析和使用Sufu等位基因或SAG21的救援实验.

主要成果:

在CTSK+细胞中Mettl3的枯竭延迟了新生儿的形成,并减少了矿化.
成年小鼠中Mettl3的丧失导致骨形成受损,透度和骨髓腔增加,骨细胞数量减少.
由于METTL3缺乏,导致 (Hh) 信号通路活动减少.
恢复Hh信号传输部分挽救了观察到的骨缺陷.

结论:

METTL3调节CTSK+血统细胞,以支持骨骨的形成和维护.
METTL3通过调节"刺"信号通路来发挥其功能.
这些发现为头骨骨性疾病提供了新的治疗策略.

关键词:

这是一种N6-甲基氨酸.骨头骨头骨头骨头甲基化疗法甲基化疗法干细胞是干细胞的组成部分.suture suture 翻译科学是翻译科学.

更多相关视频

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential

Published on: July 21, 2023

相关概念视频

Hedgehog Signaling Pathway

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

Notch Signaling Pathway

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not...