相关实验视频

Updated: Jun 6, 2025

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
07:15

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils

Published on: January 21, 2020

11.3K

牙周炎中的乌比奎丁-蛋白质体系统:机制和临床影响

Yilin Ma1, Ruiwei Jia1, Shuhong Chen1

  • 1Institute of Stomatology, School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, China.

Cell proliferation
|December 3, 2024
PubMed
概括

泛素-蛋白酶系统 (UPS) 涉及E3泛素连接酶和二化酶,在牙周炎的进展中起着关键作用. 调节这些UPS酶为牙周炎提供了一个有前途的治疗策略.

关键词:
E3 无处不在酸接酶骨的新陈代谢 骨的新陈代谢没有除酶的酶.这是一种炎症炎症炎症炎症.牙周炎是指牙周炎的一种疾病.乌比奎丁-蛋白酶体系统

更多相关视频

Isolation, Processing and Analysis of Murine Gingival Cells09:47

Isolation, Processing and Analysis of Murine Gingival Cells

Published on: July 2, 2013

18.9K
In Situ Detection of Bacteria within Paraffin-embedded Tissues Using a Digoxin-labeled DNA Probe Targeting 16S rRNA11:15

In Situ Detection of Bacteria within Paraffin-embedded Tissues Using a Digoxin-labeled DNA Probe Targeting 16S rRNA

Published on: May 21, 2015

10.9K

相关概念视频

Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
1
The Proteasome01:13

The Proteasome

Eukaryotic cells can degrade proteins through several pathways. One of the most important among these is the ubiquitin-proteasome pathway. It helps the cell eliminate the misfolded, damaged, or unwarranted cytoplasmic proteins in a highly specific manner.
In this pathway, the target proteins are first tagged with small proteins called ubiquitin. This involves participation of a series of enzymes including— E1 (ubiquitin-activating enzyme), E2 (ubiquitin-conjugating enzyme), and E3...
813
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
2.7K
Biofilms01:29

Biofilms

Biofilms are complex communities of microorganisms encased in a self-produced extracellular polysaccharide matrix attached to surfaces. These microbial consortia can include single or multiple species, providing enhanced survival benefits by forming organized, multilayered structures.The formation of biofilms occurs through four key stages: attachment, colonization, development, and dispersal.During attachment, free-swimming planktonic cells adhere to a surface, often facilitated by...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
356
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
280