ArticleRNA (New York, N.Y.)2006
Non-snRNP U1A levels decrease during mammalian B-cell differentiation and release the IgM secretory poly(A) site from repression.
Article in RNA (New York, N.Y.), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- The emerging roles of alternative splicing in modulating tumor immune responses and immunotherapies.Cell death and differentiation · 2026Review
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- U1 snRNP proteins promote proximal alternative polyadenylation sites by directly interacting with 3' end processing core factors.Journal of molecular cell biology · 2022Article
- Linking Endoplasmic Reticular Stress and Alternative Splicing.International journal of molecular sciences · 2018Review
- RNA Splicing in the Transition from B Cells to Antibody-Secreting Cells: The Influences of ELL2, Small Nuclear RNA, and Endoplasmic Reticulum Stress.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Cytoplasmic poly(A)-binding protein 1 (PABPC1) interacts with the RNA-binding protein hnRNPLL and thereby regulates immunoglobulin secretion in plasma cells.The Journal of biological chemistry · 2017Article
- Splicing in immune cells-mechanistic insights and emerging topics.International immunology · 2017Review
- The reciprocal regulation between splicing and 3'-end processing.Wiley interdisciplinary reviews. RNA · 2016Review
- Coordination of RNA Polymerase II Pausing and 3' End Processing Factor Recruitment with Alternative Polyadenylation.Molecular and cellular biology · 2016Article
- Zfp318 regulates IgD expression by abrogating transcription termination within the Ighm/Ighd locus.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Plasma cell formation, secretion, and persistence: the short and the long of it.Critical reviews in immunology · 2014Review
- A novel intra-U1 snRNP cross-regulation mechanism: alternative splicing switch links U1C and U1-70K expression.PLoS genetics · 2013Article
- U1 snRNP-Dependent Suppression of Polyadenylation: Physiological Role and Therapeutic Opportunities in Cancer.International journal of cell biology · 2013Review
- Transcription elongation factor ELL2 directs immunoglobulin secretion in plasma cells by stimulating altered RNA processing.Nature immunology · 2009Article
- Regulation of bovine papillomavirus type 1 gene expression by RNA processing.Frontiers in bioscience (Landmark edition) · 2009Review
- Article
- A bipartite U1 site represses U1A expression by synergizing with PIE to inhibit nuclear polyadenylation.RNA (New York, N.Y.) · 2007Article
- Mechanisms controlling production of membrane and secreted immunoglobulin during B cell development.Immunologic research · 2007Review
- Multiple features contribute to the use of the immunoglobulin M secretion-specific poly(A) signal but are not required for developmental regulation.Molecular and cellular biology · 2006Article
- The role of RNA structure in the interaction of U1A protein with U1 hairpin II RNA.RNA (New York, N.Y.) · 2006Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
A regulated shift from the production of membrane to secretory forms of Immunoglobulin M (IgM) mRNA occurs during B cell differentiation due to the activation of an upstream secretory poly(A) site. U1A plays a key role in inhibiting the expression of the secretory poly(A) site by inhibiting both cleavage at the poly(A) site and subsequent poly(A) tail addition. However, how the inhibitory effect of U1A is alleviated in differentiated cells, which express the secretory poly(A) site, is not known. Using B cell lines representing different stages of B cell differentiation, we show that the amount of U1A available to inhibit the secretory poly(A) site is reduced in differentiated cells. Undifferentiated B cells have more total U1A than differentiated cells and a greater proportion of this is not associated with the U1snRNP. We show that this is available to inhibit poly(A) addition at the secretory poly(A) site using cold competitor RNA oligos to de-repress poly(A) addition in nuclear extracts from the respective cell lines. In addition, endogenous non-snRNP associated U1A-immunopurified from the different cell lines-inhibits poly(A) polymerase activity proportional to U1A recovered, suggesting that available U1A level alone is responsible for changes in its inhibitory effect at the secretory IgM poly (A) site.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.