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mir-184

February 20, 2024

In molecular biology, miR-184 microRNA is a short non-coding RNA molecule. MicroRNAs (miRNAs) function as posttranscriptional regulators of expression levels of other genes by several mechanisms.[1] Several targets for miR-184 have been described, including that of mediators of neurological development, apoptosis and it has been suggested that miR-184 plays an essential role in development.[2]

mir-184
miR-184 microRNA secondary structure and sequence conservation
Identifiers
Symbolmir-184
RfamRF00657
miRBase familyMIPF0000059
NCBI Gene406960
HGNC31555
OMIM613146
Other data
RNA typemicroRNA
Domain(s)Eukaryota; Chordata
PDB structuresPDBe

MicroRNAs can bind to the three prime untranslated region (3'UTR) of the target messenger RNA (mRNA).[3] Binding of the miRNA can hinder translation of mRNA by promoting degradation or inducing deadenylation.[4]

Genomic location edit

miR-184 is a single copy gene and evolutionarily conserved at the nucleotide level from flies to humans.[5] In humans, miR-184 is located within region 25.1 on the q-arm of chromosome 15, and its corresponding transcript is comparatively small (84bp) which is not encoded near other clustered miRNAs.[6] In the mouse genome, miR-184 is located in an imprinted locus on mouse chromosome 9, and it is 55 kb away from the nearest coding gene.[7]

The genomic region immediately surrounding miR-184 does not contain a classic CpG island, but does contain several CpG-rich sequences that are suitable for MBD1 binding.[8]

Expression edit

miR-184 displays a tissue- and developmental-specific expression pattern. In mammals, mature miR-184 is particularly enriched in the brain and testis,[7] along with the corneal epithelium.[9] Depolarization of cortical neurons results in pri-miR-184 expression in an allele specific manner.[7] High expression is observed in suprabasal cells of the corneal epithelium in the mouse model, along with expression in mouse testis and brain tissue.[7][9] In Zebrafish, it is expressed in lens, hatching gland and epidermis (shown by Northern blot).[10] miR-184 is expressed ubiquitously in Drosophila embryos, larvae and adults, and its expression pattern displays dynamic changes during the development of embryo, especially in the central nervous system.[2][5] However, the temporal and spatial expression pattern of miR-184 is still being debated.

Role in neuronal cells edit

C. Liu et al. showed that Methyl-CpG binding protein 1 (MBD1) regulates the expression of several miRNAs in adult neural stem/progenitor cells (aNSCs) and, specifically, that miR-184 is directly repressed by MBD1. High levels of miR-184 promotes cell proliferation but inhibits differentiation of aNSCs, whereas inhibition of miR-184 rescued phenotypes associated with MBD1 deficiency.[11]

Numblike (Numbl) is known to be important in embryonic neural stem cell function and cortical brain development and has been identified as a downstream target of miR-184.[12][13] It has been found that exogenously expressed Numbl could rescue aNSC proliferation and differentiation deficits resulting from either elevated miR-184 or MBD1 deficiency.[11]

Other Targets edit

An analysis of the primary transcript of miR-184 (pri-mir-184) in several mouse tissues revealed specific expression in the brain and testis. Its expression is repressed by the binding of methyl-CpG binding protein 2 (MeCP2) to its promoter, but is upregulated by the release of MeCP2 after depolarization, suggesting a link between miRNAs and DNA methylation pathways .[7] J. Yu et al. demonstrated that the lipid phosphatase SH2-containing phosphoinositide 5'phosphatase 2 (SHIP2) is a target of miRNA-205 (miR-205) in epithelial cells, and that the corneal epithelial-specific miR-184 can interfere with the ability of miR-205 to suppress SHIP2 levels. The mechanism by which miR-184 negatively regulates miR-205 appears to be unique, and is the first example of a miRNA negatively regulating another to maintain levels of a target protein. miR-184 does not directly affect SHIP2 translation, but instead prevents miR-205 from interacting with SHIP2 mRNA. Interfering with miR-205 function by using a synthetic antagomir, or by the ectopic expression of miR-184, is thought to lead to a coordinated damping of the Akt signaling pathway via SHIP2 induction.[14]

