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Autophagy and Cellular Signaling: A Two-Way Relationship
Autophagy and Cellular Signaling: A Two-Way Relationship
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20250211152736
- ISBN
- 9798384456735
- DDC
- 574
- 서명/저자
- Autophagy and Cellular Signaling: A Two-Way Relationship
- 발행사항
- [Sl] : University of California, Berkeley, 2024
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2024
- 형태사항
- 60 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 86-04, Section: B.
- 주기사항
- Includes supplementary digital materials.
- 주기사항
- Advisor: Zoncu, Roberto.
- 학위논문주기
- Thesis (Ph.D.)--University of California, Berkeley, 2024.
- 초록/해제
- 요약The correct function of organisms ranging from bacteria to humans critically depends on the cells' ability to rapidly change its metabolism through dedicated signaling cascades that transduce signals present in the surrounding environment. Two examples of these signaling cascades: mechanistic target of rapamycin complex 1 (mTORC1) and cAMP-dependent protein kinase A (PKA) work in tangent with cellular processes like autophagy to maintain cellular homeostasis. The two-way regulation between mTORC1 and autophagy is clear but the relationship between autophagy and PKA is more complex. Here I will focus on this complex interaction and propose a model where autophagy is regulating the PKA holoenzyme but also becomes a signaling scaffold for AKAP11-bound PKA. Furthermore, I also talk about the implications of our findings in the context of schizophrenia and bipolar disorder.
- 일반주제명
- Cellular biology
- 일반주제명
- Biology
- 일반주제명
- Molecular biology
- 키워드
- Protein kinase A
- 키워드
- Bipolar disorder
- 기타저자
- University of California, Berkeley Molecular & Cell Biology
- 기본자료저록
- Dissertations Abstracts International. 86-04B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■00520250211152736
■006m o d
■007cr#unu||||||||
■020 ▼a9798384456735
■035 ▼a(MiAaPQ)AAI31491378
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aSegura-Roman, Ashley.
■24510▼aAutophagy and Cellular Signaling: A Two-Way Relationship
■260 ▼a[Sl]▼bUniversity of California, Berkeley▼c2024
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2024
■300 ▼a60 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 86-04, Section: B.
■500 ▼aIncludes supplementary digital materials.
■500 ▼aAdvisor: Zoncu, Roberto.
■5021 ▼aThesis (Ph.D.)--University of California, Berkeley, 2024.
■520 ▼aThe correct function of organisms ranging from bacteria to humans critically depends on the cells' ability to rapidly change its metabolism through dedicated signaling cascades that transduce signals present in the surrounding environment. Two examples of these signaling cascades: mechanistic target of rapamycin complex 1 (mTORC1) and cAMP-dependent protein kinase A (PKA) work in tangent with cellular processes like autophagy to maintain cellular homeostasis. The two-way regulation between mTORC1 and autophagy is clear but the relationship between autophagy and PKA is more complex. Here I will focus on this complex interaction and propose a model where autophagy is regulating the PKA holoenzyme but also becomes a signaling scaffold for AKAP11-bound PKA. Furthermore, I also talk about the implications of our findings in the context of schizophrenia and bipolar disorder.
■590 ▼aSchool code: 0028.
■650 4▼aCellular biology
■650 4▼aBiology
■650 4▼aMolecular biology
■653 ▼aMechanistic target of rapamycin complex 1
■653 ▼aProtein kinase A
■653 ▼aBipolar disorder
■653 ▼aSchizophrenia disorder
■690 ▼a0379
■690 ▼a0306
■690 ▼a0307
■71020▼aUniversity of California, Berkeley▼bMolecular & Cell Biology.
■7730 ▼tDissertations Abstracts International▼g86-04B.
■790 ▼a0028
■791 ▼aPh.D.
■792 ▼a2024
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17163652▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
