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MT-RNR2 is a gene that codes for 16S RNA and is found in the mitochondria. It has been identified to have methylated cytosines in the mouse D-loop and MT-RNR2 itself, with different levels of methylation observed in the brain, liver, and testes [PMC4357308]. The regulation of MT-RNR2 is also influenced by three miRNAs: hsa-miR-mit3, hsa-miR-mit6, and hsa-miR-mit4 [PMC4324738]. A study has shown that PU-91, an FDA-approved drug, promotes mitochondrial stabilization and upregulation of PGC-1α. It also protects AMD ARPE-19 transmitochondrial cybrid cells by preserving mitochondrial health, reducing apoptotic cell loss, and inducing upregulation of the MT-RNR2 gene [PMC6756897]. Furthermore, in an analysis of gene expression in various tissues, 10 out of 15 differentially expressed genes were found to be pseudogenes or isoforms of mitochondrial genes such as MT-ND1 (MTND1P20, MTND1P21 and MTND1P23), MT-ND2 (MTND2P12 and MTND2P28), MT-ND4 (MTND4P9), MT-ND5 (MTND5P11), MT-ND6 (MTND6P3), and also including isoforms of the MTRNR2 gene (MTRNR2L1 and MTRNR2L2) [PMC9028063]. These findings highlight the importance of understanding the regulation and function of MT-RNR2 in various biological processes.
SNORA73B is a small nucleolar RNA (snoRNA) that has been found to be overexpressed in Huh7 cells [PMC8763008]. It is also downregulated in histone encoding genes and spliceosome-associated small nuclear ribonucleoproteins (RNP) [PMC7191197]. In the context of age-related macular degeneration (AMD), SNORA73B has been found to be expressed at higher levels in both retina and PRCS tissues compared to normal tissues, suggesting a potential role in AMD [PMC5813239]. SNORA73B is associated with SIRT7 and is involved in the processing of pre-rRNAs to produce mature rRNAs [PMC4754350] [PMC8410784]. Overexpression of SNORA73B has been shown to inhibit the expression of its host genes [PMC8763008]. The snoRNABase database provides accession numbers and approved symbols for snoRNAs, including SNORA73B [PMC1687206]. The expression of SNORA23 and SNORA73B is regulated by the AKT molecular inhibitor, GSK2141795, suggesting their involvement in the PI3K/Akt/mTOR signaling pathway [PMC8763008]. In terms of cancer prognosis, SNORA73B has been identified as a potential predicting factor for outcome in cutaneous melanoma (CM) [PMC7550331]. In summary, SNORA73B is a snoRNA that shows differential expression patterns in various cellular contexts and diseases. It plays a role in RNA processing and may have implications for AMD and cancer prognosis.
mmu-mir-1195 is a small non-coding RNA molecule, specifically a microRNA, that has been studied in relation to its effects on tumoral cells' viability [PMC7139390]. In a study conducted on PC14 cells, the exogenous expression of mmu-mir-1195, along with mmu-miR-16*, mmu-miR-709, and endo-siRNA-1196, was found to increase the viability of tumoral cells [PMC4914300]. These sRNAs were chosen for analysis due to their significant differences in fold change and their reported gene targets that may have protective activity in relation to apoptosis, cell cycle, and p53-signaling pathways [PMC4914300]. Furthermore, it was observed that mmu-mir-1195 and endo-siRNA-1196 may contribute to the protective effect when administered in combination with miR-709 [PMC4914300]. Treatment with CBX significantly decreased the levels of mmu-mir-1195 by 82% compared to CBX-untreated cells [PMC4914300]. Additionally, it was found that several miRNAs can target circ-Vps54 and circ-Gm49339 along with mmu-mir-1195 [PMC9230989]. NONMMUT147434.1 was identified as a regulator of mmu-mir-1195 among other miRNAs [PMC7339411]. Primer/probe Taqman assays were used for the quantitation of several miRNAs including mmu-mir-1195 [PMC7603330]. It is worth noting that hsa-miR584 shares partial homology with mmu-mir 1195 but requires further analysis for validation [PMC4335692]
