Non-coding RNA

From Wikipedia the free encyclopedia

The roles of non-coding RNAs: Ribonucleoproteins are shown in red, non-coding RNAs in blue.

A non-coding RNA (ncRNA) is a functional RNA molecule that is not translated into a protein. The DNA sequence from which a functional non-coding RNA is transcribed is often called an RNA gene. Abundant and functionally important types of non-coding RNAs include transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), as well as small RNAs such as microRNAs, siRNAs, piRNAs, snoRNAs, snRNAs, exRNAs, scaRNAs and the long ncRNAs such as Xist and HOTAIR.

The number of non-coding RNAs within the human genome is unknown; however, recent transcriptomic and bioinformatic studies suggest that there are thousands of non-coding transcripts.[1][2][3][4][5][6][7] Many of the newly identified ncRNAs have not been validated for their function.[8] There is no consensus in the literature on how much of non-coding transcription is functional. Some researchers have argued that many ncRNAs are non-functional (sometimes referred to as "junk RNA"), spurious transcriptions.[9][10] Others, however, disagree, arguing instead that many non-coding transcripts do have functions and that those functions are being and will continue to be discovered.[11][12]

History and discovery[edit]

Nucleic acids were first discovered in 1868 by Friedrich Miescher,[13] and by 1939, RNA had been implicated in protein synthesis.[14] Two decades later, Francis Crick predicted a functional RNA component which mediated translation; he reasoned that RNA is better suited to base-pair with an mRNA transcript than a pure polypeptide.[15]

The cloverleaf structure of Yeast tRNAPhe (inset) and the 3D structure determined by X-ray analysis.

The first non-coding RNA to be characterised was an alanine tRNA found in baker's yeast, its structure was published in 1965.[16] To produce a purified alanine tRNA sample, Robert W. Holley et al. used 140kg of commercial baker's yeast to give just 1g of purified tRNAAla for analysis.[17] The 80 nucleotide tRNA was sequenced by first being digested with Pancreatic ribonuclease (producing fragments ending in Cytosine or Uridine) and then with takadiastase ribonuclease Tl (producing fragments which finished with Guanosine). Chromatography and identification of the 5' and 3' ends then helped arrange the fragments to establish the RNA sequence.[17] Of the three structures originally proposed for this tRNA,[16] the 'cloverleaf' structure was independently proposed in several following publications.[18][19][20][21] The cloverleaf secondary structure was finalised following X-ray crystallography analysis performed by two independent research groups in 1974.[22][23]

Ribosomal RNA was next to be discovered, followed by URNA in the early 1980s. Since then, the discovery of new non-coding RNAs has continued with snoRNAs, Xist, CRISPR and many more.[24] Recent notable additions include riboswitches and miRNA; the discovery of the RNAi mechanism associated with the latter earned Craig C. Mello and Andrew Fire the 2006 Nobel Prize in Physiology or Medicine.[25]

Recent discoveries of ncRNAs have been achieved through both experimental and bioinformatic methods.

Biological roles[edit]

Noncoding RNAs belong to several groups and are involved in many cellular processes.[26] These range from ncRNAs of central importance that are conserved across all or most cellular life through to more transient ncRNAs specific to one or a few closely related species. The more conserved ncRNAs are thought to be molecular fossils or relics from the last universal common ancestor and the RNA world, and their current roles remain mostly in regulation of information flow from DNA to protein.[27][28][29]

In translation[edit]

Atomic structure of the 50S Subunit from Haloarcula marismortui. Proteins are shown in blue and the two RNA strands in orange and yellow.[30] The small patch of green in the center of the subunit is the active site.

Many of the conserved, essential and abundant ncRNAs are involved in translation. Ribonucleoprotein (RNP) particles called ribosomes are the 'factories' where translation takes place in the cell. The ribosome consists of more than 60% ribosomal RNA; these are made up of 3 ncRNAs in prokaryotes and 4 ncRNAs in eukaryotes. Ribosomal RNAs catalyse the translation of nucleotide sequences to protein. Another set of ncRNAs, Transfer RNAs, form an 'adaptor molecule' between mRNA and protein. The H/ACA box and C/D box snoRNAs are ncRNAs found in archaea and eukaryotes. RNase MRP is restricted to eukaryotes. Both groups of ncRNA are involved in the maturation of rRNA. The snoRNAs guide covalent modifications of rRNA, tRNA and snRNAs; RNase MRP cleaves the internal transcribed spacer 1 between 18S and 5.8S rRNAs. The ubiquitous ncRNA, RNase P, is an evolutionary relative of RNase MRP.[31] RNase P matures tRNA sequences by generating mature 5'-ends of tRNAs through cleaving the 5'-leader elements of precursor-tRNAs. Another ubiquitous RNP called SRP recognizes and transports specific nascent proteins to the endoplasmic reticulum in eukaryotes and the plasma membrane in prokaryotes. In bacteria, Transfer-messenger RNA (tmRNA) is an RNP involved in rescuing stalled ribosomes, tagging incomplete polypeptides and promoting the degradation of aberrant mRNA.[citation needed]

In RNA splicing[edit]

Electron microscopy images of the yeast spliceosome. Note the bulk of the complex is in fact ncRNA.

In eukaryotes, the spliceosome performs the splicing reactions essential for removing intron sequences, this process is required for the formation of mature mRNA. The spliceosome is another RNP often known as the snRNP or tri-snRNP. There are two different forms of the spliceosome, the major and minor forms. The ncRNA components of the major spliceosome are U1, U2, U4, U5, and U6. The ncRNA components of the minor spliceosome are U11, U12, U5, U4atac and U6atac.[citation needed]

Another group of introns can catalyse their own removal from host transcripts; these are called self-splicing RNAs. There are two main groups of self-splicing RNAs: group I catalytic intron and group II catalytic intron. These ncRNAs catalyze their own excision from mRNA, tRNA and rRNA precursors in a wide range of organisms.[citation needed]

In mammals it has been found that snoRNAs can also regulate the alternative splicing of mRNA, for example snoRNA HBII-52 regulates the splicing of serotonin receptor 2C.[32]

In nematodes, the SmY ncRNA appears to be involved in mRNA trans-splicing.[citation needed]

In DNA replication[edit]

The Ro autoantigen protein (white) binds the end of a double-stranded Y RNA (red) and a single stranded RNA (blue). (PDB: 1YVP [1]).[33]

Y RNAs are stem loops, necessary for DNA replication through interactions with chromatin and initiation proteins (including the origin recognition complex).[34][35] They are also components of the Ro60 ribonucleoprotein particle[36] which is a target of autoimmune antibodies in patients with systemic lupus erythematosus.[37]

In gene regulation[edit]

The expression of many thousands of genes are regulated by ncRNAs. This regulation can occur in trans or in cis. There is increasing evidence that a special type of ncRNAs called enhancer RNAs, transcribed from the enhancer region of a gene, act to promote gene expression.[citation needed]


In higher eukaryotes microRNAs regulate gene expression. A single miRNA can reduce the expression levels of hundreds of genes. The mechanism by which mature miRNA molecules act is through partial complementarity to one or more messenger RNA (mRNA) molecules, generally in 3' UTRs. The main function of miRNAs is to down-regulate gene expression.

