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相关概念视频

The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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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...
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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Updated: May 31, 2025

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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通过JAK/STAT信号通路,CDCA4促进了膀癌的进展.

Peng Wan1, Yuan Ren1, Hao Deng2

  • 1Department of Oncology, The First Affiliated Hospital of Yangtze University, Jingzhou, 434000, China.

Journal of cancer research and clinical oncology
|January 24, 2025
PubMed
概括

细胞分裂周期相关的4 (CDCA4) 通过激活JAK/STAT通路,促进膀癌的进展. 抑制CDCA4可能为膀癌患者提供新的治疗策略.

关键词:
AG49090 AG49090 AG49090 AG490 AG490 AG490 AG490 AG490 AG490 AG490 AG490 AG490膀癌是一种癌症.这是一个CDCA4CDCA4CDCA4CDCA4CDCA.这就是JAK/STAT.分子点是分子点.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 癌症研究 癌症研究

背景情况:

  • 细胞分裂周期相关的4 (CDCA4) 参与瘤进展.
  • 它在膀癌发病过程中的具体作用尚不清楚.

研究的目的:

  • 研究CDCA4在膀癌中的作用和机制.
  • 评估CDCA4作为潜在的治疗点.

主要方法:

  • 对CDCA4表达和预后的TCGA和GEO膀癌数据集的分析.
  • 在体外实验中使用CDCA4过度表达和淘汰的膀癌细胞系.
  • 对细胞增殖,迁移,入侵和上皮-介质细胞过渡 (EMT) 的检测.
  • 西部斑点和路径分析以确定下游目标.

主要成果:

  • 膀癌中CDCA4的表达上调,与预后不佳有关.
  • 抑制CDCA4抑制了膀癌细胞的增殖,迁移,入侵和EMT.
  • 过度表达CDCA4增强了膀癌细胞恶性.
  • CDCA4激活了JAK/STAT信号通路,促进了膀癌的进展.

结论:

  • CDCA4通过JAK/STAT通路促进膀癌细胞的增殖,迁移和入侵.
  • CDCA4代表了膀癌治疗的潜在新型分子标.