mir-181 microRNA precursor

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mir-181 microRNA precursor
Predicted secondary structure and sequence conservation of mir-181
Identifiers
SymbolmiR-181
RfamRF00076
miRBaseMI0000269
miRBase familyMIPF0000007
Other data
RNA typeGene; miRNA
Domain(s)Eukaryota
GOGO:0035195 GO:0035068
SOSO:0001244
PDB structuresPDBe

In molecular biology miR-181 microRNA precursor is a small non-coding RNA molecule. MicroRNAs (miRNAs) are transcribed as ~70 nucleotide precursors and subsequently processed by the RNase-III type enzyme Dicer to give a ~22 nucleotide mature product. In this case the mature sequence comes from the 5' arm of the precursor. They target and modulate protein expression by inhibiting translation and / or inducing degradation of target messenger RNAs. This new class of genes has recently been shown to play a central role in malignant transformation. miRNA are downregulated in many tumors and thus appear to function as tumor suppressor genes.[1] The mature products miR-181a, miR-181b, miR-181c or miR-181d are thought to have regulatory roles at posttranscriptional level, through complementarity to target mRNAs.[2] miR-181 has been predicted or experimentally confirmed in a wide number of vertebrate species such as rat, zebrafish, and pufferfish (see below) (MIPF0000007).

Expression[edit]

It has been shown that miR-181 is preferentially expressed in the B-lymphoid cells of mouse bone marrow,[3] but also in the retina and brain.[4] In humans, this microRNA is involved in the mechanisms of immunity, and in many different cancers (see below) it was found to be expressed at a particularly low level.[5]

Genome location[edit]

Human
miR-181a1 and miR-181b1 are clustered together and located on the chromosome 1 (37.p5), miR-181a2 and miR-181b2 are clustered together and located on the chromosome 9 (37.p5).[6][7][8] miR-181c and miR-181d are clustered together and located on the chromosome 19 (37.p5).[2][9][10]

Organisms[edit]

miR-181 family are present in vertebrates and nematodes[citation needed] (this list is not exhaustive):

miR-181[edit]

Chronic lymphocytic leukemia[edit]

miR-181 may have a regulatory role with tumor suppressors genes of the human chromosome 1.[5] It has been shown that the Tcl1 oncogene is a target of miR-181a in an inhibition relation (downregulated) that would result in an action on the tumor cell growth process. miR-181 expression has a reverse correlation with Tcl1 protein expression.[31]

Neuroblastoma[edit]

mir-181 a and b are over-expressed and act as bad prognosis maker of aggressive neuroblastoma (Stage 4) as compare to low grade stage (Stage 1;2;3 and 4S) whereas mir-181 c and d isoforms are not. In these conditions, they regulate the tumor suppressor gene CDON.[32]

Myoblast differentiation[edit]

It has been shown that miR-181 targets the homeobox protein Hox-A11 and participates in establishing muscle tissue downregulating it (a repressor of the differentiation process in mammalians and lower organisms).[33]

Breast cancer[edit]

miR-181a, miR-181b, miR-181c and miR-181d are activated by the human gene ERBB2, located on the chromosome 17. The expression of miR-181c is relevant to characterize a Breast cancer form, the HER2/neu.[34]
miR-181 is also activated by the small molecule tamoxifen.[35] One selective modulators of estrogen receptor having specific activities of tissue. Tamoxifen acts as an anti-estrogen (inhibitor) in breast tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and the proliferation of endometrial cells. miR-181 could acquire a resistance to tamoxifen, the drug is successfully used to treat women with estrogen receptor-positive breast cancer.[35]

Acute myeloid leukemia[edit]

Downregulation of miR-181 family contributes to aggressive leukemia phenotype through mechanisms related to the activation pathways of innate immunity mediated by toll-like receptors TLR2, TLR4, TLR7 and TLR8 and interleukin-1β IL1B (humans on chromose 2).[1]

Glioblastoma[edit]

miR-181a, miR-181b, and miR-181c, which are down-regulated in glioblastoma.[36] miR-181b is downregulated in glioma samples compared with the normal brain tissue. It is suggested that the downregulation of miR-181 may play a role in the development of cancer. It is shown that transfection of miR-181a and miR-181b triggers growth inhibition, apoptosis and inhibits invasion. In addition, the expression of miR-181a was found to be inversely correlated with tumor grading while miR-181b was uniformly downregulated in gliomas with different grades of malignancy.[37]