The ncRNA RNase P has also been shown to influence gene expression. In the human nucleus, RNase P is required for the normal and efficient transcription of various ncRNAs transcribed by RNA polymerase III. These include tRNA, 5S rRNA, SRP RNA, and U6 snRNA genes. RNase P exerts its role in transcription through association with Pol III and chromatin of active tRNA and 5S rRNA genes.[38]

It has been shown that 7SK RNA, a metazoan ncRNA, acts as a negative regulator of the RNA polymerase II elongation factor P-TEFb, and that this activity is influenced by stress response pathways.[citation needed]

The bacterial ncRNA, 6S RNA, specifically associates with RNA polymerase holoenzyme containing the sigma70 specificity factor. This interaction represses expression from a sigma70-dependent promoter during stationary phase.[citation needed]

Another bacterial ncRNA, OxyS RNA represses translation by binding to Shine-Dalgarno sequences thereby occluding ribosome binding. OxyS RNA is induced in response to oxidative stress in Escherichia coli.[citation needed]

The B2 RNA is a small noncoding RNA polymerase III transcript that represses mRNA transcription in response to heat shock in mouse cells. B2 RNA inhibits transcription by binding to core Pol II. Through this interaction, B2 RNA assembles into preinitiation complexes at the promoter and blocks RNA synthesis.[39]

A recent study has shown that just the act of transcription of ncRNA sequence can have an influence on gene expression. RNA polymerase II transcription of ncRNAs is required for chromatin remodelling in the Schizosaccharomyces pombe. Chromatin is progressively converted to an open configuration, as several species of ncRNAs are transcribed.[40]


A number of ncRNAs are embedded in the 5' UTRs (Untranslated Regions) of protein coding genes and influence their expression in various ways. For example, a riboswitch can directly bind a small target molecule; the binding of the target affects the gene's activity.[citation needed]

RNA leader sequences are found upstream of the first gene of amino acid biosynthetic operons. These RNA elements form one of two possible structures in regions encoding very short peptide sequences that are rich in the end product amino acid of the operon. A terminator structure forms when there is an excess of the regulatory amino acid and ribosome movement over the leader transcript is not impeded. When there is a deficiency of the charged tRNA of the regulatory amino acid the ribosome translating the leader peptide stalls and the antiterminator structure forms. This allows RNA polymerase to transcribe the operon. Known RNA leaders are Histidine operon leader, Leucine operon leader, Threonine operon leader and the Tryptophan operon leader.[citation needed]

Iron response elements (IRE) are bound by iron response proteins (IRP). The IRE is found in UTRs of various mRNAs whose products are involved in iron metabolism. When iron concentration is low, IRPs bind the ferritin mRNA IRE leading to translation repression.[citation needed]

Internal ribosome entry sites (IRES) are RNA structures that allow for translation initiation in the middle of a mRNA sequence as part of the process of protein synthesis.[citation needed]

In genome defense[edit]

Piwi-interacting RNAs (piRNAs) expressed in mammalian testes and somatic cells form RNA-protein complexes with Piwi proteins. These piRNA complexes (piRCs) have been linked to transcriptional gene silencing of retrotransposons and other genetic elements in germline cells, particularly those in spermatogenesis.

Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) are repeats found in the DNA of many bacteria and archaea. The repeats are separated by spacers of similar length. It has been demonstrated that these spacers can be derived from phage and subsequently help protect the cell from infection.

Chromosome structure[edit]

Telomerase is an RNP enzyme that adds specific DNA sequence repeats ("TTAGGG" in vertebrates) to telomeric regions, which are found at the ends of eukaryotic chromosomes. The telomeres contain condensed DNA material, giving stability to the chromosomes. The enzyme is a reverse transcriptase that carries Telomerase RNA, which is used as a template when it elongates telomeres, which are shortened after each replication cycle.

Xist (X-inactive-specific transcript) is a long ncRNA gene on the X chromosome of the placental mammals that acts as major effector of the X chromosome inactivation process forming Barr bodies. An antisense RNA, Tsix, is a negative regulator of Xist. X chromosomes lacking Tsix expression (and thus having high levels of Xist transcription) are inactivated more frequently than normal chromosomes. In drosophilids, which also use an XY sex-determination system, the roX (RNA on the X) RNAs are involved in dosage compensation.[41] Both Xist and roX operate by epigenetic regulation of transcription through the recruitment of histone-modifying enzymes.

Bifunctional RNA[edit]

Bifunctional RNAs, or dual-function RNAs, are RNAs that have two distinct functions.[42][43] The majority of the known bifunctional RNAs are mRNAs that encode both a protein and ncRNAs. However, a growing number of ncRNAs fall into two different ncRNA categories; e.g., H/ACA box snoRNA and miRNA.[44][45]

Two well known examples of bifunctional RNAs are SgrS RNA and RNAIII. However, a handful of other bifunctional RNAs are known to exist (e.g., steroid receptor activator/SRA,[46] VegT RNA,[47][48] Oskar RNA,[49] ENOD40,[50] p53 RNA[51] SR1 RNA,[52] and Spot 42 RNA.[53]) Bifunctional RNAs were the subject of a 2011 special issue of Biochimie.[54]

As a hormone[edit]

There is an important link between certain non-coding RNAs and the control of hormone-regulated pathways. In Drosophila, hormones such as ecdysone and juvenile hormone can promote the expression of certain miRNAs. Furthermore, this regulation occurs at distinct temporal points within Caenorhabditis elegans development.[55] In mammals, miR-206 is a crucial regulator of estrogen-receptor-alpha.[56]

Non-coding RNAs are crucial in the development of several endocrine organs, as well as in endocrine diseases such as diabetes mellitus.[57] Specifically in the MCF-7 cell line, addition of 17β-estradiol increased global transcription of the noncoding RNAs called lncRNAs near estrogen-activated coding genes.[58]

In pathogenic avoidance[edit]

C. elegans was shown to learn and inherit pathogenic avoidance after exposure to a single non-coding RNA of a bacterial pathogen.[59][60]

Roles in disease[edit]

As with proteins, mutations or imbalances in the ncRNA repertoire within the body can cause a variety of diseases.


