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Role of ER in the Secretory Pathway01:17

Role of ER in the Secretory Pathway

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Eukaryotic cells have a special pathway that enables communication between various intracellular membrane-bound compartments and also with the extracellular environment. This pathway is termed as the secretory pathway.
Components of the secretory pathway
About a third of proteins synthesized in the cell are sorted via the secretory route. They shuffle between different compartments in membrane-bound vesicles until they reach their final destination. The main intracellular compartments involved...
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Export of Misfolded Proteins out of the ER01:32

Export of Misfolded Proteins out of the ER

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After folding, the ER assesses the quality of secretory and membrane proteins. The correctly folded proteins are cleared by the calnexin cycle for transport to their final destination, while misfolded proteins are held back in the ER lumen. The ER chaperones attempt to unfold and refold the misfolded proteins but sometimes fail to achieve the correct native conformation. Such terminally misfolded proteins are then exported to the cytosol by ER-associated degradation or ERAD pathway for...
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
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Tail-anchoring of Proteins in the ER Membrane01:45

Tail-anchoring of Proteins in the ER Membrane

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Tail-anchored, or TA, proteins are estimated to make up to 3-5% of membrane proteins found in the eukaryotic cell. Such proteins have a single transmembrane domain located approximately 30 amino acid residues upstream from the C-terminal end. As a result, the signal recognition particle (SRP) cannot guide a TA protein to the ER membrane for cotranslational insertion. Hence, they are integrated into the ER membrane post-translationally using their C-terminal end as the anchor. TA proteins...
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ER Retrieval Pathway01:45

ER Retrieval Pathway

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In the secretory pathway, vesicles transport proteins from one cellular compartment to another in forward transport to deliver the protein to its correct location. Occasionally, misfolded proteins and incorrect proteins escape their original compartments, and a retrieval pathway is used to return the escaped proteins to their original compartment.
The ER uses many checkpoints to prevent the entry of incorrectly folded or a resident protein as cargo onto a transport vesicle. These mechanisms...
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Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

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Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Systems Biology of Metabolic Regulation by Estrogen Receptor Signaling in Breast Cancer
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内分泌療法に抵抗する乳がんにおける標的となる脆弱性として,セラミド誘発の内分泌網膜ストレス

Purab Pal1, Shweta Chitkara2, Godwin K Sarpey1

  • 1Department of Physiology and Biophysics, University of Illinois Chicago, IL, USA.

bioRxiv : the preprint server for biology
|September 2, 2025
PubMed
まとめ
この要約は機械生成です。

乳がんにおける内分泌療法抵抗は,セラミドの減少とセラミド誘発の細胞死に対する感受性の増加を伴う. セラミドは,PERK経由でエンドプラズマ網膜ストレス (EnRS) 経路を活性化し,特にTRAM1の相互作用により,抵抗性細胞の細胞死を引き起こす.

キーワード:
セラミドセラミドと相互作用するタンパク質内分泌療法に対する耐性エンドプラズマの網膜のストレス乳がん 乳がんPERK (ペーク)トラム1

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An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
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科学分野:

  • 腫瘍学
  • 分子生物学
  • 細胞生物学

背景:

  • 内分泌療法 (ET) は,ホルモン受容体陽性乳がんに有効ですが,治療抵抗性や患者の再発によって課題に直面しています.
  • ET耐性乳がん細胞はセラミド代謝が変化し,セラミド誘発の細胞死に対するレベルが低下し,敏感性が高まっている.

研究 の 目的:

  • セラミドがET耐性乳がん細胞の細胞死を誘発するメカニズムを調査する.
  • ET耐性におけるセラミド媒介細胞死経路に関与する特定のタンパク質を特定する.

主な方法:

  • セラミド治療によるET抵抗性細胞の転写再プログラム分析.
  • セラミド誘発細胞死におけるエンドプラズマ網膜ストレス (EnRS) とPERK経路の役割の評価
  • 光活性化セラミドプローブを使用してセラミド相互作用タンパク質 (CIP) を特定する.
  • ET耐性モデルと患者データにおけるTRAM1の機能を調査する.

主要な成果:

  • セラミドは,ET耐性細胞の特異的な転写再プログラムを引き起こし,EnRS経路を向上させる.
  • セラミド誘発のEnRSはPERK経路に依存し,複数のET抵抗モデルで細胞死を媒介する.
  • TRAM1は,ET耐性細胞における重要なセラミド相互作用タンパク質 (CIP) として特定され,再発のない生存率の低下と攻撃的な乳がんのフェノタイプに関連していました.
  • TRAM1のノックダウンは,セラミドによる細胞死におけるセラミドの作用を模倣し,その役割を強調した.

結論:

  • ETに抵抗する乳がん細胞は,ETに敏感な細胞と比較してPERK媒介のEnRSに対してより敏感である.
  • セラミドは,TRAM1のようなCIPと相互作用し,PERKを活性化し,ET耐性モデルで細胞死を誘発することで,この敏感性を利用します.
  • セラミド-TRAM1-PERK軸を標的とした治療は,乳がんにおけるET抵抗を克服するための潜在的な治療戦略です.