MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00010240-T01
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- MRPS31 NIH gene
- Name:
- mitochondrial ribosomal protein S31
- Previous symbol:
- -
- Synonyms:
- IMOGN38
- Chromosome:
- 13q14.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-20
- Date modifiied:
- 2014-11-19
- Gene:
- MRPS31P5 NIH gene
- Name:
- mitochondrial ribosomal protein S31 pseudogene 5
- Previous symbol:
- MRPS31P3
- Synonyms:
- -
- Chromosome:
- 13q14.3
- Locus Type:
- pseudogene
- Date approved:
- 2010-11-24
- Date modifiied:
- 2012-11-14
Related products to: MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: MRPS31 293T Cell Transient Overexpression Lysate(Denatured)
- Fusion genes and epigenetic regulators (i.e., miRNAs and long non-coding RNAs) constitute essential pieces of the puzzle of the tumor genomic landscape, in particular in mechanisms behind the adenoma-to-carcinoma progression of colorectal cancer (CRC). In this work, we aimed to identify molecular signatures of the different steps of sporadic CRC development in eleven patients, of which synchronous samples of adenomas, tumors, and normal tissues were analyzed by RNA-Seq. At a functional level, tumors and adenomas were all characterized by increased activity of the cell cycle, cell development, cell growth, and biological proliferation functions. In contrast, organic survival and apoptosis-related functions were inhibited both in tumors and adenomas at different levels. At a molecular level, we found that three individuals shared a tumor-specific fusion named MRPS31-SUGT1, generated through an intra-chromosomal translocation on chromosome 13, whose sequence resulted in being 100% identical to the long non-coding RNA (lncRNA) MRPS31P5. Our analyses suggest that MRPS31P5 could take part to a competitive endogenous (ce)RNA network by acting as a miRNA sponge or/and as an interactor of other mRNAs, and thus it may be an important gene expression regulatory factor and could be used as a potential biomarker for the detection of early CRC events. - Source: PubMed
Publication date: 2020/09/27
Panza AnnaCastellana StefanoBiscaglia GiuseppePiepoli AdaParca LucaGentile AnnamariaLatiano AnnaMazza TommasoPerri FrancescoAndriulli AngeloPalmieri Orazio - Once believed to be unique features of neoplasia, chimeric RNAs are now being discovered in normal physiology. We speculated that some chimeric RNAs may be functional precursors of genes, and that forming chimeric RNA at the transcriptional level may be a 'trial' mechanism before the functional element is fixed into the genome. Supporting this idea, we identified a chimeric RNA, , whose sequence is highly similar to that of a 'pseudogene' . Sequence analysis revealed that transcript is more similar to chimeric RNA than its 'parent' gene, . Evolutionarily, precedes , as it can be detected bioinformatically and experimentally in marmosets, which do not yet possess in their genome. Conversely, is minimally expressed in humans, while instead, is abundantly expressed. Silencing in marmoset cells resulted in similar phenotype as silencing in human cells. In addition, whole transcriptome analysis and candidate downstream target validation revealed common signalling pathways shared by the two transcripts. Interestingly, failed to rescue the phenotype caused by silencing in human and rhesus cells, whereas can at least partially rescue the phenotype caused by silencing H-S in marmoset cells, suggesting that may have further evolved into a distinct entity. Thus, multiple lines of evidence support that is not truly a pseudogene of , but a likely functional descendent of chimera. Instead being a gene fusion product, is a product of cis-splicing between adjacent genes, while is likely produced by genome rearrangement. - Source: PubMed
Publication date: 2019/09/29
Wu HaoSingh SandeepShi XinruiXie ZhongqiuLin EmilyLi XiaorongLi Hui