Many ncRNAs show abnormal expression patterns in cancerous tissues.[6] These include miRNAs, long mRNA-like ncRNAs,[61][62] GAS5,[63] SNORD50,[64] telomerase RNA and Y RNAs.[65] The miRNAs are involved in the large scale regulation of many protein coding genes,[66][67] the Y RNAs are important for the initiation of DNA replication,[34] telomerase RNA that serves as a primer for telomerase, an RNP that extends telomeric regions at chromosome ends (see telomeres and disease for more information). The direct function of the long mRNA-like ncRNAs is less clear.

Germline mutations in miR-16-1 and miR-15 primary precursors have been shown to be much more frequent in patients with chronic lymphocytic leukemia compared to control populations.[68][69]

It has been suggested that a rare SNP (rs11614913) that overlaps hsa-mir-196a-2 has been found to be associated with non-small cell lung carcinoma.[70] Likewise, a screen of 17 miRNAs that have been predicted to regulate a number of breast cancer associated genes found variations in the microRNAs miR-17 and miR-30c-1of patients; these patients were noncarriers of BRCA1 or BRCA2 mutations, lending the possibility that familial breast cancer may be caused by variation in these miRNAs.[71] The p53 tumor suppressor is arguably the most important agent in preventing tumor formation and progression. The p53 protein functions as a transcription factor with a crucial role in orchestrating the cellular stress response. In addition to its crucial role in cancer, p53 has been implicated in other diseases including diabetes, cell death after ischemia, and various neurodegenerative diseases such as Huntington, Parkinson, and Alzheimer. Studies have suggested that p53 expression is subject to regulation by non-coding RNA.[5]

Another example of non-coding RNA dysregulated in cancer cells is the long non-coding RNA Linc00707. Linc00707 is upregulated and sponges miRNAs in human bone marrow-derived mesenchymal stem cells,[72] in hepatocellular carcinoma,[73] gastric cancer[74] or breast cancer,[75][76] and thus promotes osteogenesis, contributes to hepatocellular carcinoma progression, promotes proliferation and metastasis, or indirectly regulates expression of proteins involved in cancer aggressiveness, respectively.

Prader–Willi syndrome[edit]

The deletion of the 48 copies of the C/D box snoRNA SNORD116 has been shown to be the primary cause of Prader–Willi syndrome.[77][78][79][80] Prader–Willi is a developmental disorder associated with over-eating and learning difficulties. SNORD116 has potential target sites within a number of protein-coding genes, and could have a role in regulating alternative splicing.[81]


The chromosomal locus containing the small nucleolar RNA SNORD115 gene cluster has been duplicated in approximately 5% of individuals with autistic traits.[82][83] A mouse model engineered to have a duplication of the SNORD115 cluster displays autistic-like behaviour.[84] A recent small study of post-mortem brain tissue demonstrated altered expression of long non-coding RNAs in the prefrontal cortex and cerebellum of autistic brains as compared to controls.[85]

Cartilage–hair hypoplasia[edit]

Mutations within RNase MRP have been shown to cause cartilage–hair hypoplasia, a disease associated with an array of symptoms such as short stature, sparse hair, skeletal abnormalities and a suppressed immune system that is frequent among Amish and Finnish.[86][87][88] The best characterised variant is an A-to-G transition at nucleotide 70 that is in a loop region two bases 5' of a conserved pseudoknot. However, many other mutations within RNase MRP also cause CHH.

Alzheimer's disease[edit]

The antisense RNA, BACE1-AS is transcribed from the opposite strand to BACE1 and is upregulated in patients with Alzheimer's disease.[89] BACE1-AS regulates the expression of BACE1 by increasing BACE1 mRNA stability and generating additional BACE1 through a post-transcriptional feed-forward mechanism. By the same mechanism it also raises concentrations of beta amyloid, the main constituent of senile plaques. BACE1-AS concentrations are elevated in subjects with Alzheimer's disease and in amyloid precursor protein transgenic mice.

miR-96 and hearing loss[edit]

Variation within the seed region of mature miR-96 has been associated with autosomal dominant, progressive hearing loss in humans and mice. The homozygous mutant mice were profoundly deaf, showing no cochlear responses. Heterozygous mice and humans progressively lose the ability to hear.[90][91][92]

Mitochondrial transfer RNAs[edit]

A number of mutations within mitochondrial tRNAs have been linked to diseases such as MELAS syndrome, MERRF syndrome, and chronic progressive external ophthalmoplegia.[93][94][95][96]

Distinction between functional RNA (fRNA) and ncRNA[edit]

Scientists have started to distinguish functional RNA (fRNA) from ncRNA, to describe regions functional at the RNA level that may or may not be stand-alone RNA transcripts.[97][98][99] This implies that fRNA (such as riboswitches, SECIS elements, and other cis-regulatory regions) is not ncRNA. Yet fRNA could also include mRNA, as this is RNA coding for protein, and hence is functional. Additionally artificially evolved RNAs also fall under the fRNA umbrella term. Some publications[24] state that ncRNA and fRNA are nearly synonymous, however others have pointed out that a large proportion of annotated ncRNAs likely have no function.[9][10] It also has been suggested to simply use the term RNA, since the distinction from a protein coding RNA (messenger RNA) is already given by the qualifier mRNA.[100] This eliminates the ambiguity when addressing a gene "encoding a non-coding" RNA. Besides, there may be a number of ncRNAs that are misannoted in published literature and datasets.[101][102][103]

See also[edit]


