التفاصيل البيبلوغرافية
العنوان: |
Genomic functions of U2AF in constitutive and regulated splicing |
المؤلفون: |
Wu, Tongbin, Fu, Xiang-Dong |
المصدر: |
RNA Biology, vol 12, iss 5 |
بيانات النشر: |
eScholarship, University of California |
سنة النشر: |
2015 |
المجموعة: |
University of California: eScholarship |
مصطلحات موضوعية: |
Biological Sciences, Bioinformatics and Computational Biology, Human Genome, Biotechnology, Genetics, 1.1 Normal biological development and functioning, Underpinning research, Generic health relevance, Alternative Splicing, Conserved Sequence, Disease, Genome, Humans, Models, Biological, Nuclear Proteins, Protein Binding, Protein Structure, Tertiary, Ribonucleoproteins, Spliceosomes, Splicing Factor U2AF, regulated splicing, genomic binding profile, definition of functional 3 ', U2AF heterodimer, splice sites, cooperation and competition in RNA binding, disease mechanism, definition of functional 3′ |
جغرافية الموضوع: |
479 - 485 |
الوصف: |
The U2AF heterodimer is generally accepted to play a vital role in defining functional 3' splice sites in pre-mRNA splicing. Given prevalent mutations in U2AF, particularly in the U2AF1 gene (which encodes for the U2AF35 subunit) in blood disorders and other human cancers, there are renewed interests in these classic splicing factors to further understand their regulatory functions in RNA metabolism in both physiological and disease settings. We recently reported that U2AF has a maximal capacity to directly bind ˜88% of functional 3' splice sites in the human genome and that numerous U2AF binding events also occur in various exonic and intronic locations, thus providing additional mechanisms for the regulation of alternative splicing besides their traditional role in titrating weak splice sites in the cell. These findings, coupled with the existence of multiple related proteins to both U2AF65 and U2AF35, beg a series of questions on the universal role of U2AF in functional 3' splice site definition, their binding specificities in vivo, potential mechanisms to bypass their requirement for certain intron removal events, contribution of splicing-independent functions of U2AF to important cellular functions, and the mechanism for U2AF mutations to invoke specific diseases in humans. |
نوع الوثيقة: |
article in journal/newspaper |
وصف الملف: |
application/pdf |
اللغة: |
unknown |
العلاقة: |
qt60730790; https://escholarship.org/uc/item/60730790Test |
الإتاحة: |
https://escholarship.org/uc/item/60730790Test |
حقوق: |
public |
رقم الانضمام: |
edsbas.CF9BDAAA |
قاعدة البيانات: |
BASE |