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相关概念视频

The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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mTOR Signaling and Cancer Progression03:03

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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.
The mTOR pathway or the...
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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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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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PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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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...
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Cancer-Critical Genes I: Proto-oncogenes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
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Updated: Jun 24, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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在KRAS突变癌症中定义KRAS和ERK依赖的转录组

Jeffrey A Klomp1,2, Jennifer E Klomp1, Clint A Stalnecker1,2

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.

Science (New York, N.Y.)
|June 6, 2024
PubMed
概括

虽然KRAS促使癌症生长,但其机制尚不清楚. 我们的研究显示ERK信号是KRAS突变癌症生长和针对性治疗的关键.

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科学领域:

  • 癌症学
  • 分子生物学
  • 癌症遗传学

背景情况:

  • KRAS瘤基因是各种癌症的关键驱动因素,但其瘤活性和相关的治疗耐药性背后的精确分子机制仍然不完全理解.
  • 了解KRAS驱动的基因转录对于开发有效的癌症治疗至关重要.

研究的目的:

  • 在KRAS突变癌症中建立KRAS和细胞外信号调节激酶 (ERK) 的全系统转录形象.
  • 确定驱动癌症生长和抑制剂耐药性的分子机制.
  • 在KRAS突变癌症中确定ERK信号调节的关键途径.

主要方法:

  • 在KRAS突变癌症模型中进行全系统基因转录分析.
  • 转录组数据与蛋白质组分析 (蛋白质组和总蛋白质组) 的整合.
  • 分析ERK中位基激活蛋白激酶 (MAPK) 级联活性.

主要成果:

  • 发现了一种新的KRAS依赖基因特征,与之前报告的特征不同.
  • 由KRAS驱动的转录主要由ERK MAPK级联介导.
  • 在胰腺管腺癌 (PDAC) 的生长中,对促进复合体/循环体 (APC/ C) 和细胞循环机制的ERK放松调控被认为是关键的.

结论:

  • 在推动KRAS突变瘤生长方面,ERK信号发挥着关键的机制作用.
  • 在KRAS- ERK MAPK向疗法的耐药性方面,ERK信号传递有所影响.
  • 这项研究为KRAS驱动的瘤发生和潜在的治疗策略提供了新的见解.