  1. ^ Cheng J, Kapranov P, Drenkow J, Dike S, Brubaker S, Patel S, et al. (May 2005). "Transcriptional maps of 10 human chromosomes at 5-nucleotide resolution". Science. 308 (5725): 1149–1154. Bibcode:2005Sci...308.1149C. doi:10.1126/science.1108625. PMID 15790807. S2CID 13047538.
  2. ^ Birney E, Stamatoyannopoulos JA, Dutta A, Guigó R, Gingeras TR, Margulies EH, et al. (ENCODE Project Consortium) (June 2007). "Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project". Nature. 447 (7146): 799–816. Bibcode:2007Natur.447..799B. doi:10.1038/nature05874. PMC 2212820. PMID 17571346.
  3. ^ Thind AS, Monga I, Thakur PK, Kumari P, Dindhoria K, Krzak M, et al. (November 2021). "Demystifying emerging bulk RNA-Seq applications: the application and utility of bioinformatic methodology". Briefings in Bioinformatics. 22 (6). doi:10.1093/bib/bbab259. PMID 34329375.
  4. ^ Washietl S, Pedersen JS, Korbel JO, Stocsits C, Gruber AR, Hackermüller J, et al. (June 2007). "Structured RNAs in the ENCODE selected regions of the human genome". Genome Research. 17 (6): 852–864. doi:10.1101/gr.5650707. PMC 1891344. PMID 17568003.
  5. ^ a b Morris KV, ed. (2012). Non-coding RNAs and Epigenetic Regulation of Gene Expression: Drivers of Natural Selection. Caister Academic Press. ISBN 978-1-904455-94-3.
  6. ^ a b Shahrouki P, Larsson E (2012). "The non-coding oncogene: a case of missing DNA evidence?". Frontiers in Genetics. 3: 170. doi:10.3389/fgene.2012.00170. PMC 3439828. PMID 22988449.
  7. ^ van Bakel H, Nislow C, Blencowe BJ, Hughes TR (May 2010). Eddy SR (ed.). "Most "dark matter" transcripts are associated with known genes". PLOS Biology. 8 (5): e1000371. doi:10.1371/journal.pbio.1000371. PMC 2872640. PMID 20502517.
  8. ^ Hüttenhofer A, Schattner P, Polacek N (May 2005). "Non-coding RNAs: hope or hype?". Trends in Genetics. 21 (5): 289–297. doi:10.1016/j.tig.2005.03.007. PMID 15851066.
  9. ^ a b Brosius J (May 2005). "Waste not, want not--transcript excess in multicellular eukaryotes". Trends in Genetics. 21 (5): 287–288. doi:10.1016/j.tig.2005.02.014. PMID 15851065.
  10. ^ a b Palazzo AF, Lee ES (2015). "Non-coding RNA: what is functional and what is junk?". Frontiers in Genetics. 6: 2. doi:10.3389/fgene.2015.00002. PMC 4306305. PMID 25674102.
  11. ^ Mattick J, Amaral P (2022). RNA, The Epicenter of Genetic Information : A New Understanding of Molecular Biology. CRC Press. ISBN 9780367623920.
  12. ^ Lee H, Zhang Z, Krause HM (December 2019). "Long Noncoding RNAs and Repetitive Elements: Junk or Intimate Evolutionary Partners?". Trends in Genetics. 35 (12): 892–902. doi:10.1016/j.tig.2019.09.006. PMID 31662190. S2CID 204975291.
  13. ^ Dahm R (February 2005). "Friedrich Miescher and the discovery of DNA". Developmental Biology. 278 (2): 274–288. doi:10.1016/j.ydbio.2004.11.028. PMID 15680349.
  14. ^ Caspersson T, Schultz J (1939). "Pentose nucleotides in the cytoplasm of growing tissues". Nature. 143 (3623): 602–3. Bibcode:1939Natur.143..602C. doi:10.1038/143602c0. S2CID 4140563.
  15. ^ Crick FH (1958). "On protein synthesis". Symposia of the Society for Experimental Biology. 12: 138–163. PMID 13580867.
  16. ^ a b Holley RW, Apgar J, Everett GA, Madison JT, Marquisee M, Merrill SH, et al. (March 1965). "Structure of a Ribonucleic Acid". Science. 147 (3664): 1462–1465. Bibcode:1965Sci...147.1462H. doi:10.1126/science.147.3664.1462. PMID 14263761. S2CID 40989800.
  17. ^ a b "The Nobel Prize in Physiology or Medicine 1968". Nobel Foundation. Retrieved 2007-07-28.
  18. ^ Madison JT, Everett GA, Kung H (July 1966). "Nucleotide sequence of a yeast tyrosine transfer RNA". Science. 153 (3735): 531–534. Bibcode:1966Sci...153..531M. CiteSeerX doi:10.1126/science.153.3735.531. PMID 5938777. S2CID 9265016.
  19. ^ Zachau HG, Dütting D, Feldmann H, Melchers F, Karau W (1966). "Serine specific transfer ribonucleic acids. XIV. Comparison of nucleotide sequences and secondary structure models". Cold Spring Harbor Symposia on Quantitative Biology. 31: 417–424. doi:10.1101/SQB.1966.031.01.054. PMID 5237198.
  20. ^ Dudock BS, Katz G, Taylor EK, Holley RW (March 1969). "Primary structure of wheat germ phenylalanine transfer RNA". Proceedings of the National Academy of Sciences of the United States of America. 62 (3): 941–945. Bibcode:1969PNAS...62..941D. doi:10.1073/pnas.62.3.941. PMC 223689. PMID 5257014.
  21. ^ Cramer F, Doepner H, Haar F VD, Schlimme E, Seidel H (December 1968). "On the conformation of transfer RNA". Proceedings of the National Academy of Sciences of the United States of America. 61 (4): 1384–1391. Bibcode:1968PNAS...61.1384C. doi:10.1073/pnas.61.4.1384. PMC 225267. PMID 4884685.
  22. ^ Ladner JE, Jack A, Robertus JD, Brown RS, Rhodes D, Clark BF, Klug A (November 1975). "Structure of yeast phenylalanine transfer RNA at 2.5 A resolution". Proceedings of the National Academy of Sciences of the United States of America. 72 (11): 4414–4418. Bibcode:1975PNAS...72.4414L. doi:10.1073/pnas.72.11.4414. PMC 388732. PMID 1105583.
  23. ^ Kim SH, Quigley GJ, Suddath FL, McPherson A, Sneden D, Kim JJ, et al. (January 1973). "Three-dimensional structure of yeast phenylalanine transfer RNA: folding of the polynucleotide chain". Science. 179 (4070): 285–288. Bibcode:1973Sci...179..285K. doi:10.1126/science.179.4070.285. PMID 4566654. S2CID 28916938.
