Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Abnormal Proliferation02:23

Abnormal Proliferation

4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

12.8K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
12.8K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.0K

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

Demographics, Clinical Characteristics, and a Stage-Based Analysis of Treatments and Outcomes for Squamous Cell Carcinoma of the Penis.

Cancer reports (Hoboken, N.J.)·2025
Same author

PTP Inhibition Improves the Macrophage Antitumor Immune Response and the Efficacy of Chemo- and Radiotherapy.

Cancer immunology research·2025
Same author

The University of North Carolina Cancer Survivorship Cohort: A Resource for Collaborative Survivorship Research.

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology·2024
Same author

MERTK Is a Potential Therapeutic Target in Ewing Sarcoma.

Cancers·2024
Same author

MERTK Inhibition as a Targeted Novel Cancer Therapy.

International journal of molecular sciences·2024
Same author

Differences in 21-Gene and PAM50 Recurrence Scores in Younger and Black Women With Breast Cancer.

JCO precision oncology·2024

相关实验视频

Updated: Jun 21, 2025

Generation of Immature, Mature and Tolerogenic Dendritic Cells with Differing Metabolic Phenotypes
06:09

Generation of Immature, Mature and Tolerogenic Dendritic Cells with Differing Metabolic Phenotypes

Published on: June 22, 2016

23.1K

通过代谢重编程,MerTK诱导功能障碍的树突细胞.

Eden Y Zewdie1,2, George M Edwards1, Debra M Hunter1

  • 1UNC Lineberger Comprehensive Cancer Center, Chapel Hill, North Carolina.

Cancer immunology research
|July 8, 2024
PubMed
概括

向树突细胞 (DC) 中的MerTK可以克服对黑色素瘤抗编程细胞死亡蛋白1 (PD1) 治疗的抗性. 抑制MerTK恢复了DC功能,增强了抗PD1的有效性,并改善了抗瘤免疫反应.

更多相关视频

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro
06:12

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro

Published on: March 7, 2022

3.4K
Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells
06:07

Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells

Published on: March 28, 2025

239

相关实验视频

Last Updated: Jun 21, 2025

Generation of Immature, Mature and Tolerogenic Dendritic Cells with Differing Metabolic Phenotypes
06:09

Generation of Immature, Mature and Tolerogenic Dendritic Cells with Differing Metabolic Phenotypes

Published on: June 22, 2016

23.1K
Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro
06:12

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro

Published on: March 7, 2022

3.4K
Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells
06:07

Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells

Published on: March 28, 2025

239

科学领域:

  • 免疫学 免疫学 免疫学
  • 癌症生物学 癌症生物学
  • 代谢过程中的代谢.

背景情况:

  • 像抗PD1这样的检查点抑制剂对转移性黑色素瘤有效,但面临抗药性.
  • 树突细胞 (DCs) 对于免疫反应至关重要,但在瘤中可能变得功能障碍.
  • 作为受体氨酸激酶的一种受体,MerTK调解了髓状细胞对死细胞的清除.

研究的目的:

  • 研究MerTK在调节瘤微环境中的DC功能和新陈代谢中的作用.
  • 为了确定MerTK是否有助于黑色素瘤中抗PD1耐药性.

主要方法:

  • 从抗PD1耐药瘤的DC中评估了MerTK水平.
  • 在实验室中用缩性黑色素瘤细胞治疗了野生型和MerTK缺乏的DCs.
  • 分析了DC代谢 (线粒体呼吸,脂肪酸氧化) 和T细胞刺激能力.
  • 在DCs中选择性MerTK切除的小鼠中评估了抗PD1疗效.

主要成果:

  • 抗PD1耐药瘤显示MerTK+DCs的增加.
  • 异位性黑色素瘤细胞诱导了MerTK表达,改变了新陈代谢,并在野生类型的DC中减少了T细胞刺激.
  • 缺乏MerTK的DCs在暴露于死细胞时保持了功能和刺激能力.
  • 在DC中MertK消去显著增强了抗PD1疗法的疗效和T细胞透.

结论:

  • 在DC中MerTK信号传递促进了代谢功能障碍,并损害了抗瘤免疫力.
  • 在DC中准MerTK是克服黑色素瘤中抗PD1耐药性的潜在策略.
  • 通过抑制MerTK调节DC代谢可以增强当前的免疫疗法.