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Investigating Non-Canonical Roles of ATR and CHK1 Throughout the Cell Cycle
Investigating Non-Canonical Roles of ATR and CHK1 Throughout the Cell Cycle
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202103033
- ISBN
- 9798286445127
- DDC
- 574
- 저자명
- Joo, Yoon Ki.
- 서명/저자
- Investigating Non-Canonical Roles of ATR and CHK1 Throughout the Cell Cycle
- 발행사항
- [Sl] : Yale University, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 157 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-12, Section: B.
- 주기사항
- Advisor: Kabeche, Lilian;Solomon, Mark.
- 학위논문주기
- Thesis (Ph.D.)--Yale University, 2025.
- 초록/해제
- 요약Chromosome Instability (CIN), which results from DNA damage in interphase and chromosome missegregation in mitosis, is considered to be a potent driver of cancer. To prevent CIN, cells harbor the DNA Damage Response (DDR) pathway, which is responsible for detecting and repairing damaged DNA. Because of their importance in preventing CIN, the core members of the DDR pathway such as Ataxia Telangiectasia and Rad3-related (ATR) and Checkpoint kinase 1 (CHK1) have been studied as promising targets in cancer therapy. However, clinical trials show that ATR and CHK1 inhibitors elicit adverse side effects with unknown reasons. Recent research suggests that one of the reasons for the unexpected side effects is that ATR and CHK1 are multi-faceted proteins that are involved in multiple different pathways while the current clinical strategies only focus on their role in the DDR pathway. In this dissertation, we show that ATR and CHK1 have multiple roles throughout the cell cycle that is not limited to the DDR pathway in both promoting the rupture of micronucleus (MN) in interphase and faithful chromosome segregation during mitosis.
- 일반주제명
- Biology
- 일반주제명
- Microbiology
- 일반주제명
- Cellular biology
- 일반주제명
- Molecular biology
- 일반주제명
- Genetics
- 키워드
- Micronucleus
- 기타저자
- Yale University Molecular Biophysics and Biochemistry
- 기본자료저록
- Dissertations Abstracts International. 86-12B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■007cr#unu||||||||
■020 ▼a9798286445127
■035 ▼a(MiAaPQ)AAI31846008
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aJoo, Yoon Ki.
■24510▼aInvestigating Non-Canonical Roles of ATR and CHK1 Throughout the Cell Cycle
■260 ▼a[Sl]▼bYale University▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a157 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-12, Section: B.
■500 ▼aAdvisor: Kabeche, Lilian;Solomon, Mark.
■5021 ▼aThesis (Ph.D.)--Yale University, 2025.
■520 ▼aChromosome Instability (CIN), which results from DNA damage in interphase and chromosome missegregation in mitosis, is considered to be a potent driver of cancer. To prevent CIN, cells harbor the DNA Damage Response (DDR) pathway, which is responsible for detecting and repairing damaged DNA. Because of their importance in preventing CIN, the core members of the DDR pathway such as Ataxia Telangiectasia and Rad3-related (ATR) and Checkpoint kinase 1 (CHK1) have been studied as promising targets in cancer therapy. However, clinical trials show that ATR and CHK1 inhibitors elicit adverse side effects with unknown reasons. Recent research suggests that one of the reasons for the unexpected side effects is that ATR and CHK1 are multi-faceted proteins that are involved in multiple different pathways while the current clinical strategies only focus on their role in the DDR pathway. In this dissertation, we show that ATR and CHK1 have multiple roles throughout the cell cycle that is not limited to the DDR pathway in both promoting the rupture of micronucleus (MN) in interphase and faithful chromosome segregation during mitosis.
■590 ▼aSchool code: 0265.
■650 4▼aBiology
■650 4▼aMicrobiology
■650 4▼aCellular biology
■650 4▼aMolecular biology
■650 4▼aGenetics
■653 ▼aChromosome Instability
■653 ▼aDNA Damage Response
■653 ▼aCheckpoint kinase 1
■653 ▼aMicronucleus
■690 ▼a0306
■690 ▼a0379
■690 ▼a0410
■690 ▼a0369
■690 ▼a0307
■71020▼aYale University▼bMolecular Biophysics and Biochemistry.
■7730 ▼tDissertations Abstracts International▼g86-12B.
■790 ▼a0265
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17356776▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