  24. ^ a b Eddy SR (December 2001). "Non-coding RNA genes and the modern RNA world". Nature Reviews. Genetics. 2 (12): 919–929. doi:10.1038/35103511. PMID 11733745. S2CID 18347629.
  25. ^ Daneholt B. "Advanced Information: RNA interference". The Nobel Prize in Physiology or Medicine 2006. Archived from the original on 2007-01-20. Retrieved 2007-01-25.
  26. ^ Monga I, Banerjee I (November 2019). "Computational Identification of piRNAs Using Features Based on RNA Sequence, Structure, Thermodynamic and Physicochemical Properties". Current Genomics. 20 (7): 508–518. doi:10.2174/1389202920666191129112705. PMC 7327968. PMID 32655289.
  27. ^ Jeffares DC, Poole AM, Penny D (January 1998). "Relics from the RNA world". Journal of Molecular Evolution. 46 (1): 18–36. Bibcode:1998JMolE..46...18J. doi:10.1007/PL00006280. PMID 9419222. S2CID 2029318.
  28. ^ Poole AM, Jeffares DC, Penny D (January 1998). "The path from the RNA world". Journal of Molecular Evolution. 46 (1): 1–17. Bibcode:1998JMolE..46....1P. doi:10.1007/PL00006275. PMID 9419221. S2CID 17968659.
  29. ^ Poole A, Jeffares D, Penny D (October 1999). "Early evolution: prokaryotes, the new kids on the block". BioEssays. 21 (10): 880–889. doi:10.1002/(SICI)1521-1878(199910)21:10<880::AID-BIES11>3.0.CO;2-P. PMID 10497339. S2CID 45607498.
  30. ^ Ban N, Nissen P, Hansen J, Moore PB, Steitz TA (August 2000). "The complete atomic structure of the large ribosomal subunit at 2.4 A resolution". Science. 289 (5481): 905–920. Bibcode:2000Sci...289..905B. CiteSeerX doi:10.1126/science.289.5481.905. PMID 10937989.
  31. ^ Zhu Y, Stribinskis V, Ramos KS, Li Y (May 2006). "Sequence analysis of RNase MRP RNA reveals its origination from eukaryotic RNase P RNA". RNA. 12 (5): 699–706. doi:10.1261/rna.2284906. PMC 1440897. PMID 16540690.
  32. ^ Kishore S, Stamm S (January 2006). "The snoRNA HBII-52 regulates alternative splicing of the serotonin receptor 2C". Science. 311 (5758): 230–232. Bibcode:2006Sci...311..230K. doi:10.1126/science.1118265. PMID 16357227. S2CID 44527461.
  33. ^ Stein AJ, Fuchs G, Fu C, Wolin SL, Reinisch KM (May 2005). "Structural insights into RNA quality control: the Ro autoantigen binds misfolded RNAs via its central cavity". Cell. 121 (4): 529–539. doi:10.1016/j.cell.2005.03.009. PMC 1769319. PMID 15907467.
  34. ^ a b Christov CP, Gardiner TJ, Szüts D, Krude T (September 2006). "Functional requirement of noncoding Y RNAs for human chromosomal DNA replication". Molecular and Cellular Biology. 26 (18): 6993–7004. doi:10.1128/MCB.01060-06. PMC 1592862. PMID 16943439.
  35. ^ Zhang AT, Langley AR, Christov CP, Kheir E, Shafee T, Gardiner TJ, Krude T (June 2011). "Dynamic interaction of Y RNAs with chromatin and initiation proteins during human DNA replication". Journal of Cell Science. 124 (Pt 12): 2058–2069. doi:10.1242/jcs.086561. PMC 3104036. PMID 21610089.
  36. ^ Hall AE, Turnbull C, Dalmay T (April 2013). "Y RNAs: recent developments". Biomolecular Concepts. 4 (2): 103–110. doi:10.1515/bmc-2012-0050. PMID 25436569. S2CID 12575326.
  37. ^ Lerner MR, Boyle JA, Hardin JA, Steitz JA (January 1981). "Two novel classes of small ribonucleoproteins detected by antibodies associated with lupus erythematosus". Science. 211 (4480): 400–402. Bibcode:1981Sci...211..400L. doi:10.1126/science.6164096. PMID 6164096.
  38. ^ Reiner R, Ben-Asouli Y, Krilovetzky I, Jarrous N (June 2006). "A role for the catalytic ribonucleoprotein RNase P in RNA polymerase III transcription". Genes & Development. 20 (12): 1621–1635. doi:10.1101/gad.386706. PMC 1482482. PMID 16778078.
  39. ^ Espinoza CA, Allen TA, Hieb AR, Kugel JF, Goodrich JA (September 2004). "B2 RNA binds directly to RNA polymerase II to repress transcript synthesis". Nature Structural & Molecular Biology. 11 (9): 822–829. doi:10.1038/nsmb812. PMID 15300239. S2CID 22199826.
  40. ^ Hirota K, Miyoshi T, Kugou K, Hoffman CS, Shibata T, Ohta K (November 2008). "Stepwise chromatin remodelling by a cascade of transcription initiation of non-coding RNAs". Nature. 456 (7218): 130–134. Bibcode:2008Natur.456..130H. doi:10.1038/nature07348. PMID 18820678. S2CID 4416402.
  41. ^ Park Y, Kelley RL, Oh H, Kuroda MI, Meller VH (November 2002). "Extent of chromatin spreading determined by roX RNA recruitment of MSL proteins". Science. 298 (5598): 1620–1623. Bibcode:2002Sci...298.1620P. doi:10.1126/science.1076686. PMID 12446910. S2CID 27167367.
  42. ^ Wadler CS, Vanderpool CK (December 2007). "A dual function for a bacterial small RNA: SgrS performs base pairing-dependent regulation and encodes a functional polypeptide". Proceedings of the National Academy of Sciences of the United States of America. 104 (51): 20454–20459. Bibcode:2007PNAS..10420454W. doi:10.1073/pnas.0708102104. PMC 2154452. PMID 18042713.
  43. ^ Dinger ME, Pang KC, Mercer TR, Mattick JS (November 2008). McEntyre J (ed.). "Differentiating protein-coding and noncoding RNA: challenges and ambiguities". PLOS Computational Biology. 4 (11): e1000176. Bibcode:2008PLSCB...4E0176D. doi:10.1371/journal.pcbi.1000176. PMC 2518207. PMID 19043537.
  44. ^ Saraiya AA, Wang CC (November 2008). Goldberg DE (ed.). "snoRNA, a novel precursor of microRNA in Giardia lamblia". PLOS Pathogens. 4 (11): e1000224. doi:10.1371/journal.ppat.1000224. PMC 2583053. PMID 19043559.
