RMI1 contributes to DNA repair and to the tolerance to camptothecin

Fang, Lianying; Sun, Xinwei; Wang, Yan; Du, Liqing; Ji, Kaihua; Wang, Jinhan; He, Ningning; Liu, Yang; Wang, Qin; Zhai, Hezheng; Hao, Jianhua; Xu, Chang; Liu, Qiang

doi:10.1096/fj.201802014r

Cited by 11 publications

(4 citation statements)

References 37 publications

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“…Two cellular RNA binding proteins of hnRNPK and NS1-BP have important roles in regulating influenza A virus RNA splicing [27] . As for the RMI1 gene, its protein is an essential component of the RMI complex, which has a crucial role in DNA repair and maintaining genome stability [28] . Since there existed important functions of these identified genes, molecular studies are warrant to illustrate the functional consequences of detected association signals.…”

Section: Discussionmentioning

confidence: 99%

Integrative Genomics Analysis Reveals a Novel 21q22.11 Locus Contributing to Susceptibility of COVID-19

Huang

Zhao

et al. 2020

Preprint

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The systematic identification of host genetic risk factors is essential for the understanding and treatment of COVID-19. By performing a meta-analysis of two independent genome-wide association (GWAS) summary datasets (N = 680,128), a novel locus at 21q22.11 was identified to be associated with COVID-19 infection (rs9976829 in IFNAR2 and upstream of IL10RB, OR = 1.16, 95% CI = 1.09 - 1.23, P = 2.57*10-6). The rs9976829 represents a strong splicing quantitative trait locus (sQTL) for both IFNAR2 and IL10RB genes, especially in lung tissue (P = 1.8*10-24). Gene-based association analysis also found IFNAR2 was significantly associated with COVID-19 infection (P = 2.58*10-7). Integrative genomics analysis of combining GWAS with eQTL data showed the expression variations of IFNAR2 and IL10RB have prominent effects on COVID-19 in various types of tissues, especially in lung tissue. The majority of IFNAR2-expressing cells were dendritic cells (40%) and plasmacytoid dendritic cells (38.5%), and IL10RB-expressing cells were mainly nonclassical monocytes (29.6%). IFNAR2 and IL10RB are targeted by several interferons-related drugs. Together, our results uncover 21q22.11 as a novel susceptibility locus for COVID-19, in which individuals with G alleles of rs9976829 have a higher probability of COVID-19 susceptibility than those with non-G alleles.

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Section: Discussionmentioning

confidence: 99%

Integrative Genomics Analysis Reveals a Novel 21q22.11 Locus Contributing to Susceptibility of COVID-19

Huang

Zhao

et al. 2020

Preprint

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“…It is a M1 marker and a key regulator of the innate immune response of the CNS during stress [ 91 – 93 ]. MIER1 , a transcriptional repressor [ 94 ], and RMI1, a DNA repair protein [ 95 ], were also positively correlated with stroke severity. Variants in these genes are associated with monocyte counts [ 96 ] and myeloid white cell counts [ 96 ], respectively; and expression positively correlates with the infiltration of monocytes, macrophages, and other immune cells in gastric carcinoma [ 97 ].…”

Section: Discussionmentioning

confidence: 99%

Monocyte, neutrophil, and whole blood transcriptome dynamics following ischemic stroke

Carmona-Mora¹,

Knepp²,

Jickling

et al. 2023

BMC Med

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Background After ischemic stroke (IS), peripheral leukocytes infiltrate the damaged region and modulate the response to injury. Peripheral blood cells display distinctive gene expression signatures post-IS and these transcriptional programs reflect changes in immune responses to IS. Dissecting the temporal dynamics of gene expression after IS improves our understanding of immune and clotting responses at the molecular and cellular level that are involved in acute brain injury and may assist with time-targeted, cell-specific therapy. Methods The transcriptomic profiles from peripheral monocytes, neutrophils, and whole blood from 38 ischemic stroke patients and 18 controls were analyzed with RNA-seq as a function of time and etiology after stroke. Differential expression analyses were performed at 0–24 h, 24–48 h, and >48 h following stroke. Results Unique patterns of temporal gene expression and pathways were distinguished for monocytes, neutrophils, and whole blood with enrichment of interleukin signaling pathways for different time points and stroke etiologies. Compared to control subjects, gene expression was generally upregulated in neutrophils and generally downregulated in monocytes over all times for cardioembolic, large vessel, and small vessel strokes. Self-organizing maps identified gene clusters with similar trajectories of gene expression over time for different stroke causes and sample types. Weighted Gene Co-expression Network Analyses identified modules of co-expressed genes that significantly varied with time after stroke and included hub genes of immunoglobulin genes in whole blood. Conclusions Altogether, the identified genes and pathways are critical for understanding how the immune and clotting systems change over time after stroke. This study identifies potential time- and cell-specific biomarkers and treatment targets.

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“…It is a M1 marker, and a key regulator of the innate immune response of the CNS during stress [86–88]. MIER1, a transcriptional repressor [89], and RMI1, a DNA repair protein [90], were also positively correlated with stroke severity. Variants in these genes are associated with monocyte counts [91], and myeloid white cell counts [91], respectively; and expression positively correlates with the infiltration of monocytes, macrophages and other immune cells in gastric carcinoma [92].…”

Section: Discussionmentioning

confidence: 99%

Monocyte, Neutrophil and Whole Blood Transcriptome Dynamics Following Ischemic Stroke

Carmona-Mora

Knepp

Jickling

et al. 2022

Preprint

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BackgroundAfter ischemic stroke (IS), peripheral leukocytes infiltrate the damaged region and modulate the response to injury. Peripheral blood cells display distinctive gene expression signatures post IS and these transcriptional programs reflect changes in immune responses to IS. Dissecting the temporal dynamics of gene expression after IS improves our understanding of immune and clotting responses at the molecular and cellular level that are involved in acute brain injury and may assist with time-targeted, cell-specific therapy.MethodsThe transcriptomic profiles from peripheral monocytes, neutrophils, and whole blood from 38 ischemic stroke patients and 18 controls were analyzed with RNAseq as a function of time and etiology after stroke. Differential expression analyses were performed at 0-24 h, 24-48 h, and >48 h following stroke.ResultsUnique patterns of temporal gene expression and pathways were distinguished for monocytes, neutrophils and whole blood with enrichment of interleukin signaling pathways for different timepoints and stroke etiologies. Compared to control subjects, gene expression was generally up-regulated in neutrophils and generally down- regulated in monocytes over all times for cardioembolic, large vessel and small vessel strokes. Self-Organizing Maps identified gene clusters with similar trajectories of gene expression over time for different stroke causes and sample types. Weighted Gene Co- expression Network Analyses identified modules of co-expressed genes that significantly varied with time after stroke and included hub genes of immunoglobulin genes in whole blood.ConclusionsAltogether, the identified genes and pathways are critical for understanding how the immune and clotting systems change over time after stroke. This study identifies potential time- and cell-specific biomarkers and treatment targets.

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RMI1 contributes to DNA repair and to the tolerance to camptothecin

Cited by 11 publications

References 37 publications

Integrative Genomics Analysis Reveals a Novel 21q22.11 Locus Contributing to Susceptibility of COVID-19

Integrative Genomics Analysis Reveals a Novel 21q22.11 Locus Contributing to Susceptibility of COVID-19

Monocyte, neutrophil, and whole blood transcriptome dynamics following ischemic stroke

Monocyte, Neutrophil and Whole Blood Transcriptome Dynamics Following Ischemic Stroke

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