Glioma[edit]

It has been shown that downregulated miR-181a and miR-181b were also involved in the oncogenesis of gliomas. miR-181a and miR-181b function as tumor suppressors that cause inhibition of growth, induce apoptosis and inhibit invasion of glioma cells. In addition, the tumor suppressive effect of miR-181b in glioma cells was apparent that the effect of miR-181a. These aberrant results suggest that downregulated miR-181a and miR-181b may be key factors that contribute to the occurrence in malignant human gliomas.[38]

Multiple myeloma[edit]

MiRNA signature for multiple myeloma (MM) has been described, including miR-181a and miR-181b, which modulate the expression of proteins essential for the pathogenesis of myeloma. Xenograft studies using human MM cell lines treated with miR-181a and miR-181b antagonists resulted in significant suppression of tumor growth in nude mice.[39]

Papillary thyroid carcinoma[edit]

It was found that miR-181a and miR-181c are overexpressed in Papillary Thyroid Carcinoma tumors, sufficiently to successfully predict cancer status.[40]

Hepatocellular carcinoma[edit]

It has been shown that conserved miR-181 family were upregulated in EpCAM+ AFP+ Hepatocellular carcinoma (HCC) cells and EpCAM+ HCC isolated from AFP+ tumors. In addition, miR-181 family members were highly expressed in the embryonic liver and isolated hepatic stem cells. Especially, inhibition of miR-181 leads to a reduction of the EpCAM+, the amount of HCC cells and initiate tumor capacity, whereas exogenous miR-181 expression in HCC cells resulted in an enrichment of EpCAM+ HCC cells. miR-181 could directly target hepatic transcriptional regulators of differentiation (like homeobox 2 CDX2 and 6 GATA proteins binding GATA6) and an inhibitor of Wnt / beta-catenin. It suggests that miR-181 may eradicate HCC.[41]

miR-181a[edit]

T-cell sensitivity[edit]

The increased expression of miR-181a in mature T cells increases susceptibility to peptide antigens, while inhibiting the expression of miR-181a in immature T cells reduces sensitivity and alters the both positive and negative selection. In addition, the quantitative regulation of the sensitivity of T cells by miR-181a allows for mature T cells recognize peptide inhibitor antagonists, like agonists. These effects are achieved in part by downregulation of multiple phosphatases, which leads to high levels of steadystate phosphorylated intermediates and reducing the threshold of T cell receptor signaling. The expression of miR-181a correlates with a greater sensitivity of immature T cells in T cells, suggesting that miR-181a acts as an antigen intrinsic sensitivity "rheostat" during the development of T cells.[42]

Vascular development[edit]

It has been shown that miR-181a binds the 3' UTR of Prox1 leading to translation repression and transcript degradation. Prox1 is a homeobox transcription factor involved in development of the lymphatic endothelium.[43]

Cerebellar neurodegeneration[edit]

miR-181a has a relatively broad expression pattern and is present in neurons in numerous parts of the mouse brain. miR-181a is essential for the survival of Purkinje cells and its absence leads to a slow degeneration of these cells.[44]

Diabetes mellitus[edit]

It has been shown that there are significant correlations between the expression of miR-181a and both adipose tissue morphology and key metabolic parameters, including visceral fat area, HbA1c, fasting plasma glucose, and circulating leptin, adiponectin, interleukin-6. The expression of miR-181a may contribute to intrinsic differences between omental and subcutaneous adipose tissue.[45]

Homozygous sickle cell disease[edit]

miR-181a is over-represented in the normal hemoglobin (HbAA) erythrocytes.[46] miR-181a has been shown to play a role in the lineage differentiation in the hematopoietic system.[3]

Breast cancer[edit]

miR-181a expression is associated with survival in triple negative breast cancer. Patients with low expression have lower probability of survival over time.[47]

miR-181b[edit]

Colorectal cancer[edit]

miR-181b was significantly overexpressed in tumors compared to normal colorectal samples, especially high miR-181b expression correlated with poor survival of only black patients with stage III colorectal cancers [48] (Sequencing analysis revealed that miR-181b expression is strongly associated with mutation status of the tumor suppressor gene p53.[49]