TSIX is a non-coding RNA that plays a crucial role in X-inactivation. It is involved in the repression of Xist, the master regulator of X-inactivation, through both indirect and direct mechanisms [PMC5064214]. TSIX is repressed by REX1 and YY1, which compete for binding sites in the F repeat region of Xist exon 1 [PMC5064214]. The transcription level of TSIX is repressed by Oct4 gene, leading to the activation of Xist and subsequent chromosome inactivation [PMC3347565]. TSIX also affects gene expression in other contexts, such as reducing type I collagen expression in SSc fibroblasts [PMC6595547]. The absence of SPEN prevents the silencing of TSIX, which acts as a brake on Xist transcription [PMC8636516]. TSIX is less conserved in humans compared to mice at the sequence level [PMC8775829]. It has been shown that TSIX regulates X chromosome inactivation through its association with CTCF sites at the Xist locus [PMC3091324]. The presence or absence of TSIX signals does not always indicate an active or reactivated state of the X chromosome [PMC6403393]. Methylation differences are not observed for mutant pSS1Δ2.7 with normal TSIX transcription and random X-inactivation observed in female heterozygotes [PMC2577046]. The expression patterns between TSIX and Xist are correlated with compaction levels within their embedding topologically associated domains (TADs) [PMC5346151].
RNA18SN1 is an 18S ribosomal RNA (rRNA) [PMC9458444]. It is commonly used as an endogenous control or reference gene in gene expression studies [PMC8002893]. RNA18SN1 has been shown to remain unaffected by experimental conditions in various cell types, including HepG2 cells [PMC6487699]. It is used as a reference gene to normalize gene expression levels in different experimental settings [PMC6173743]. RNA18SN1 has also been used as a reference RNA for quantification of mitochondrial DNA (mtDNA) content [PMC5986740]. In addition, it has been used as a reference RNA for normalization of target gene expression in various tissues, including bronchoalveolar lavage fluid (BALF) and placental tissue samples [PMC6307268] [PMC9588925]. The expression of RNA18SN1 can be measured by quantitative PCR (qPCR) using specific primers designed for this gene [PMC8774144]. It is important to note that the DNA sequence of the RNA18SN1 gene has high identity with other ribosomal RNAs, such as RNA18SN2 and RNA18SP3 [PMC10114345]. Overall, RNA18SN1 serves as a reliable and stable reference gene for normalization purposes in various experimental studies.
MALAT1, a long non-coding RNA (lncRNA), has been extensively studied in various diseases, including osteoporosis [PMC10059267]. It is highly expressed in proliferating and differentiating myoblasts [PMC6755471]. Researchers have systematically screened for therapeutic approaches targeting MALAT1 and its associated factors, such as KDM5B, to improve clinical outcomes [PMC4768424]. MALAT1 has been implicated in various cancers, including osteosarcoma and breast cancer, where it promotes cell proliferation and metastasis through the PI3K/AKT signaling pathway [PMC6006327] [PMC6110141] [PMC8349266]. It has also been suggested that MALAT1 modulates the expression of genes involved in cell cycle regulation [PMC7531330]. In HIV-1 infection, MALAT1 expression is up-regulated and associated with viral reactivation [PMC6451131]. Additionally, MALAT1 has been implicated in hepatocellular carcinoma (HCC) progression through mTOR activation and SRSF1 elevation [PMC8352691]. In drug resistance studies, MALAT1 has been shown to alter drug distribution by regulating ABC proteins [PMC9960193]. Furthermore, downregulation of MALAT1 expression alleviates neuronal apoptosis and inhibits HIV-1 transcription by preventing polycomb repressive complex 2-mediated H3K27me3 at the HIV- 5′-LTR promoter region[ PMC8635732] . Overall, these studies highlight the diverse roles of MALAT1 in various diseases and its potential as a therapeutic target.
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