서브메뉴
검색
Ubiquitin-Dependent Control of AKT Signaling During Myogenesis
Ubiquitin-Dependent Control of AKT Signaling During Myogenesis
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202103603
- ISBN
- 9798288865800
- DDC
- 574
- 저자명
- Padovani, Chris.
- 서명/저자
- Ubiquitin-Dependent Control of AKT Signaling During Myogenesis
- 발행사항
- [Sl] : University of California, Berkeley, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 38 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 87-01, Section: B.
- 주기사항
- Includes supplementary digital materials.
- 주기사항
- Advisor: Rape, Michael.
- 학위논문주기
- Thesis (Ph.D.)--University of California, Berkeley, 2025.
- 초록/해제
- 요약Muscle development requires that cells adopt specific identities at the right time and place within an embryo. Central to the success of this process are posttranslational modifications, such as ubiquitylation, that change activity, stability or localization of crucial transducers of differentiation signals. While many studies highlighted the importance of ubiquitylation during myogenesis, only few E3 ligases have been ascribed functions in this process. Here, we report that CUL3BTBD9, an E3 ligase associated with restless leg syndrome, is essential for myogenesis in vitro. CUL3BTBD9 binds and ubiquitylates CAV1, the central component of caveolae that modulate insulin signaling during muscle formation. CUL3BTBD9 and CAV1 are both required for insulin-dependent activation of the AKT kinase in myoblasts, thereby safeguarding the ability of muscle precursors to respond to insulin signals. Together, this work identifies CUL3BTBD9 as a regulator of myogenesis that acts by modulating plasma-membrane localized events critical for cell fate specification.
- 일반주제명
- Cellular biology
- 일반주제명
- Physiology
- 일반주제명
- Medicine
- 키워드
- Insulin
- 키워드
- Myogenesis
- 키워드
- Ubiquitylation
- 기타저자
- University of California, Berkeley Molecular & Cell Biology
- 기본자료저록
- Dissertations Abstracts International. 87-01B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
008260126s2025 us c eng d■001000017357808
■00520260202103603
■006m o d
■007cr#unu||||||||
■020 ▼a9798288865800
■035 ▼a(MiAaPQ)AAI32042581
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aPadovani, Chris.
■24510▼aUbiquitin-Dependent Control of AKT Signaling During Myogenesis
■260 ▼a[Sl]▼bUniversity of California, Berkeley▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a38 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 87-01, Section: B.
■500 ▼aIncludes supplementary digital materials.
■500 ▼aAdvisor: Rape, Michael.
■5021 ▼aThesis (Ph.D.)--University of California, Berkeley, 2025.
■520 ▼aMuscle development requires that cells adopt specific identities at the right time and place within an embryo. Central to the success of this process are posttranslational modifications, such as ubiquitylation, that change activity, stability or localization of crucial transducers of differentiation signals. While many studies highlighted the importance of ubiquitylation during myogenesis, only few E3 ligases have been ascribed functions in this process. Here, we report that CUL3BTBD9, an E3 ligase associated with restless leg syndrome, is essential for myogenesis in vitro. CUL3BTBD9 binds and ubiquitylates CAV1, the central component of caveolae that modulate insulin signaling during muscle formation. CUL3BTBD9 and CAV1 are both required for insulin-dependent activation of the AKT kinase in myoblasts, thereby safeguarding the ability of muscle precursors to respond to insulin signals. Together, this work identifies CUL3BTBD9 as a regulator of myogenesis that acts by modulating plasma-membrane localized events critical for cell fate specification.
■590 ▼aSchool code: 0028.
■650 4▼aCellular biology
■650 4▼aPhysiology
■650 4▼aMedicine
■653 ▼aInsulin
■653 ▼aMyogenesis
■653 ▼aUbiquitylation
■653 ▼aMuscle development
■653 ▼aRestless leg syndrome
■690 ▼a0379
■690 ▼a0564
■690 ▼a0719
■71020▼aUniversity of California, Berkeley▼bMolecular & Cell Biology.
■7730 ▼tDissertations Abstracts International▼g87-01B.
■790 ▼a0028
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17357808▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