Cardiac hypertrophy[edit]

miR-181b is downregulated during hypertrophy, it causes a reduction in cardiomyocyte cell size.[50]

Oral carcinoma[edit]

miR-181b expression was steadily increased and is associated with increased severity of lesions during the progression of the Oral Carcinoma. Overexpression of miR-181b may play an important role in malignant transformation.[51]

Prostate cancer[edit]

miR-181b is downregulated in cancerous cells.[52]

Adrenocortical carcinoma[edit]

Mir-210 has been suggested as a useful biomarker to distinguish adrenocortical carcinoma from adrenocortical adenoma.[53]

miR-181c[edit]

in Apoptosis[citation needed]

miR-181d[edit]

Duchenne muscular dystrophy[edit]

miR-181d is disregulated in Duchenne muscular dystrophy (DMD).[54]

Nemaline myopathy[edit]

miR-181d is disregulated in nemaline myopathy (NM).[54]

References[edit]

  1. ^ a b Larson RA (March 2010). "Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia". Chemico-Biological Interactions. 184 (1–2): 21–5. doi:10.1016/j.cbi.2009.10.002. PMC 2846194. PMID 19822134.
  2. ^ a b c d Lim LP, Glasner ME, Yekta S, Burge CB, Bartel DP (March 2003). "Vertebrate microRNA genes". Science. 299 (5612): 1540. doi:10.1126/science.1080372. PMID 12624257. S2CID 37750545.
  3. ^ a b Chen CZ, Li L, Lodish HF, Bartel DP (January 2004). "MicroRNAs modulate hematopoietic lineage differentiation". Science. 303 (5654): 83–6. doi:10.1126/science.1091903. hdl:1721.1/7483. PMID 14657504. S2CID 7044929.
  4. ^ Ryan DG, Oliveira-Fernandes M, Lavker RM (October 2006). "MicroRNAs of the mammalian eye display distinct and overlapping tissue specificity". Molecular Vision. 12: 1175–84. PMID 17102797.
  5. ^ a b Marton S, Garcia MR, Robello C, Persson H, Trajtenberg F, Pritsch O, Rovira C, Naya H, Dighiero G, Cayota A (February 2008). "Small RNAs analysis in CLL reveals a deregulation of miRNA expression and novel miRNA candidates of putative relevance in CLL pathogenesis". Leukemia. 22 (2): 330–8. doi:10.1038/sj.leu.2405022. PMID 17989717.
  6. ^ Lui WO, Pourmand N, Patterson BK, Fire A (July 2007). "Patterns of known and novel small RNAs in human cervical cancer". Cancer Research. 67 (13): 6031–43. doi:10.1158/0008-5472.CAN-06-0561. PMID 17616659.
  7. ^ Cai X, Lu S, Zhang Z, Gonzalez CM, Damania B, Cullen BR (April 2005). "Kaposi's sarcoma-associated herpesvirus expresses an array of viral microRNAs in latently infected cells". Proceedings of the National Academy of Sciences of the United States of America. 102 (15): 5570–5. doi:10.1073/pnas.0408192102. PMC 556237. PMID 15800047.
  8. ^ Dostie J, Mourelatos Z, Yang M, Sharma A, Dreyfuss G (February 2003). "Numerous microRNPs in neuronal cells containing novel microRNAs". RNA. 9 (2): 180–6. doi:10.1261/rna.2141503. PMC 1370383. PMID 12554860.
  9. ^ Landgraf P, Rusu M, Sheridan R, Sewer A, Iovino N, Aravin A, et al. (June 2007). "A mammalian microRNA expression atlas based on small RNA library sequencing". Cell. 129 (7): 1401–14. doi:10.1016/j.cell.2007.04.040. PMC 2681231. PMID 17604727.
  10. ^ Bentwich I, Avniel A, Karov Y, Aharonov R, Gilad S, Barad O, Barzilai A, Einat P, Einav U, Meiri E, Sharon E, Spector Y, Bentwich Z (July 2005). "Identification of hundreds of conserved and nonconserved human microRNAs". Nature Genetics. 37 (7): 766–70. doi:10.1038/ng1590. PMID 15965474. S2CID 7746954.
