CBARA1 Plays a Role in Stemness and Proliferation of Human Embryonic Stem Cells

Chen, Kevin; Hsu, Lih-Tao; Wu, Cheng‐Yi; Chang, Shau-Feng; Huang, Hui-Ting; Chen, Wannhsin

doi:10.1371/journal.pone.0063653

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…noX5 may be able to reduce oxidative stress and may be associated with calcium ion channel-related oxidative stress in lymph nodes (44). WWP2 also exhibits protein binding and ligase activities (28); it is involved in the ubiquitination process, circulation and viral entry into host cells (28). WWP2 has a negative regulatory effect on Toll-like receptor 3-mediated innate immunity (45).…”

Section: Discussionmentioning

confidence: 99%

“…Based on P-values and the functions of related genes according to GenBank (https://www.ncbi.nlm.nih.gov/; accessed on February 18, 2018), four genes were ultimately selected for verification (Table VI). WWP2 is an e3 ubiquitin protein ligase containing a WW domain that participates in the ubiquitination process and viral entry into host cells (28). AKT2 has shown nucleotide binding, protein serine, threonine kinase, protein binding, aTP-binding and transferase activities, and participates in protein amino acid phosphorylation and diabetes development (29).…”

Section: Leukocytosis Vs Normal Controlmentioning

confidence: 99%

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Abnormal DNA methylation patterns in patients with infection‑caused leukocytopenia based on methylation microarrays

Muhataer

Wang

et al. 2020

Mol Med Report

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The present study aimed to investigate the association between gene methylation and leukocytopenia from the perspective of gene regulation. A total of 30 patients confirmed as having post-infection leukocytopenia at People's Hospital of Xinjiang uygur autonomous region between January 2016 and June 2017 were successively recruited as the leukocytopenia group; 30 patients with post-infection leukocytosis were enrolled as the leukocytosis group. in addition, 30 healthy volunteers who received a health examination at the hospital during the same period were included as the normal control group. in each group, four individuals were randomly selected for whole genome methylation screening. after selection of key methylation sites, the remaining samples in each group were used for verification using matrix-assisted laser desorption/ionization-time of flight mass spectrometry. The levels of serum complement factors c3 and c5 in the leukocytopenia group were significantly lower than those in the other two groups (P<0.05). according to whole-genome dna methylation detection, 66 and 27 methylation loci may be associated with leukocytopenia and leukocytosis, respectively. Most of these abnormal loci are located on chromosomes 2, 6, 7, 1, 17 and 11. The rates of WW domain containing e3 ubiquitin protein ligase 2 gene methylation at cytosine-phosphate-guanine (cpG)_1, cpG_5/6 and cpG_7 in the leukocytopenia group were higher than in the other two groups (P<0.05); the rate of AKT2 cpG_1 methylation was higher in the leukocytopenia group than in the other two groups (P<0.05); the rate of calcium-binding atopy-related autoantigen 1 gene cpG_2 methylation was higher in the leukocytosis group than in the normal control group (P<0.05); and the rate of nadPH oxidase 5 gene cpG_3 methylation was higher in the leukocytosis group than in the normal control group (P<0.05). chemotactic factor secretion and cell migration abnormalities, ubiquitination modification disorders and reduced oxidative burst may participate in infection-complicated leukocytopenia. The results of this study shed new light on the molecular biological mechanisms of infection-complicated leukocytopenia and provide novel avenues for diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

Section: Leukocytosis Vs Normal Controlmentioning

confidence: 99%

Abnormal DNA methylation patterns in patients with infection‑caused leukocytopenia based on methylation microarrays

Muhataer

Wang

et al. 2020

Mol Med Report

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“…15,16 Antony et al found that on liver-specific MICU1 loss, partial hepatectomy resulted in lethargic mice. Furthermore, the pro-inflammatory phase does not resolve in such mice and liver regeneration fails, with evidence of impaired cell cycle entry and extensive necrosis.…”

Section: Discussionmentioning

confidence: 99%

MICU1 may be a promising intervention target for gut-derived sepsis induced by intra-abdominal hypertension

