Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

10.3K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
10.3K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.3K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
3.3K
Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

9.1K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.1K
Negative Regulator Molecules01:23

Negative Regulator Molecules

38.8K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
38.8K
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

9.9K
Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein....
9.9K

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

Prenatal iodine supplementation and early childhood neurodevelopment: the PoppiE trial - study protocol for a multicentre randomised controlled trial.

BMJ open·2023
Same author

Corrigendum to "Feline mammary carcinoma stem cells are tumorigenic, radioresistant, chemoresistant and defective in activation of the ATM/p53 DNA damage pathway" [The Veterinary Journal 196 (2013) 414-423].

Veterinary journal (London, England : 1997)·2021
Same author

Simultaneous measurement of p53:Mdm2 and p53:Mdm4 protein-protein interactions in whole cells using fluorescence labelled foci.

Scientific reports·2019
Same author

Standard terminology for reproductive tissue and cell products for use in ART.

Human reproduction open·2019
Same author

Synthetic 10FN3-based mono- and bivalent inhibitors of MDM2/X function.

Protein engineering, design & selection : PEDS·2018
Same author

Enhancing Specific Disruption of Intracellular Protein Complexes by Hydrocarbon Stapled Peptides Using Lipid Based Delivery.

Scientific reports·2017

関連する実験動画

Updated: Mar 13, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

300

小型のペプチドは,p53の潜在配列特異的なDNA結合機能を活性化します.

T R Hupp1, A Sparks, D P Lane

  • 1Department of Biochemistry, Dundee University, Scotland.

Cell
|October 20, 1995
PubMed
まとめ

正常な細胞は,紫外線または抗体の介入によって,p53タンパク質を転写のために活性化します. この研究では,ペプチド活性化システムが導入され,p53のアロステリック調節が明らかにされ,新しいp53応答変形剤への道が開かれている.

科学分野:

  • 分子生物学は分子生物学である.
  • バイオケミストリー バイオケミストリー
  • セルラーレギュレーション セルラーレギュレーション

背景:

  • p53タンパク質は通常,細胞内に潜伏しているが,UV放射線によってシーケンス固有の転写のために活性化することができる.
  • アクティベーションは,p53タンパク質のレベルが上昇することなく起こるので,翻訳後の修正が重要なことを示唆しています.

研究 の 目的:

  • p53の活性化のメカニズムを調査する.
  • p53.5 のための特定のペプチド活性化システムを開発する.
  • p53の活性に対するアロステリック対ステリック調節を調べる.

主な方法:

  • 細胞にp53.3のC端末陰性調節ドメインを標的にする抗体を微注入する.
  • p53の負の調節ドメインから派生した小さなペプチドを使用します.
  • ペプチド活性化システムの開発.

主要な成果:

  • 抗体マイクロインジェクションは,紫外線損傷なしにp53機能を活性化させ, in vivoの翻訳後の改変が速度制限であることを示しています.
  • ペプチドは,アロステリックとステリックの負の調節メカニズムを区別するために使用されました.
  • アロステル調節と一致する特定のペプチド活性化システムが開発されました.

さらに関連する動画

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

10.1K
High Sensitivity Measurement of Transcription Factor-DNA Binding Affinities by Competitive Titration Using Fluorescence Microscopy
06:38

High Sensitivity Measurement of Transcription Factor-DNA Binding Affinities by Competitive Titration Using Fluorescence Microscopy

Published on: February 7, 2019

9.3K

関連する実験動画

Last Updated: Mar 13, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

300
Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

10.1K
High Sensitivity Measurement of Transcription Factor-DNA Binding Affinities by Competitive Titration Using Fluorescence Microscopy
06:38

High Sensitivity Measurement of Transcription Factor-DNA Binding Affinities by Competitive Titration Using Fluorescence Microscopy

Published on: February 7, 2019

9.3K

結論:

  • p53の負の調節ドメインの翻訳後の改変は,p53の活性化に重要な,速度を制限するステップです.
  • 開発されたペプチドシステムは,p53の負の調節のためのアロステリックメカニズムをサポートします.
  • この研究は,p53応答の新しい小分子修正剤の作成のための先例を確立しています.