  11. ^ Lyson TR, Sperling EA, Heimberg AM, Gauthier JA, King BL, Peterson KJ (February 2012). "MicroRNAs support a turtle + lizard clade". Biology Letters. 8 (1): 104–7. doi:10.1098/rsbl.2011.0477. PMC 3259949. PMID 21775315.
  12. ^ Strozzi F, Mazza R, Malinverni R, Williams JL (February 2009). "Annotation of 390 bovine miRNA genes by sequence similarity with other species". Animal Genetics. 40 (1): 125. doi:10.1111/j.1365-2052.2008.01780.x. PMID 18945293.
  13. ^ Jin W, Grant JR, Stothard P, Moore SS, Guan LL (September 2009). "Characterization of bovine miRNAs by sequencing and bioinformatics analysis". BMC Molecular Biology. 10: 90. doi:10.1186/1471-2199-10-90. PMC 2761914. PMID 19758457. Open access icon
  14. ^ Yan X, Ding L, Li Y, Zhang X, Liang Y, Sun X, Teng CB (2012). "Identification and profiling of microRNAs from skeletal muscle of the common carp". PLOS ONE. 7 (1): e30925. doi:10.1371/journal.pone.0030925. PMC 3267759. PMID 22303472. Open access icon
  15. ^ Friedländer MR, Chen W, Adamidi C, Maaskola J, Einspanier R, Knespel S, Rajewsky N (April 2008). "Discovering microRNAs from deep sequencing data using miRDeep". Nature Biotechnology. 26 (4): 407–15. doi:10.1038/nbt1394. PMID 18392026. S2CID 9956142.
  16. ^ Hackl M, Jakobi T, Blom J, Doppmeier D, Brinkrolf K, Szczepanowski R, Bernhart SH, Höner Zu Siederdissen C, Bort JA, Wieser M, Kunert R, Jeffs S, Hofacker IL, Goesmann A, Pühler A, Borth N, Grillari J (April 2011). "Next-generation sequencing of the Chinese hamster ovary microRNA transcriptome: Identification, annotation and profiling of microRNAs as targets for cellular engineering". Journal of Biotechnology. 153 (1–2): 62–75. doi:10.1016/j.jbiotec.2011.02.011. PMC 3119918. PMID 21392545.
  17. ^ Zhou M, Wang Q, Sun J, Li X, Xu L, Yang H, Shi H, Ning S, Chen L, Li Y, He T, Zheng Y (August 2009). "In silico detection and characteristics of novel microRNA genes in the Equus caballus genome using an integrated ab initio and comparative genomic approach". Genomics. 94 (2): 125–31. doi:10.1016/j.ygeno.2009.04.006. PMID 19406225.
  18. ^ International Chicken Genome Sequencing Consortium (December 2004). "Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution" (PDF). Nature. 432 (7018): 695–716. doi:10.1038/nature03154. PMID 15592404.
  19. ^ Yao Y, Zhao Y, Xu H, Smith LP, Lawrie CH, Watson M, Nair V (April 2008). "MicroRNA profile of Marek's disease virus-transformed T-cell line MSB-1: predominance of virus-encoded microRNAs". Journal of Virology. 82 (8): 4007–15. doi:10.1128/JVI.02659-07. PMC 2293013. PMID 18256158.
  20. ^ a b c d e f g h Berezikov E, Guryev V, van de Belt J, Wienholds E, Plasterk RH, Cuppen E (January 2005). "Phylogenetic shadowing and computational identification of human microRNA genes". Cell. 120 (1): 21–4. doi:10.1016/j.cell.2004.12.031. PMID 15652478.
  21. ^ Devor EJ, Samollow PB (2008). "In vitro and in silico annotation of conserved and nonconserved microRNAs in the genome of the marsupial Monodelphis domestica". The Journal of Heredity. 99 (1): 66–72. doi:10.1093/jhered/esm085. PMID 17965199.
  22. ^ Weber MJ (January 2005). "New human and mouse microRNA genes found by homology search". The FEBS Journal. 272 (1): 59–73. doi:10.1111/j.1432-1033.2004.04389.x. PMID 15634332. S2CID 32923462.
