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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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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
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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 transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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通过JNK开关进行酸化,使BRD4功能发挥作用.

Ballachanda N Devaiah1, Amit Kumar Singh1, Jie Mu1

  • 1Experimental Immunology Branch, NCI, NIH, Bethesda, MD 20892, USA.

Molecular cell
|October 25, 2024
PubMed
概括

odomain 4 (BRD4) 开关通过JNK酸化起作用,从染色质释放以激活转录. 这种开关是免疫反应和癌症进展的关键.

关键词:
这就是BRD4D.在EMT中,EMT是EMT.在JNK中,JNK就是JNK.细胞的压力是细胞的压力.染色素分解分解的过程基因组乙烯转移酶 (Histone Acetyltransferase) 是一种酶.激酶激酶的作用是什么这是一种-BRD4D4.甲状腺细胞刺激刺激转录激活的激活方式

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科学领域:

  • 分子生物学分子生物学
  • 细胞生物学 细胞生物学
  • 癌症研究 癌症研究

背景情况:

  • odomain 4 (BRD4) 是癌症和细胞压力的关键调节剂.
  • BRD4具有双重作用:通过HAT活性重塑染色质,通过激酶活性调节转录.
  • BRD4的活性取决于环境,在与染色质相结合时具有不同的功能,而不是促进剂.

研究的目的:

  • 阐明BRD4在染色质调节和转录激活之间的功能切换背后的机制.
  • 调查c-Jun N-终端激酶 (JNK) 在调解BRD4功能转换中的作用.

主要方法:

  • 人类BRD4.4的酸化部位映射.
  • 在刺激时从染色质中释放BRD4的分析.
  • 对RNA聚合酶II (RNA Pol II),PTEFb和c-Myc.的BRD4激酶活性的评估.
  • 在胸细胞和前列腺癌细胞中评估BRD4介导的基因表达变化.

主要成果:

  • 在Thr1186和Thr1212的BRD4的JNK介导酸化诱导其从染色质释放.
  • 释放的BRD4表现出增强的激酶活性,酸化RNA Pol II,PTEFb和c-Myc.
  • 这种功能性开关促进了免疫/炎症基因的转录,胸细胞中的CD8表达,以及前列腺癌中的上皮转介质过渡 (EMT).

结论:

  • 通过JNK介导的酸化是BRD4功能切换的关键机制.
  • 通过JNK信号传递,BRD4从染色质修饰剂过渡到转录激活剂.
  • 这种开关对免疫反应和癌症的发展,特别是前列腺癌,有重大影响.