  45. ^ Ender C, Krek A, Friedländer MR, Beitzinger M, Weinmann L, Chen W, et al. (November 2008). "A human snoRNA with microRNA-like functions". Molecular Cell. 32 (4): 519–528. doi:10.1016/j.molcel.2008.10.017. PMID 19026782.
  46. ^ Leygue E (August 2007). "Steroid receptor RNA activator (SRA1): unusual bifaceted gene products with suspected relevance to breast cancer". Nuclear Receptor Signaling. 5: e006. doi:10.1621/nrs.05006. PMC 1948073. PMID 17710122.
  47. ^ Zhang J, King ML (December 1996). "Xenopus VegT RNA is localized to the vegetal cortex during oogenesis and encodes a novel T-box transcription factor involved in mesodermal patterning". Development. 122 (12): 4119–4129. doi:10.1242/dev.122.12.4119. PMID 9012531. S2CID 28462527.
  48. ^ Kloc M, Wilk K, Vargas D, Shirato Y, Bilinski S, Etkin LD (August 2005). "Potential structural role of non-coding and coding RNAs in the organization of the cytoskeleton at the vegetal cortex of Xenopus oocytes". Development. 132 (15): 3445–3457. doi:10.1242/dev.01919. PMID 16000384.
  49. ^ Jenny A, Hachet O, Závorszky P, Cyrklaff A, Weston MD, Johnston DS, et al. (August 2006). "A translation-independent role of oskar RNA in early Drosophila oogenesis". Development. 133 (15): 2827–2833. doi:10.1242/dev.02456. PMID 16835436.
  50. ^ Gultyaev AP, Roussis A (2007). "Identification of conserved secondary structures and expansion segments in enod40 RNAs reveals new enod40 homologues in plants". Nucleic Acids Research. 35 (9): 3144–3152. doi:10.1093/nar/gkm173. PMC 1888808. PMID 17452360.
  51. ^ Candeias MM, Malbert-Colas L, Powell DJ, Daskalogianni C, Maslon MM, Naski N, et al. (September 2008). "P53 mRNA controls p53 activity by managing Mdm2 functions". Nature Cell Biology. 10 (9): 1098–1105. doi:10.1038/ncb1770. PMID 19160491. S2CID 5122088.
  52. ^ Gimpel M, Preis H, Barth E, Gramzow L, Brantl S (December 2012). "SR1--a small RNA with two remarkably conserved functions". Nucleic Acids Research. 40 (22): 11659–11672. doi:10.1093/nar/gks895. PMC 3526287. PMID 23034808.
  53. ^ Aoyama JJ, Raina M, Zhong A, Storz G (March 2022). "Dual-function Spot 42 RNA encodes a 15-amino acid protein that regulates the CRP transcription factor". Proceedings of the National Academy of Sciences of the United States of America. 119 (10): e2119866119. Bibcode:2022PNAS..11919866A. doi:10.1073/pnas.2119866119. PMC 8916003. PMID 35239441.
  54. ^ Francastel C, Hubé F (November 2011). "Coding or non-coding: Need they be exclusive?". Biochimie. 93 (11): vi–vii. doi:10.1016/S0300-9084(11)00322-1. PMID 21963143.
  55. ^ Sempere LF, Sokol NS, Dubrovsky EB, Berger EM, Ambros V (July 2003). "Temporal regulation of microRNA expression in Drosophila melanogaster mediated by hormonal signals and broad-Complex gene activity". Developmental Biology. 259 (1): 9–18. doi:10.1016/S0012-1606(03)00208-2. PMID 12812784. S2CID 17249847.
  56. ^ Adams BD, Furneaux H, White BA (May 2007). "The micro-ribonucleic acid (miRNA) miR-206 targets the human estrogen receptor-alpha (ERalpha) and represses ERalpha messenger RNA and protein expression in breast cancer cell lines". Molecular Endocrinology. 21 (5): 1132–1147. doi:10.1210/me.2007-0022. PMID 17312270.
  57. ^ Knoll M, Lodish HF, Sun L (March 2015). "Long non-coding RNAs as regulators of the endocrine system". Nature Reviews. Endocrinology. 11 (3): 151–160. doi:10.1038/nrendo.2014.229. hdl:1721.1/116703. PMC 4376378. PMID 25560704.
  58. ^ Li W, Notani D, Ma Q, Tanasa B, Nunez E, Chen AY, et al. (June 2013). "Functional roles of enhancer RNAs for oestrogen-dependent transcriptional activation". Nature. 498 (7455): 516–520. Bibcode:2013Natur.498..516L. doi:10.1038/nature12210. PMC 3718886. PMID 23728302.
  59. ^ "Researchers discover how worms pass knowledge of a pathogen to offspring". Retrieved 11 October 2020.
  60. ^ Kaletsky R, Moore RS, Vrla GD, Parsons LR, Gitai Z, Murphy CT (October 2020). "C. elegans interprets bacterial non-coding RNAs to learn pathogenic avoidance". Nature. 586 (7829): 445–451. Bibcode:2020Natur.586..445K. doi:10.1038/s41586-020-2699-5. PMC 8547118. PMID 32908307. S2CID 221626129.
  61. ^ Pibouin L, Villaudy J, Ferbus D, Muleris M, Prospéri MT, Remvikos Y, Goubin G (February 2002). "Cloning of the mRNA of overexpression in colon carcinoma-1: a sequence overexpressed in a subset of colon carcinomas". Cancer Genetics and Cytogenetics. 133 (1): 55–60. doi:10.1016/S0165-4608(01)00634-3. PMID 11890990.
  62. ^ Fu X, Ravindranath L, Tran N, Petrovics G, Srivastava S (March 2006). "Regulation of apoptosis by a prostate-specific and prostate cancer-associated noncoding gene, PCGEM1". DNA and Cell Biology. 25 (3): 135–141. doi:10.1089/dna.2006.25.135. PMID 16569192.
  63. ^ Mourtada-Maarabouni M, Pickard MR, Hedge VL, Farzaneh F, Williams GT (January 2009). "GAS5, a non-protein-coding RNA, controls apoptosis and is downregulated in breast cancer". Oncogene. 28 (2): 195–208. doi:10.1038/onc.2008.373. PMID 18836484.
  64. ^ Dong XY, Guo P, Boyd J, Sun X, Li Q, Zhou W, Dong JT (August 2009). "Implication of snoRNA U50 in human breast cancer". Journal of Genetics and Genomics = Yi Chuan Xue Bao. 36 (8): 447–454. doi:10.1016/S1673-8527(08)60134-4. PMC 2854654. PMID 19683667.
