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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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MAPK Signaling Cascades01:07

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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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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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PI3K/mTOR/AKT Signaling Pathway01:22

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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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Rab Proteins01:14

Rab Proteins

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Rab proteins constitute the largest family of monomeric GTPases, of which 70 members are present in humans. Rab proteins and their effectors regulate consecutive stages of vesicle transport such as vesicle transport, docking, and fusion to the correct recipient membrane.
Rab proteins switch between a cytosolic, GDP-bound inactive state and a membrane-anchored, GTP-bound active state. By themselves, Rabs show slow rates of GDP/GTP exchange and GTP hydrolysis. Thus, Rab proteins are considered...
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Rab Cascades01:25

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Rab GTPases act in a regulated cascade during membrane fusion, helping the lipid bilayers mix. The Rab family of proteins are active when bound to GTP, and inactive when bound to GDP. Hence, they act as guanine nucleotide-dependent molecular switches. Rab-GTP recognizes and binds to long or short-range tethering proteins to capture the target vesicle. These tethers coordinate with SNAREs on the vesicle and the target membrane to assemble the trans SNARE complex that locks the mixing bilayers.
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相关实验视频

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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通过扩大其与GAP蛋白的结合接口,K128无处不在限制了RAS活性.

Wout Magits1, Mikhail Steklov1, Hyunbum Jang2

  • 1VIB-KU Leuven Center for Cancer Biology, VIB, 3000, Leuven, Belgium.

The EMBO journal
|June 10, 2024
PubMed
概括

氨酸128对RAS蛋白的泛化增强了它们与GTPase激活蛋白 (GAPs) 的相互作用,抑制了癌细胞的生长. 减少无处不在促进RAS信号传递和胰腺瘤的发展.

关键词:
NF1 NF1 是一个字母.在 RAS 互动组中.在 RAS 信号传输中.与衰老相关的分泌体表现型在Ubiquitination中使用.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 细胞信号传递 细胞信号传递

背景情况:

  • 在各种癌症中,RAS信号通路经常失调.
  • 控制人类病理中的RAS活动的机制需要进一步阐明.
  • 氨酸128 (K128) NRAS和KRAS的无处不在是癌症中普遍发生的修饰性降低.

研究的目的:

  • 调查K128无化在RAS信号传递和癌症中的功能作用.
  • 确定K128的无处不在如何影响RAS与GTPase激活蛋白 (GAPs) 的相互作用.
  • 探索改变K128无处不在的后果在野生类型和突变RAS驱动的癌症中.

主要方法:

  • 在癌症细胞系和组织中研究K128的无处不在.
  • 利用细胞培养刺激与生长因子和细胞因子.
  • 分析了RAS-GAP相互作用和下游信号通路 (RAL/TBK1).
  • 评估了对瘤生长和衰老相关的分泌表型的影响.

主要成果:

  • K128无处不在增强了与GAPs (NF1,RASA1) 的结合,促进了GTP的水解,并限制了野生类型的RAS激活.
  • 暂时的K128无处可见性限制了在生长因子刺激时RAS激活.
  • 在KRAS突变细胞中,K128无处不在抑制瘤生长,通过抑制RAL/TBK1信号传递和自身隐性回路.
  • 降低的K128无处不在激活野生型和突变RAS,诱导与衰老相关的分泌表型并促进胰腺瘤发生.

结论:

  • K128的无处不在作用是RAS信号的关键负调节器.
  • 这种修改会影响正常和癌症条件下的RAS活性.
  • 准K128无处不在可能为RAS驱动的癌症提供治疗策略,特别是胰腺癌.