자료유형 | 학위논문 |
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서명/저자사항 | Networks of Splice Factor Regulation by Unproductive Splicing Coupled With NMD. |
개인저자 | Desai, Anna Maria. |
단체저자명 | University of California, Berkeley. Biological Science. |
발행사항 | [S.l.]: University of California, Berkeley., 2017. |
발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2017. |
형태사항 | 80 p. |
기본자료 저록 | Dissertation Abstracts International 79-08B(E). Dissertation Abstract International |
ISBN | 9780355832174 |
학위논문주기 | Thesis (Ph.D.)--University of California, Berkeley, 2017. |
일반주기 |
Source: Dissertation Abstracts International, Volume: 79-08(E), Section: B.
Adviser: Steven E. Brenner. |
이용제한사항 | This item is not available from ProQuest Dissertations & Theses. |
요약 | Virtually all multi-exon genes undergo alternative splicing (AS) to generate multiple protein isoforms. Alternative splicing is regulated by splicing factors, such as the serine/arginine rich (SR) protein family and the heterogeneous nuclear rib |
요약 | The NMD pathway has a role in preventing accumulation of erroneous transcripts with dominant negative phenotypes. During the pioneer round of translation, NMD recognizes mRNA transcripts with in-frame premature termination codons (PTCs) and degr |
요약 | Approximately 18% of expressed genes are reported to be natural targets of NMD, yet it still remains unclear why the human genome would express mRNAs that are immediately degraded by the NMD pathway. It is especially intriguing that splicing fac |
요약 | Regulation via alternative splicing coupled to NMD requires binding of a splicing factor to the regulated mRNA. CLIP-seq and related studies reveal that splicing factors bind abundantly to all transcripts of our selected 100 splicing factors. In |
요약 | Dr. Courtney French, Dr. Hu, and I combined experimental data and a model for NMD mechanism to identify targets of NMD. I inhibited NMD in HeLa and GM12878 cells via knockdown of UPF1 and SMG6, two core NMD factors, and by exposure to cyclohexim |
일반주제명 | Genetics. Biochemistry. |
언어 | 영어 |
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