scholarly journals Changes in the process of alternative RNA splicing results in soluble B and T lymphocyte attenuator with biological and clinical implications in critical illness

2018 ◽  
Vol 24 (1) ◽  
Author(s):  
Sean F. Monaghan ◽  
Debasree Banerjee ◽  
Chun-Shiang Chung ◽  
Joanne Lomas-Neira ◽  
Kamil J. Cygan ◽  
...  
Author(s):  
Hengzhen Li ◽  
WenFeng Xiao ◽  
Yuqiong He ◽  
Zeqin Wen ◽  
Siyuan Cheng ◽  
...  

N6-methyladenosine (m6A) is an important modification of eukaryotic mRNA. Since the first discovery of the corresponding demethylase and the subsequent identification of m6A as a dynamic modification, the function and mechanism of m6A in mammalian gene regulation have been extensively investigated. “Writer”, “eraser” and “reader” proteins are key proteins involved in the dynamic regulation of m6A modifications, through the anchoring, removal, and interpretation of m6A modifications, respectively. Remarkably, such dynamic modifications can regulate the progression of many diseases by affecting RNA splicing, translation, export and degradation. Emerging evidence has identified the relationship between m6A modifications and degenerative musculoskeletal diseases, such as osteoarthritis, osteoporosis, sarcopenia and degenerative spinal disorders. Here, we have comprehensively summarized the evidence of the pathogenesis of m6A modifications in degenerative musculoskeletal diseases. Moreover, the potential molecular mechanisms, regulatory functions and clinical implications of m6A modifications are thoroughly discussed. Our review may provide potential prospects for addressing key issues in further studies.


2019 ◽  
Vol 219 (1) ◽  
Author(s):  
Elizabeth M. Park ◽  
Phillip M. Scott ◽  
Kevin Clutario ◽  
Katelyn B. Cassidy ◽  
Kevin Zhan ◽  
...  

Centriole duplication occurs once in each cell cycle to maintain centrosome number. A previous genome-wide screen revealed that depletion of 14 RNA splicing factors leads to a specific defect in centriole duplication, but the cause of this deficit remains unknown. Here, we identified an additional pre-mRNA splicing factor, WBP11, as a novel protein required for centriole duplication. Loss of WBP11 results in the retention of ∼200 introns, including multiple introns in TUBGCP6, a central component of the γ-TuRC. WBP11 depletion causes centriole duplication defects, in part by causing a rapid decline in the level of TUBGCP6. Several additional splicing factors that are required for centriole duplication interact with WBP11 and are required for TUBGCP6 expression. These findings provide insight into how the loss of a subset of splicing factors leads to a failure of centriole duplication. This may have clinical implications because mutations in some spliceosome proteins cause microcephaly and/or growth retardation, phenotypes that are strongly linked to centriole defects.


1996 ◽  
Vol 22 (2) ◽  
pp. 145-150 ◽  
Author(s):  
T. C. Hunter ◽  
S. B. Melancon ◽  
L. Dallaire ◽  
S. Taft ◽  
T. R. Skopek ◽  
...  

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