  23. ^ Murchison EP, Kheradpour P, Sachidanandam R, Smith C, Hodges E, Xuan Z, Kellis M, Grützner F, Stark A, Hannon GJ (June 2008). "Conservation of small RNA pathways in platypus". Genome Research. 18 (6): 995–1004. doi:10.1101/gr.073056.107. PMC 2413167. PMID 18463306.
  24. ^ Li SC, Chan WC, Ho MR, Tsai KW, Hu LY, Lai CH, Hsu CN, Hwang PP, Lin WC (December 2010). "Discovery and characterization of medaka miRNA genes by next generation sequencing platform". BMC Genomics. 11 (Suppl 4): S8. doi:10.1186/1471-2164-11-S4-S8. PMC 3005926. PMID 21143817. Open access icon
  25. ^ Heimberg AM, Cowper-Sal-lari R, Sémon M, Donoghue PC, Peterson KJ (November 2010). "microRNAs reveal the interrelationships of hagfish, lampreys, and gnathostomes and the nature of the ancestral vertebrate". Proceedings of the National Academy of Sciences of the United States of America. 107 (45): 19379–83. doi:10.1073/pnas.1010350107. PMC 2984222. PMID 20959416.
  26. ^ Linsen SE, de Wit E, de Bruijn E, Cuppen E (April 2010). "Small RNA expression and strain specificity in the rat". BMC Genomics. 11: 249. doi:10.1186/1471-2164-11-249. PMC 2864251. PMID 20403161. Open access icon
  27. ^ Murchison EP, Tovar C, Hsu A, Bender HS, Kheradpour P, Rebbeck CA, Obendorf D, Conlan C, Bahlo M, Blizzard CA, Pyecroft S, Kreiss A, Kellis M, Stark A, Harkins TT, Marshall Graves JA, Woods GM, Hannon GJ, Papenfuss AT (January 2010). "The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer". Science. 327 (5961): 84–7. doi:10.1126/science.1180616. PMC 2982769. PMID 20044575.
  28. ^ Reddy AM, Zheng Y, Jagadeeswaran G, Macmil SL, Graham WB, Roe BA, Desilva U, Zhang W, Sunkar R (February 2009). "Cloning, characterization and expression analysis of porcine microRNAs". BMC Genomics. 10: 65. doi:10.1186/1471-2164-10-65. PMC 2644714. PMID 19196471. Open access icon
  29. ^ Warren WC, Clayton DF, Ellegren H, Arnold AP, Hillier LW, Künstner A, et al. (April 2010). "The genome of a songbird". Nature. 464 (7289): 757–62. doi:10.1038/nature08819. PMC 3187626. PMID 20360741.
  30. ^ Tang GQ, Maxwell ES (January 2008). "Xenopus microRNA genes are predominantly located within introns and are differentially expressed in adult frog tissues via post-transcriptional regulation". Genome Research. 18 (1): 104–12. doi:10.1101/gr.6539108. PMC 2134782. PMID 18032731.
  31. ^ Pekarsky Y, Santanam U, Cimmino A, Palamarchuk A, Efanov A, Maximov V, Volinia S, Alder H, Liu CG, Rassenti L, Calin GA, Hagan JP, Kipps T, Croce CM (December 2006). "Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181". Cancer Research. 66 (24): 11590–3. doi:10.1158/0008-5472.CAN-06-3613. PMID 17178851.
  32. ^ Gibert B, Delloye-Bourgeois C, Gattolliat CH, Meurette O, Le Guernevel S, Fombonne J, Ducarouge B, Lavial F, Bouhallier F, Creveaux M, Negulescu AM, Bénard J, Janoueix-Lerosey I, Harel-Bellan A, Delattre O, Mehlen P (November 2014). "Regulation by miR181 family of the dependence receptor CDON tumor suppressive activity in neuroblastoma". Journal of the National Cancer Institute. 106 (11): dju318. doi:10.1093/jnci/dju318. PMID 25313246.
  33. ^ Naguibneva I, Ameyar-Zazoua M, Polesskaya A, Ait-Si-Ali S, Groisman R, Souidi M, Cuvellier S, Harel-Bellan A (March 2006). "The microRNA miR-181 targets the homeobox protein Hox-A11 during mammalian myoblast differentiation". Nature Cell Biology. 8 (3): 278–84. doi:10.1038/ncb1373. PMID 16489342. S2CID 24759490.