Leng

Zhao

et al. 2016

Cell Death Discovery

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Intra-abdominal hypertension (IAH) is a common and serious complication in critically ill patients, for which there is no targeted therapy. IAH-induced dysfunction of intestinal barriers is closely associated with oxidative imbalances, which are considered to provide a pathophysiological basis for subsequent gut-derived sepsis. However, the upstream mechanism that produces oxidative damage during IAH remains unknown. It is not clear whether ‘mitochondrial Ca2+ uptake 1’ (MICU1, the key protein regulating the oxidative process) is involved in preventing Ca2+m (mitochondrial Ca2+) overload. Here, we detected changes in the expression of MICU1 during the development of increased intestinal permeability in rats with IAH, and we explored the related mechanism regulating epithelial-barrier functions by knocking-down micu1 in Caco-2 cells. Our results demonstrated that, to combat IAH-induced dysfunction of intestinal barriers, MICU1 undergoes a compensatory increase in expression, whereas ‘mitochondrial calcium uniporter’ (MCU) – a conserved Ca2+ transporter – becomes transcriptionally suppressed. Silencing the expression of MICU1 destroyed Caco-2 cell barrier integrity, promoted paracellular permeability, and impaired the expression of tight junction proteins (occludin, ZO-1, and claudin 1). Meanwhile, oxidative imbalances were induced; malondialdehyde (MDA), a product of oxidation, was increased and antioxidant products (GSH-Px, CAT, and SOD) were decreased. In MICU1-deficient Caco-2 cells, proliferation was inhibited and apoptosis was promoted. Collectively, our results indicate that MICU1-related oxidation/antioxidation disequilibrium is strongly involved in IAH-induced damage to intestinal barriers. MICU1-targeted treatment may hold promise for preventing the progression of IAH to gut-derived sepsis.

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“…MICU1 (Gene ID: 10367) could encode an essential regulator of mitochondrial Ca 2+ uptake under basal conditions. The encoded protein interacts with the mitochondrial calcium uniporter and is essential in preventing mitochondrial Ca 2+ overload that could cause excessive production of reactive oxygen species and cell stress (Mallilankaraman et al, 2012;Arvizo et al, 2013;Chen et al, 2013;Hoffman et al, 2013;Logan et al, 2014). OIT3 didn't obtain any annotated results from Gene database, but get some other annotated messages from GO, INTERPRO, PFAM, SMART annotation analysis provided by DAVID (Table 2).…”

Section: Gene Annotationmentioning

confidence: 99%

Loss of Heterozygosity at the Calcium Regulation Gene Locus on Chromosome 10q in Human Pancreatic Cancer

Jin

Zhang²,

Liu³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: Loss of heterozygosity (LOH) on chromosomal regions is crucial in tumor progression and this study aimed to identify genome-wide LOH in pancreatic cancer. Materials and Methods: Single-nucleotide polymorphism (SNP) profiling data GSE32682 of human pancreatic samples snap-frozen during surgery were downloaded from Gene Expression Omnibus database. Genotype console software was used to perform data processing. Candidate genes with LOH were screened based on the genotype calls, SNP loci of LOH and dbSNP database. Gene annotation was performed to identify the functions of candidate genes using NCBI (the National Center for Biotechnology Information) database, followed by Gene Ontology, INTERPRO, PFAM and SMART annotation and UCSC Genome Browser track to the unannotated genes using DAVID (the Database for Annotation, Visualization and Integration Discovery). Results: The candidate genes with LOH identified in this study were MCU, MICU1 and OIT3 on chromosome 10. MCU was found to encode a calcium transporter and MICU1 could encode an essential regulator of mitochondrial Ca 2+ uptake. OIT3 possibly correlated with calcium binding revealed by the annotation analyses and was regulated by a large number of transcription factors including STAT, SOX9, CREB, NF-kB, PPARG and p53. Conclusions: Global genomic analysis of SNPs identified MICU1, MCU and OIT3 with LOH on chromosome 10, implying involvement of these genes in progression of pancreatic cancer.

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CBARA1 Plays a Role in Stemness and Proliferation of Human Embryonic Stem Cells

Cited by 6 publications

References 39 publications

Abnormal DNA methylation patterns in patients with infection‑caused leukocytopenia based on methylation microarrays

Abnormal DNA methylation patterns in patients with infection‑caused leukocytopenia based on methylation microarrays

MICU1 may be a promising intervention target for gut-derived sepsis induced by intra-abdominal hypertension

Loss of Heterozygosity at the Calcium Regulation Gene Locus on Chromosome 10q in Human Pancreatic Cancer

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