Jove
Visualize
お問い合わせ
このページは機械翻訳されています。他のページは英語で表示される場合があります。View in English
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 腫瘍学とがん発生
  9. 分子標的
  11. Hpf1は,dna損傷によるadpリボシライゼーションのためのparp活性部位を完了する.
  1. ホーム
  3. 研究分野
  5. 生物医学と臨床科学
  7. 腫瘍学とがん発生
  9. 分子標的
  11. Hpf1は,dna損傷によるadpリボシライゼーションのためのparp活性部位を完了する.

関連する実験動画

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

10.6K

HPF1は,DNA損傷によるADPリボシライゼーションのためのPARP活性部位を完了する.

Marcin J Suskiewicz1, Florian Zobel1, Tom E H Ogden2

  • 1Sir William Dunn School of Pathology, University of Oxford, Oxford, UK.

Nature
|February 7, 2020

PubMed で要約を見る

まとめ
この要約は機械生成です。

HPF1は,PARP1/PARP2との複合活性サイトを形成し,セリンADPリボシレーションによるDNA損傷修復に不可欠である. この相互作用は,DNA損傷と臨床PARP阻害剤に対する細胞の反応に不可欠です.

科学分野:

  • 生物化学
  • 分子生物学
  • 遺伝学

背景:

  • ポリ ((ADP-リボース) ポリメラーゼ1 (PARP1) とPARP2はDNA損傷に対する主要な反応因子である.
  • ADP-リボース信号でタンパク質を修正し,クロマチンの分解と修復因子の徴集を助けます.
  • 血清関連改変は,DNA損傷応答のPARP1/PARP2特異性を変化させるHPF1を必要とします.

研究 の 目的:

  • PARP媒介によるDNA損傷反応におけるHPF1の構造的および機能的役割を明らかにする.
  • HPF1およびPARP酵素を含む複合活性部位の形成を調査する.
  • DNA損傷に対するHPF1-PARP相互作用の調節を理解する.

主な方法:

  • PARP2の触媒領域とHPF1の共構造の決定
  • 核磁共振 (NMR) スペクトロスコーピー
  • 酵素の活性と相互作用を評価するための生化学的測定法

主要な成果:

  • HPF1とPARP1/PARP2の残留物によって形成された複合活性サイトが検出されました.
  • この触媒センターはADP-リボース添加後のDNA損傷に不可欠です.

さらに関連する動画

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

4.5K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

3.4K

関連する実験動画

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
10:44

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

10.6K
Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging
06:44

Assessment of Global DNA Double-Strand End Resection using BrdU-DNA Labeling coupled with Cell Cycle Discrimination Imaging

Published on: April 28, 2021

4.5K
Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications
10:12

Author Spotlight: Quantitative Detection of DNA Protein Crosslinks and Their Post-Translational Modifications

Published on: April 21, 2023

3.4K

関連する概念動画

Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

6.2K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
6.2K
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

9.9K
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...
9.9K
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

3.0K
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...
3.0K
Long-patch Base Excision Repair01:02

Long-patch Base Excision Repair

7.7K
Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
7.7K
Homologous Recombination02:31

Homologous Recombination

62.0K
The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
62.0K
Translesion DNA Polymerases02:10

Translesion DNA Polymerases

10.9K
Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
TLS polymerases are found in all three domains of life - archaea, bacteria, and eukaryotes. Of the different classes of TLS polymerases, members of the Y family are fitted with specialized structures that...
10.9K
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
  • アロステリックネットワークは,DNA損傷とNAD+結合の際のHPF1-PARP相互作用を強化し,DNA損傷反応を調節する.

    • 結論:

    • HPF1は,DNA損傷修復のためのPARP1とPARP2の活性部位の形成に不可欠です.
    • HPF1は,DNA損傷に対する細胞反応の決定的要素として作用する.
    • 複合活性部位におけるHPF1の役割は,臨床PARP阻害剤の有効性に関与する.