  34. ^ Lowery AJ, Miller N, Devaney A, McNeill RE, Davoren PA, Lemetre C, Benes V, Schmidt S, Blake J, Ball G, Kerin MJ (2009). "MicroRNA signatures predict oestrogen receptor, progesterone receptor and HER2/neu receptor status in breast cancer". Breast Cancer Research. 11 (3): R27. doi:10.1186/bcr2257. PMC 2716495. PMID 19432961.
  35. ^ a b Miller TE, Ghoshal K, Ramaswamy B, Roy S, Datta J, Shapiro CL, Jacob S, Majumder S (October 2008). "MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1". The Journal of Biological Chemistry. 283 (44): 29897–903. doi:10.1074/jbc.M804612200. PMC 2573063. PMID 18708351.
  36. ^ Ciafrè SA, Galardi S, Mangiola A, Ferracin M, Liu CG, Sabatino G, Negrini M, Maira G, Croce CM, Farace MG (September 2005). "Extensive modulation of a set of microRNAs in primary glioblastoma". Biochemical and Biophysical Research Communications. 334 (4): 1351–8. doi:10.1016/j.bbrc.2005.07.030. PMID 16039986.
  37. ^ Conti A, Aguennouz M, La Torre D, Tomasello C, Cardali S, Angileri FF, Maio F, Cama A, Germanò A, Vita G, Tomasello F (July 2009). "miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors". Journal of Neuro-Oncology. 93 (3): 325–32. doi:10.1007/s11060-009-9797-4. PMID 19159078. S2CID 10220565.
  38. ^ Shi L, Cheng Z, Zhang J, Li R, Zhao P, Fu Z, You Y (October 2008). "hsa-mir-181a and hsa-mir-181b function as tumor suppressors in human glioma cells". Brain Research. 1236: 185–93. doi:10.1016/j.brainres.2008.07.085. PMID 18710654. S2CID 28258522.
  39. ^ Pichiorri F, Suh SS, Ladetto M, Kuehl M, Palumbo T, Drandi D, Taccioli C, Zanesi N, Alder H, Hagan JP, Munker R, Volinia S, Boccadoro M, Garzon R, Palumbo A, Aqeilan RI, Croce CM (September 2008). "MicroRNAs regulate critical genes associated with multiple myeloma pathogenesis". Proceedings of the National Academy of Sciences of the United States of America. 105 (35): 12885–90. doi:10.1073/pnas.0806202105. PMC 2529070. PMID 18728182.
  40. ^ He H, Jazdzewski K, Li W, Liyanarachchi S, Nagy R, Volinia S, Calin GA, Liu CG, Franssila K, Suster S, Kloos RT, Croce CM, de la Chapelle A (December 2005). "The role of microRNA genes in papillary thyroid carcinoma". Proceedings of the National Academy of Sciences of the United States of America. 102 (52): 19075–80. doi:10.1073/pnas.0509603102. PMC 1323209. PMID 16365291.
  41. ^ Ji J, Yamashita T, Budhu A, Forgues M, Jia HL, Li C, Deng C, Wauthier E, Reid LM, Ye QH, Qin LX, Yang W, Wang HY, Tang ZY, Croce CM, Wang XW (August 2009). "Identification of microRNA-181 by genome-wide screening as a critical player in EpCAM-positive hepatic cancer stem cells". Hepatology. 50 (2): 472–80. doi:10.1002/hep.22989. PMC 2721019. PMID 19585654.
  42. ^ Li QJ, Chau J, Ebert PJ, Sylvester G, Min H, Liu G, Braich R, Manoharan M, Soutschek J, Skare P, Klein LO, Davis MM, Chen CZ (April 2007). "miR-181a is an intrinsic modulator of T cell sensitivity and selection". Cell. 129 (1): 147–61. doi:10.1016/j.cell.2007.03.008. PMID 17382377.
  43. ^ Kazenwadel J, Michael MZ, Harvey NL (September 2010). "Prox1 expression is negatively regulated by miR-181 in endothelial cells". Blood. 116 (13): 2395–401. doi:10.1182/blood-2009-12-256297. PMID 20558617.
