The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function

Yin, Jianwen; Cao, Dayan; Xiao, Deyong; Zhou, Zhongjun; Liu, Ying; Shou, Weinian

doi:10.3389/fcell.2021.668659

Cited by 19 publications

(14 citation statements)

References 71 publications

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“…S5B). Some of these RBP motifs were correlated with a higher effective transport rate, e.g., HNRNPK and QKI [13][14][15][16] . Conversely, there are some RBP motifs on the 3′-UTR that correlate with a lower effective transport rate, e.g., HNRNPLL [17][18][19] and YBX1 [20][21][22][23] .…”

Section: Transport Parameters Correlate With Gene Structure and Seque...mentioning

confidence: 99%

Kinetics of mRNA nuclear export regulate innate immune response gene expression

et al. 2022

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The abundance and stimulus-responsiveness of mature mRNA is thought to be determined by nuclear synthesis, processing, and cytoplasmic decay. However, the rate and efficiency of moving mRNA to the cytoplasm almost certainly contributes, but has rarely been measured. Here, we investigated mRNA export rates for innate immune genes. We generated high spatio-temporal resolution RNA-seq data from endotoxin-stimulated macrophages and parameterized a mathematical model to infer kinetic parameters with confidence intervals. We find that the effective chromatin-to-cytoplasm export rate is gene-specific, varying 100-fold: for some genes, less than 5% of synthesized transcripts arrive in the cytoplasm as mature mRNAs, while others show high export efficiency. Interestingly, effective export rates do not determine temporal gene responsiveness, but complement the wide range of mRNA decay rates; this ensures similar abundances of short- and long-lived mRNAs, which form successive innate immune response expression waves.

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Section: Transport Parameters Correlate With Gene Structure and Seque...mentioning

confidence: 99%

Kinetics of mRNA nuclear export regulate innate immune response gene expression

et al. 2022

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“…As the member of the signal transduction and activation of RNA (STAR) family, QKI-5 is critical in regulating pre-mRNA posttranscriptional processing, intracellular migration, and mRNA stability. QKI-5 can regulate pre-mRNA splicing, transportation or stability differently in a unique cell type-speci c manner [23]. QKI-5 inhibits pro-metastasis processes of lung cancer cells through interdicting β-catenin signaling pathway, and that QKI-5 promoter hypermethylation is a crucial epigenetic regulation reducing QKI-5 expression in lung cancer cells [24].…”

Section: Discussionmentioning

confidence: 99%

MiR-183-5p Promotes the Cell Proliferation of Colorectal Cancer by Targeting QKI-5

Liu¹,

Mei

Qin

et al. 2022

Preprint

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Background Colorectal cancer is the third most common malignant tumor in the world and the fourth most common cancer-related death cause. Previous studies have confirmed that miR-183-5P is considered to be a cancer-associated miRNA in several tumor types. Methods We analyzed the expression of miR-183-5P in cancer tissues and adjacent tissues in TCGA database. The expression of miR-183-5P and QKI-5 mRNA was measured by RT-qPCR and western blot. CCK-8 were used to indicate the proliferation capacity. BALB/c nude mice were used to simulate in vivo experiments. Results In this study, we identified miR-183-5p as a tumor promoter in colorectal cancer. The expression of miR-183-5p was found upregulated in human colorectal cancer tissues while QKI-5 was down-regulated. CCK-8 assay demonstrated that miR-183-5p promoted colorectal cancer cell proliferation. We also found miR183-5P can target QKI-5 and inhibit its expression in CRC cell lines. Restoration of QKI-5 reversed the effects of miR-183-5p in colorectal cancer cells. Conclusion Taken together, our results suggest that miR-183-5p might function as a tumor-promoting factor in colorectal cancer and might contribute to its proliferation.

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“…TBX20 and DSG2 are localized in humans on chromosome 7 and 18, respectively. TBX20 encodes a transcription factor, which is involved in embryonic cardiac development and organogenesis (for a review, see [32]). Mutations in TBX20 cause a complex and broad spectrum of heart defects, including septal defects, DCM, and arrhythmia [31].…”

Section: Discussionmentioning

confidence: 99%

The Double Mutation DSG2-p.S363X and TBX20-p.D278X Is Associated with Left Ventricular Non-Compaction Cardiomyopathy: Case Report

Myasnikov

Brodehl

Мешков

et al. 2021

IJMS

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Left ventricular non-compaction cardiomyopathy (LVNC) is a rare heart disease, with or without left ventricular dysfunction, which is characterized by a two-layer structure of the myocardium and an increased number of trabeculae. The study of familial forms of LVNC is helpful for risk prediction and genetic counseling of relatives. Here, we present a family consisting of three members with LVNC. Using a next-generation sequencing approach a combination of two (likely) pathogenic nonsense mutations DSG2-p.S363X and TBX20-p.D278X was identified in all three patients. TBX20 encodes the cardiac T-box transcription factor 20. DSG2 encodes desmoglein–2, which is part of the cardiac desmosomes and belongs to the cadherin family. Since the identified nonsense variant (DSG2-p.S363X) is localized in the extracellular domain of DSG2, we performed in vitro cell transfection experiments. These experiments revealed the absence of truncated DSG2 at the plasma membrane, supporting the pathogenic relevance of DSG2-p.S363X. In conclusion, we suggest that in the future, these findings might be helpful for genetic screening and counseling of patients with LVNC.

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The Emerging Roles of the RNA Binding Protein QKI in Cardiovascular Development and Function

Cited by 19 publications

References 71 publications

Kinetics of mRNA nuclear export regulate innate immune response gene expression

Kinetics of mRNA nuclear export regulate innate immune response gene expression

MiR-183-5p Promotes the Cell Proliferation of Colorectal Cancer by Targeting QKI-5

The Double Mutation DSG2-p.S363X and TBX20-p.D278X Is Associated with Left Ventricular Non-Compaction Cardiomyopathy: Case Report

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