Modulation of Gene Expression by RNA Binding Proteins: mRNA Stability and Translation

Abdelmohsen, Kotb

doi:10.5772/48485

Cited by 8 publications

(4 citation statements)

References 98 publications

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“…CELF1 can act by relieving secondary structures on a subset of target RNAs that exhibit G-rich sequence stretches with a high-degree of secondary structure, thereby promoting their translatability. Furthermore, if (hyper)phosphorylated, CELF1 may form a multisubunit complex with eukaryotic initiation factor eIF2 and other translation initiation factors, promoting the translation of protein products from alternative start codons in mRNAs that bear an IRES motif ( 100 , 101 ). Importantly, the different effects of CELF1 on the translation of target mRNAs depend on its phosphorylation status and on the overall level of available protein, which is controlled in accordance with the stage of myogenic differentiation.…”

Section: Myotonic Dystrophymentioning

confidence: 99%

Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy

et al. 2018

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Myotonic dystrophy type 1 (DM1) and 2 (DM2) are autosomal dominant degenerative neuromuscular disorders characterized by progressive skeletal muscle weakness, atrophy, and myotonia with progeroid features. Although both DM1 and DM2 are characterized by skeletal muscle dysfunction and also share other clinical features, the diseases differ in the muscle groups that are affected. In DM1, distal muscles are mainly affected, whereas in DM2 problems are mostly found in proximal muscles. In addition, manifestation in DM1 is generally more severe, with possible congenital or childhood-onset of disease and prominent CNS involvement. DM1 and DM2 are caused by expansion of (CTG•CAG)n and (CCTG•CAGG)n repeats in the 3′ non-coding region of DMPK and in intron 1 of CNBP, respectively, and in overlapping antisense genes. This critical review will focus on the pleiotropic problems that occur during development, growth, regeneration, and aging of skeletal muscle in patients who inherited these expansions. The current best-accepted idea is that most muscle symptoms can be explained by pathomechanistic effects of repeat expansion on RNA-mediated pathways. However, aberrations in DNA replication and transcription of the DM loci or in protein translation and proteome homeostasis could also affect the control of proliferation and differentiation of muscle progenitor cells or the maintenance and physiological integrity of muscle fibers during a patient’s lifetime. Here, we will discuss these molecular and cellular processes and summarize current knowledge about the role of embryonic and adult muscle-resident stem cells in growth, homeostasis, regeneration, and premature aging of healthy and diseased muscle tissue. Of particular interest is that also progenitor cells from extramuscular sources, such as pericytes and mesoangioblasts, can participate in myogenic differentiation. We will examine the potential of all these types of cells in the application of regenerative medicine for muscular dystrophies and evaluate new possibilities for their use in future therapy of DM.

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Section: Myotonic Dystrophymentioning

confidence: 99%

Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy

et al. 2018

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“…Gene expression regulation is an essential process by which cells react to microenvironment changes. One of the key mechanisms of gene expression regulation occurs at post-transcriptional levels, i.e on mRNA [ 1 ]. RNA regulation allows cells to react to environmental stimuli more quickly than de novo transcription.…”

Section: Introductionmentioning

confidence: 99%

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

et al. 2016

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RNA binding proteins (RBPs) play a central role in cell physiology and pathology. Among them, HuR is a nuclear RBP, which shuttles to the cytoplasm to allow its RNA targets processing. HuR over-expression and delocalization are often associated to cell transformation. Numerous cancers display increased HuR protein levels and its high cytoplasmic levels has been associated with a worse prognosis.In our study, we first evaluated HuR expression in normal and cancer thyroid tissues and then evaluated its function in thyroid cell lines. HuR is over-expressed in all thyroid tumor tissues; high cytoplasmic levels are detected in all thyroid carcinomas. HuR silencing decreased cell viability and determined apoptotic cell death, in a non-tumorigenic (Nthy-ori-3.1) and a tumorigenic (BCPAP) thyroid cell line. Global transcriptome analysis indicated that HuR silencing, though having similar biological effects, induces distinct gene expression modifications in the two cell lines. By using the RIP-seq approach, the HuR-bound RNA profiles of different thyroid cell lines were evaluated. We show that in distinct cell lines HuR-bound RNA profiles are different. A set of 114 HuR-bound RNAs distinguishing tumorigenic cell lines from the non-tumorigenic one was identified.Altogether, our data indicate that HuR plays a role in thyroid tumorigenesis. Moreover, our findings are a proof of concept that RBP targets differ between cells with the same origin but with distinct biological behavior.

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“…RIG-I Enhances RNA Stability and Up-Regulates the Transcription of TRIM25. It has been reported that RNA-binding proteins usually play key roles in the regulation of mRNA stability (36). To investigate the mechanism underlying the up-regulation of TRIM25 mediated by RIG-I, we tested the stability of TRIM25 mRNA through an actinomycin D (ActD) chase experiment in NB4 cells before and after ATRA induction.…”

Section: Resultsmentioning

confidence: 99%

RIG-I regulates myeloid differentiation by promoting TRIM25-mediated ISGylation

Shi

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Retinoic acid-inducible gene I (RIG-I) is up-regulated during granulocytic differentiation of acute promyelocytic leukemia (APL) cells induced by all-transretinoic acid (ATRA). It has been reported that RIG-I recognizes virus-specific 5′-ppp-double-stranded RNA (dsRNA) and activates the type I interferons signaling pathways in innate immunity. However, the functions of RIG-I in hematopoiesis remain unclear, especially regarding its possible interaction with endogenous RNAs and the associated pathways that could contribute to the cellular differentiation and maturation. Herein, we identified a number of RIG-I–binding endogenous RNAs in APL cells following ATRA treatment, including the tripartite motif-containing protein 25 (TRIM25) messenger RNA (mRNA).TRIM25encodes the protein known as an E3 ligase for ubiquitin/interferon (IFN)-induced 15-kDa protein (ISG15) that is involved in RIG-I–mediated antiviral signaling. We show that RIG-I could bindTRIM25mRNA via its helicase domain and C-terminal regulatory domain, enhancing the stability ofTRIM25transcripts. RIG-I could increase the transcriptional expression ofTRIM25by caspase recruitment domain (CARD) domain through an IFN-stimulated response element. In addition, RIG-I activated other key genes in the ISGylation pathway by activating signal transducer and activator of transcription 1 (STAT1), including the modifier ISG15 and several enzymes responsible for the conjugation of ISG15 to protein substrates. RIG-I cooperated with STAT1/2 and interferon regulatory factor 1 (IRF1) to promote the activation of the ISGylation pathway. The integrity of ISGylation in ATRA or RIG-I–induced cell differentiation was essential given that knockdown of TRIM25 or ISG15 resulted in significant inhibition of this process. Our results provide insight into the role of the RIG-I-TRIM25-ISGylation axis in myeloid differentiation.

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Modulation of Gene Expression by RNA Binding Proteins: mRNA Stability and Translation

Cited by 8 publications

References 98 publications

Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy

Abnormalities in Skeletal Muscle Myogenesis, Growth, and Regeneration in Myotonic Dystrophy

Identification of tumorigenesis-related mRNAs associated with RNA-binding protein HuR in thyroid cancer cells

RIG-I regulates myeloid differentiation by promoting TRIM25-mediated ISGylation

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