  44. ^ Schaefer A, O'Carroll D, Tan CL, Hillman D, Sugimori M, Llinas R, Greengard P (July 2007). "Cerebellar neurodegeneration in the absence of microRNAs". The Journal of Experimental Medicine. 204 (7): 1553–8. doi:10.1084/jem.20070823. PMC 2118654. PMID 17606634.
  45. ^ Klöting N, Berthold S, Kovacs P, Schön MR, Fasshauer M, Ruschke K, Stumvoll M, Blüher M (2009). "MicroRNA expression in human omental and subcutaneous adipose tissue". PLOS ONE. 4 (3): e4699. doi:10.1371/journal.pone.0004699. PMC 2649537. PMID 19259271. Open access icon
  46. ^ Chen SY, Wang Y, Telen MJ, Chi JT (June 2008). "The genomic analysis of erythrocyte microRNA expression in sickle cell diseases". PLOS ONE. 3 (6): e2360. doi:10.1371/journal.pone.0002360. PMC 2408759. PMID 18523662. Open access icon
  47. ^ Lánczky A, Nagy Á, Bottai G, Munkácsy G, Szabó A, Santarpia L, Győrffy B (December 2016). "miRpower: a web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients". Breast Cancer Research and Treatment. 160 (3): 439–446. doi:10.1007/s10549-016-4013-7. PMID 27744485. S2CID 11165696.
  48. ^ Bovell LC, Shanmugam C, Putcha BD, Katkoori VR, Zhang B, Bae S, Singh KP, Grizzle WE, Manne U (July 2013). "The prognostic value of microRNAs varies with patient race/ethnicity and stage of colorectal cancer". Clinical Cancer Research. 19 (14): 3955–65. doi:10.1158/1078-0432.CCR-12-3302. PMC 3746330. PMID 23719259.
  49. ^ Xi Y, Formentini A, Chien M, Weir DB, Russo JJ, Ju J, Kornmann M, Ju J (2006). "Prognostic Values of microRNAs in Colorectal Cancer". Biomarker Insights. 2: 113–121. PMC 2134920. PMID 18079988.
  50. ^ van Rooij E, Sutherland LB, Liu N, Williams AH, McAnally J, Gerard RD, Richardson JA, Olson EN (November 2006). "A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure". Proceedings of the National Academy of Sciences of the United States of America. 103 (48): 18255–60. doi:10.1073/pnas.0608791103. PMC 1838739. PMID 17108080.
  51. ^ Cervigne NK, Reis PP, Machado J, Sadikovic B, Bradley G, Galloni NN, Pintilie M, Jurisica I, Perez-Ordonez B, Gilbert R, Gullane P, Irish J, Kamel-Reid S (December 2009). "Identification of a microRNA signature associated with progression of leukoplakia to oral carcinoma". Human Molecular Genetics. 18 (24): 4818–29. doi:10.1093/hmg/ddp446. PMID 19776030.
  52. ^ Schaefer A, Jung M, Mollenkopf HJ, Wagner I, Stephan C, Jentzmik F, Miller K, Lein M, Kristiansen G, Jung K (March 2010). "Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma". International Journal of Cancer. 126 (5): 1166–76. doi:10.1002/ijc.24827. PMID 19676045.
  53. ^ Szabó DR, Luconi M, Szabó PM, Tóth M, Szücs N, Horányi J, Nagy Z, Mannelli M, Patócs A, Rácz K, Igaz P (March 2014). "Analysis of circulating microRNAs in adrenocortical tumors". Laboratory Investigation; A Journal of Technical Methods and Pathology. 94 (3): 331–9. doi:10.1038/labinvest.2013.148. PMID 24336071.
  54. ^ a b Eisenberg I, Eran A, Nishino I, Moggio M, Lamperti C, Amato AA, Lidov HG, Kang PB, North KN, Mitrani-Rosenbaum S, Flanigan KM, Neely LA, Whitney D, Beggs AH, Kohane IS, Kunkel LM (October 2007). "Distinctive patterns of microRNA expression in primary muscular disorders". Proceedings of the National Academy of Sciences of the United States of America. 104 (43): 17016–21. doi:10.1073/pnas.0708115104. PMC 2040449. PMID 17942673.

Further reading[edit]

External links[edit]


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