  65. ^ Christov CP, Trivier E, Krude T (March 2008). "Noncoding human Y RNAs are overexpressed in tumours and required for cell proliferation". British Journal of Cancer. 98 (5): 981–988. doi:10.1038/sj.bjc.6604254. PMC 2266855. PMID 18283318.
  66. ^ Farh KK, Grimson A, Jan C, Lewis BP, Johnston WK, Lim LP, et al. (December 2005). "The widespread impact of mammalian MicroRNAs on mRNA repression and evolution". Science. 310 (5755): 1817–1821. Bibcode:2005Sci...310.1817F. doi:10.1126/science.1121158. PMID 16308420. S2CID 1849875.
  67. ^ Lim LP, Lau NC, Garrett-Engele P, Grimson A, Schelter JM, Castle J, et al. (February 2005). "Microarray analysis shows that some microRNAs downregulate large numbers of target mRNAs". Nature. 433 (7027): 769–773. Bibcode:2005Natur.433..769L. doi:10.1038/nature03315. PMID 15685193. S2CID 4430576.
  68. ^ Calin GA, Ferracin M, Cimmino A, Di Leva G, Shimizu M, Wojcik SE, et al. (October 2005). "A MicroRNA signature associated with prognosis and progression in chronic lymphocytic leukemia". The New England Journal of Medicine. 353 (17): 1793–1801. doi:10.1056/NEJMoa050995. PMID 16251535.
  69. ^ Calin GA, Dumitru CD, Shimizu M, Bichi R, Zupo S, Noch E, et al. (November 2002). "Frequent deletions and down-regulation of micro- RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia". Proceedings of the National Academy of Sciences of the United States of America. 99 (24): 15524–15529. Bibcode:2002PNAS...9915524C. doi:10.1073/pnas.242606799. PMC 137750. PMID 12434020.
  70. ^ Hu Z, Chen J, Tian T, Zhou X, Gu H, Xu L, et al. (July 2008). "Genetic variants of miRNA sequences and non-small cell lung cancer survival". The Journal of Clinical Investigation. 118 (7): 2600–2608. doi:10.1172/JCI34934. PMC 2402113. PMID 18521189.
  71. ^ Shen J, Ambrosone CB, Zhao H (March 2009). "Novel genetic variants in microRNA genes and familial breast cancer". International Journal of Cancer. 124 (5): 1178–1182. doi:10.1002/ijc.24008. PMID 19048628. S2CID 20960029.
  72. ^ Jia B, Wang Z, Sun X, Chen J, Zhao J, Qiu X (February 2019). "Long noncoding RNA LINC00707 sponges miR-370-3p to promote osteogenesis of human bone marrow-derived mesenchymal stem cells through upregulating WNT2B". Stem Cell Research & Therapy. 10 (1): 67. doi:10.1186/s13287-019-1161-9. PMC 6387535. PMID 30795799.
  73. ^ Tu J, Zhao Z, Xu M, Chen M, Weng Q, Wang J, Ji J (July 2019). "LINC00707 contributes to hepatocellular carcinoma progression via sponging miR-206 to increase CDK14". Journal of Cellular Physiology. 234 (7): 10615–10624. doi:10.1002/jcp.27737. PMID 30488589. S2CID 54119752.
  74. ^ Xie M, Ma T, Xue J, Ma H, Sun M, Zhang Z, et al. (February 2019). "The long intergenic non-protein coding RNA 707 promotes proliferation and metastasis of gastric cancer by interacting with mRNA stabilizing protein HuR". Cancer Letters. 443: 67–79. doi:10.1016/j.canlet.2018.11.032. PMID 30502359. S2CID 54611497.
  75. ^ Li T, Li Y, Sun H (2019-06-06). "MicroRNA-876 is sponged by long noncoding RNA LINC00707 and directly targets metadherin to inhibit breast cancer malignancy". Cancer Management and Research. 11: 5255–5269. doi:10.2147/cmar.s210845. PMC 6559252. PMID 31239777.
  76. ^ Yuan RX, Bao D, Zhang Y (May 2020). "Linc00707 promotes cell proliferation, invasion, and migration via the miR-30c/CTHRC1 regulatory loop in breast cancer". European Review for Medical and Pharmacological Sciences. 24 (9): 4863–4872. doi:10.26355/eurrev_202005_21175. PMID 32432749. S2CID 218759508.
  77. ^ Sahoo T, del Gaudio D, German JR, Shinawi M, Peters SU, Person RE, et al. (June 2008). "Prader-Willi phenotype caused by paternal deficiency for the HBII-85 C/D box small nucleolar RNA cluster". Nature Genetics. 40 (6): 719–721. doi:10.1038/ng.158. PMC 2705197. PMID 18500341.
  78. ^ Skryabin BV, Gubar LV, Seeger B, Pfeiffer J, Handel S, Robeck T, et al. (December 2007). "Deletion of the MBII-85 snoRNA gene cluster in mice results in postnatal growth retardation". PLOS Genetics. 3 (12): e235. doi:10.1371/journal.pgen.0030235. PMC 2323313. PMID 18166085.
  79. ^ Ding F, Li HH, Zhang S, Solomon NM, Camper SA, Cohen P, Francke U (March 2008). Akbarian S (ed.). "SnoRNA Snord116 (Pwcr1/MBII-85) deletion causes growth deficiency and hyperphagia in mice". PLOS ONE. 3 (3): e1709. Bibcode:2008PLoSO...3.1709D. doi:10.1371/journal.pone.0001709. PMC 2248623. PMID 18320030.
  80. ^ Ding F, Prints Y, Dhar MS, Johnson DK, Garnacho-Montero C, Nicholls RD, Francke U (June 2005). "Lack of Pwcr1/MBII-85 snoRNA is critical for neonatal lethality in Prader-Willi syndrome mouse models". Mammalian Genome. 16 (6): 424–431. doi:10.1007/s00335-005-2460-2. PMID 16075369. S2CID 12256515.
  81. ^ Bazeley PS, Shepelev V, Talebizadeh Z, Butler MG, Fedorova L, Filatov V, Fedorov A (January 2008). "snoTARGET shows that human orphan snoRNA targets locate close to alternative splice junctions". Gene. 408 (1–2): 172–179. doi:10.1016/j.gene.2007.10.037. PMC 6800007. PMID 18160232.
  82. ^ Bolton PF, Veltman MW, Weisblatt E, Holmes JR, Thomas NS, Youings SA, et al. (September 2004). "Chromosome 15q11-13 abnormalities and other medical conditions in individuals with autism spectrum disorders". Psychiatric Genetics. 14 (3): 131–137. doi:10.1097/00041444-200409000-00002. PMID 15318025. S2CID 37344935.