R. Weitzel et al. showed that miR-184 mediates NFAT1 translational regulation in umbilical cord blood (UCB) graft CD4+ T-cells leading to blunted allogenic responses.[15]

J. Roberts et al. found that miR-184 repressed the expression of Argonaute 2 in epidermal keratinocytes.[16] Similarly, Tattikota et al. showed miR-184 reduced Argonaute 2 levels in the MIN6 mouse pancreatic beta islet cell line.[17]

Furthermore, miR-184 has multiple roles in Drosophila female germline development.[18]

Finally, a recent study identified miR-184 as essential for embryonic corneal commitment of pluripotent stem cells.[19]

Disease relevance edit

• A single base mutation in the seed region of miR-184 causes EDICT syndrome, a hereditary eye disease.[20]
• A mutation altering the miR-184 seed region causes familial keratoconus with cataract.[21]
• Rett syndrome.[7]
• Several forms of cancer (see below) including elevation of miR-184 levels in squamous cell carcinoma of the tongue.[22] All-trans-retinoic acid induces miR-184 expression in neuroblastoma cell line and ectopic miR-184 causes apoptosis.[23]
• miR-184 has been implicated in ischemia-induced retinal neovascularization.[24]

Angiogenesis and cancer edit

Dysregulation of miRNA expression is thought to play a part in abnormal gene expression in cancer cells, and miR-184 has been implicated in several forms of cancer.[22][25] MYCN has been found to contribute to tumorigenesis, in part, by repressing miR-184, leading to increased levels of the serine/threonine kinase, AKT2. AKT2 is a major effector of the phosphatidylinositol 3-kinase (PI3K) pathways, one of the most potent survival pathways in cancer, and is a direct target of miR-184. It has been suggested that MYCN provides a tumourigenic effect, in part, by protecting AKT2 mRNA from degradation by miR-184, permitting the PI3K pathway to remain functional.[26]

miR-184 has been found to be significantly increased in the tumor cells in comparison with the normal epithelial cells of the tongue. High miR-184 levels were not only detected in the tumor tissues, but also in the plasma of patients with tongue squamous cell carcinoma (SCC). Decreased plasma levels of miR-184 were observed in patients after surgical removal of the primary tumor, suggesting that it is a potential oncogenic miRNA in tongue SCC. Inhibiting miR-184 promotes apoptosis as well as hindering cell proliferation in cultured tongue SCC cells.[27] Furthermore, over expression of miR-184 in neuroblastoma cell lines results in apoptosis.[23] SND1 expression is regulated by miR-184 in gliomas.[28]

See also edit

References edit

  1. ^ Cullen BR (December 2004). "Transcription and processing of human microRNA precursors". Mol. Cell. 16 (6): 861–5. doi:10.1016/j.molcel.2004.12.002. PMID 15610730.
  2. ^ a b Li P, Peng J, Hu J, Xu Z, Xie W, Yuan L (March 2010). "Localized expression pattern of miR-184 in Drosophila". Mol Biol Rep. 38 (1): 355–8. doi:10.1007/s11033-010-0115-1. PMID 20339929. S2CID 2939105.
  3. ^ Hutvágner G, Zamore PD (April 2002). "RNAi: nature abhors a double-strand". Curr. Opin. Genet. Dev. 12 (2): 225–32. doi:10.1016/S0959-437X(02)00290-3. PMID 11893497.
  4. ^ Hutvágner G, Zamore PD (September 2002). "A microRNA in a multiple-turnover RNAi enzyme complex". Science. 297 (5589): 2056–60. Bibcode:2002Sci...297.2056H. doi:10.1126/science.1073827. PMID 12154197. S2CID 16969059.
  5. ^ a b Aboobaker AA, Tomancak P, Patel N, Rubin GM, Lai EC (December 2005). "Drosophila microRNAs exhibit diverse spatial expression patterns during embryonic development". Proc. Natl. Acad. Sci. U.S.A. 102 (50): 18017–22. Bibcode:2005PNAS..10218017A. doi:10.1073/pnas.0508823102. PMC 1306796. PMID 16330759.
  6. ^ Weitzel RP, Lesniewski ML, Greco NJ, Laughlin MJ (October 2010). "Reduced methyl-CpG protein binding contributing to miR-184 expression in umbilical cord blood CD4(+) T-cells". Leukemia. 25 (1): 169–72. doi:10.1038/leu.2010.227. PMID 20927133.
  7. ^ a b c d e f Nomura T, Kimura M, Horii T, et al. (April 2008). "MeCP2-dependent repression of an imprinted miR-184 released by depolarization". Hum. Mol. Genet. 17 (8): 1192–9. doi:10.1093/hmg/ddn011. PMID 18203756.
  8. ^ Jørgensen HF, Ben-Porath I, Bird AP (April 2004). "Mbd1 is recruited to both methylated and nonmethylated CpGs via distinct DNA binding domains". Mol. Cell. Biol. 24 (8): 3387–95. doi:10.1128/mcb.24.8.3387-3395.2004. PMC 381685. PMID 15060159.
  9. ^ a b Ryan DG, Oliveira-Fernandes M, Lavker RM (2006). "MicroRNAs of the mammalian eye display distinct and overlapping tissue specificity". Mol. Vis. 12: 1175–84. PMID 17102797.
  10. ^ Wienholds E, Kloosterman WP, Miska E, et al. (July 2005). "MicroRNA expression in zebrafish embryonic development". Science. 309 (5732): 310–1. Bibcode:2005Sci...309..310W. doi:10.1126/science.1114519. PMID 15919954. S2CID 38939571.
  11. ^ a b Liu C, Teng ZQ, Santistevan NJ, et al. (May 2010). "Epigenetic regulation of miR-184 by MBD1 governs neural stem cell proliferation and differentiation". Cell Stem Cell. 6 (5): 433–44. doi:10.1016/j.stem.2010.02.017. PMC 2867837. PMID 20452318.
  12. ^ Li HS, Wang D, Shen Q, et al. (December 2003). "Inactivation of Numb and Numblike in embryonic dorsal forebrain impairs neurogenesis and disrupts cortical morphogenesis". Neuron. 40 (6): 1105–18. doi:10.1016/S0896-6273(03)00755-4. PMID 14687546.
  13. ^ Petersen PH, Zou K, Hwang JK, Jan YN, Zhong W (October 2002). "Progenitor cell maintenance requires numb and numblike during mouse neurogenesis". Nature. 419 (6910): 929–34. Bibcode:2002Natur.419..929P. doi:10.1038/nature01124. PMID 12410312. S2CID 4412567.
  14. ^ Yu J, Ryan DG, Getsios S, Oliveira-Fernandes M, Fatima A, Lavker RM (December 2008). "MicroRNA-184 antagonizes microRNA-205 to maintain SHIP2 levels in epithelia". Proc. Natl. Acad. Sci. U.S.A. 105 (49): 19300–5. Bibcode:2008PNAS..10519300Y. doi:10.1073/pnas.0803992105. PMC 2587229. PMID 19033458.
  15. ^ Weitzel RP, Lesniewski ML, Haviernik P, et al. (June 2009). "microRNA 184 regulates expression of NFAT1 in umbilical cord blood CD4+ T cells". Blood. 113 (26): 6648–57. doi:10.1182/blood-2008-09-181156. PMC 2710921. PMID 19286996.