  83. ^ Cook EH, Scherer SW (October 2008). "Copy-number variations associated with neuropsychiatric conditions". Nature. 455 (7215): 919–923. Bibcode:2008Natur.455..919C. doi:10.1038/nature07458. PMID 18923514. S2CID 4377899.
  84. ^ Nakatani J, Tamada K, Hatanaka F, Ise S, Ohta H, Inoue K, et al. (June 2009). "Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism". Cell. 137 (7): 1235–1246. doi:10.1016/j.cell.2009.04.024. PMC 3710970. PMID 19563756.
  85. ^ Ziats MN, Rennert OM (March 2013). "Aberrant expression of long noncoding RNAs in autistic brain". Journal of Molecular Neuroscience. 49 (3): 589–593. doi:10.1007/s12031-012-9880-8. PMC 3566384. PMID 22949041.
  86. ^ Ridanpää M, van Eenennaam H, Pelin K, Chadwick R, Johnson C, Yuan B, et al. (January 2001). "Mutations in the RNA component of RNase MRP cause a pleiotropic human disease, cartilage-hair hypoplasia". Cell. 104 (2): 195–203. doi:10.1016/S0092-8674(01)00205-7. hdl:2066/185709. PMID 11207361. S2CID 13977736.
  87. ^ Martin AN, Li Y (March 2007). "RNase MRP RNA and human genetic diseases". Cell Research. 17 (3): 219–226. doi:10.1038/ PMID 17189938.
  88. ^ Kavadas FD, Giliani S, Gu Y, Mazzolari E, Bates A, Pegoiani E, et al. (December 2008). "Variability of clinical and laboratory features among patients with ribonuclease mitochondrial RNA processing endoribonuclease gene mutations". The Journal of Allergy and Clinical Immunology. 122 (6): 1178–1184. doi:10.1016/j.jaci.2008.07.036. PMID 18804272.
  89. ^ Faghihi MA, Modarresi F, Khalil AM, Wood DE, Sahagan BG, Morgan TE, et al. (July 2008). "Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of beta-secretase". Nature Medicine. 14 (7): 723–730. doi:10.1038/nm1784. PMC 2826895. PMID 18587408.
  90. ^ Mencía A, Modamio-Høybjør S, Redshaw N, Morín M, Mayo-Merino F, Olavarrieta L, et al. (May 2009). "Mutations in the seed region of human miR-96 are responsible for nonsyndromic progressive hearing loss". Nature Genetics. 41 (5): 609–613. doi:10.1038/ng.355. PMID 19363479. S2CID 11113852.
  91. ^ Lewis MA, Quint E, Glazier AM, Fuchs H, De Angelis MH, Langford C, et al. (May 2009). "An ENU-induced mutation of miR-96 associated with progressive hearing loss in mice". Nature Genetics. 41 (5): 614–618. doi:10.1038/ng.369. PMC 2705913. PMID 19363478.
  92. ^ Soukup GA (June 2009). "Little but loud: small RNAs have a resounding affect on ear development". Brain Research. 1277: 104–114. doi:10.1016/j.brainres.2009.02.027. PMC 2700218. PMID 19245798.
  93. ^ Taylor RW, Turnbull DM (May 2005). "Mitochondrial DNA mutations in human disease". Nature Reviews. Genetics. 6 (5): 389–402. doi:10.1038/nrg1606. PMC 1762815. PMID 15861210.
  94. ^ Yarham JW, Elson JL, Blakely EL, McFarland R, Taylor RW (September 2010). "Mitochondrial tRNA mutations and disease". Wiley Interdisciplinary Reviews. RNA. 1 (2): 304–324. doi:10.1002/wrna.27. PMID 21935892. S2CID 43123827.
  95. ^ Zifa E, Giannouli S, Theotokis P, Stamatis C, Mamuris Z, Stathopoulos C (January 2007). "Mitochondrial tRNA mutations: clinical and functional perturbations". RNA Biology. 4 (1): 38–66. doi:10.4161/rna.4.1.4548. PMID 17617745. S2CID 11965790.
  96. ^ Abbott JA, Francklyn CS, Robey-Bond SM (2014). "Transfer RNA and human disease". Frontiers in Genetics. 5: 158. doi:10.3389/fgene.2014.00158. PMC 4042891. PMID 24917879.
  97. ^ Carter RJ, Dubchak I, Holbrook SR (October 2001). "A computational approach to identify genes for functional RNAs in genomic sequences". Nucleic Acids Research. 29 (19): 3928–3938. doi:10.1093/nar/29.19.3928. PMC 60242. PMID 11574674.
  98. ^ Pedersen JS, Bejerano G, Siepel A, Rosenbloom K, Lindblad-Toh K, Lander ES, et al. (April 2006). "Identification and classification of conserved RNA secondary structures in the human genome". PLOS Computational Biology. 2 (4): e33. Bibcode:2006PLSCB...2...33P. doi:10.1371/journal.pcbi.0020033. PMC 1440920. PMID 16628248.
  99. ^ Thomas JM, Horspool D, Brown G, Tcherepanov V, Upton C (January 2007). "GraphDNA: a Java program for graphical display of DNA composition analyses". BMC Bioinformatics. 8: 21. doi:10.1186/1471-2105-8-21. PMC 1783863. PMID 17244370.
  100. ^ Brosius J, Raabe CA (February 2015). "What is an RNA? A top layer for RNA classification". RNA Biology. 13 (2): 140–144. doi:10.1080/15476286.2015.1128064. PMC 4829331. PMID 26818079.
  101. ^ Ji Z, Song R, Regev A, Struhl K (December 2015). "Many lncRNAs, 5'UTRs, and pseudogenes are translated and some are likely to express functional proteins". eLife. 4: e08890. doi:10.7554/eLife.08890. PMC 4739776. PMID 26687005.
  102. ^ Tosar JP, Rovira C, Cayota A (2018-01-22). "Non-coding RNA fragments account for the majority of annotated piRNAs expressed in somatic non-gonadal tissues". Communications Biology. 1 (1): 2. doi:10.1038/s42003-017-0001-7. PMC 6052916. PMID 30271890.
  103. ^ Housman G, Ulitsky I (January 2016). "Methods for distinguishing between protein-coding and long noncoding RNAs and the elusive biological purpose of translation of long noncoding RNAs". Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms. 1859 (1): 31–40. doi:10.1016/j.bbagrm.2015.07.017. PMID 26265145.

External links[edit]