  16. ^ Roberts JC, Warren RB, Griffiths CE, Ross K (2013). "Expression of microRNA-184 in keratinocytes represses argonaute 2". J. Cell. Physiol. 228 (12): 2314–23. doi:10.1002/jcp.24401. PMID 23696368. S2CID 206052733.
  17. ^ Tattikota SG, Rathjen T, McAnulty SJ, Wessels HH, Akerman I, van de Bunt M, Hausser J, Esguerra JL, Musahl A, Pandey AK, You X, Chen W, Herrera PL, Johnson PR, O'Carroll D, Eliasson L, Zavolan M, Gloyn AL, Ferrer J, Shalom-Feuerstein R, Aberdam D, Poy MN (2014). "Argonaute2 mediates compensatory expansion of the pancreatic β cell". Cell Metab. 19 (1): 122–34. doi:10.1016/j.cmet.2013.11.015. PMC 3945818. PMID 24361012.
  18. ^ Iovino N, Pane A, Gaul U (July 2009). "miR-184 has multiple roles in Drosophila female germline development". Dev. Cell. 17 (1): 123–33. doi:10.1016/j.devcel.2009.06.008. hdl:21.11116/0000-0007-F64E-D. PMID 19619497.
  19. ^ Shalom-Feuerstein R, Serror L, De La Forest Divonne S, Petit I, Aberdam E, Camargo L, Damour O, Vigouroux C, Solomon A, Gaggioli C, Itskovitz-Eldor J, Ahmad S, Aberdam D (May 2012). "Pluripotent stem cell model reveals essential roles for miR-450b-5p and miR-184 in embryonic corneal lineage specification". Stem Cells. 30 (5): 898–909. doi:10.1002/stem.1068. PMID 22367714.
  20. ^ Iliff BW, Riazuddin SA, Gottsch JD (January 2012), "A Single-Base Substitution in the Seed Region of miR-184 Causes EDICT Syndrome", Invest. Ophthalmol. Vis. Sci., 53 (1): 348–53, doi:10.1167/iovs.11-8783, PMC 3292370, PMID 22131394
  21. ^ Hughes AE, Bradley DT, Campbell M, Lechner J, Dash DP, Simpson DA, Willoughby CE (2011). "Mutation Altering the miR-184 Seed Region Causes Familial Keratoconus with Cataract". American Journal of Human Genetics. 89 (5): 628–33. doi:10.1016/j.ajhg.2011.09.014. PMC 3213395. PMID 21996275.
  22. ^ a b Wong TS, Liu XB, Wong BY, Ng RW, Yuen AP, Wei WI (May 2008). "Mature miR-184 as Potential Oncogenic microRNA of Squamous Cell Carcinoma of Tongue". Clin. Cancer Res. 14 (9): 2588–92. doi:10.1158/1078-0432.CCR-07-0666. PMID 18451220.
  23. ^ a b Chen Y, Stallings RL (February 2007). "Differential patterns of microRNA expression in neuroblastoma are correlated with prognosis, differentiation, and apoptosis". Cancer Res. 67 (3): 976–83. doi:10.1158/0008-5472.CAN-06-3667. PMID 17283129.
  24. ^ Shen J, Yang X, Xie B, et al. (July 2008). "MicroRNAs regulate ocular neovascularization". Mol. Ther. 16 (7): 1208–16. doi:10.1038/mt.2008.104. PMC 3033219. PMID 18500251.
  25. ^ Hayashita Y, Osada H, Tatematsu Y, et al. (November 2005). "A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation". Cancer Res. 65 (21): 9628–32. doi:10.1158/0008-5472.CAN-05-2352. PMID 16266980.
  26. ^ Foley NH, Bray IM, Tivnan A, et al. (2010). "MicroRNA-184 inhibits neuroblastoma cell survival through targeting the serine/threonine kinase AKT2". Mol. Cancer. 9: 83. doi:10.1186/1476-4598-9-83. PMC 2864218. PMID 20409325.
  27. ^ Wong TS, Ho WK, Chan JY, Ng RW, Wei WI (2009). "Mature miR-184 and squamous cell carcinoma of the tongue". ScientificWorldJournal. 9: 130–2. doi:10.1100/tsw.2009.12. PMC 5823126. PMID 19219377.
  28. ^ Emdad L, Janjic A, Alzubi MA, Hu B, Santhekadur PK, Menezes ME, Shen XN, Das SK, Sarkar D, Fisher PB (2015). "Suppression of miR-184 in malignant gliomas upregulates SND1 and promotes tumor aggressiveness". Neuro-Oncology. 17 (3): 419–29. doi:10.1093/neuonc/nou220. PMC 4483100. PMID 25216670.

External links edit

  • Page for mir-184 microRNA precursor family at Rfam

February 20, 2024
molecular, biology, microrna, short, coding, molecule, micrornas, mirnas, function, posttranscriptional, regulators, expression, levels, other, genes, several, mechanisms, several, targets, have, been, described, including, that, mediators, neurological, devel. In molecular biology miR 184 microRNA is a short non coding RNA molecule MicroRNAs miRNAs function as posttranscriptional regulators of expression levels of other genes by several mechanisms 1 Several targets for miR 184 have been described including that of mediators of neurological development apoptosis and it has been suggested that miR 184 plays an essential role in development 2 mir 184miR 184 microRNA secondary structure and sequence conservationIdentifiersSymbolmir 184RfamRF00657miRBase familyMIPF0000059NCBI Gene406960HGNC31555OMIM613146Other dataRNA typemicroRNADomain s Eukaryota ChordataPDB structuresPDBeMicroRNAs can bind to the three prime untranslated region 3 UTR of the target messenger RNA mRNA 3 Binding of the miRNA can hinder translation of mRNA by promoting degradation or inducing deadenylation 4 Contents 1 Genomic location 2 Expression 3 Role in neuronal cells 4 Other Targets 5 Disease relevance 5 1 Angiogenesis and cancer 6 See also 7 References 8 External linksGenomic location editmiR 184 is a single copy gene and evolutionarily conserved at the nucleotide level from flies to humans 5 In humans miR 184 is located within region 25 1 on the q arm of chromosome 15 and its corresponding transcript is comparatively small 84bp which is not encoded near other clustered miRNAs 6 In the mouse genome miR 184 is located in an imprinted locus on mouse chromosome 9 and it is 55 kb away from the nearest coding gene 7 The genomic region immediately surrounding miR 184 does not contain a classic CpG island but does contain several CpG rich sequences that are suitable for MBD1 binding 8 Expression editmiR 184 displays a tissue and developmental specific expression pattern In mammals mature miR 184 is particularly enriched in the brain and testis 7 along with the corneal epithelium 9 Depolarization of cortical neurons results in pri miR 184 expression in an allele specific manner 7 High expression is observed in suprabasal cells of the corneal epithelium in the mouse model along with expression in mouse testis and brain tissue 7 9 In Zebrafish it is expressed in lens hatching gland and epidermis shown by Northern blot 10 miR 184 is expressed ubiquitously in Drosophila embryos larvae and adults and its expression pattern displays dynamic changes during the development of embryo especially in the central nervous system 2 5 However the temporal and spatial expression pattern of miR 184 is still being debated Role in neuronal cells editC Liu et al showed that Methyl CpG binding protein 1 MBD1 regulates the expression of several miRNAs in adult neural stem progenitor cells aNSCs and specifically that miR 184 is directly repressed by MBD1 High levels of miR 184 promotes cell proliferation but inhibits differentiation of aNSCs whereas inhibition of miR 184 rescued phenotypes associated with MBD1 deficiency 11 Numblike Numbl is known to be important in embryonic neural stem cell function and cortical brain development and has been identified as a downstream target of miR 184 12 13 It has been found that exogenously expressed Numbl could rescue aNSC proliferation and differentiation deficits resulting from either elevated miR 184 or MBD1 deficiency 11 Other Targets editAn analysis of the primary transcript of miR 184 pri mir 184 in several mouse tissues revealed specific expression in the brain and testis Its expression is repressed by the binding of methyl CpG binding protein 2 MeCP2 to its promoter but is upregulated by the release of MeCP2 after depolarization suggesting a link between miRNAs and DNA methylation pathways 7 J Yu et al demonstrated that the lipid phosphatase SH2 containing phosphoinositide 5 phosphatase 2 SHIP2 is a target of miRNA 205 miR 205 in epithelial cells and that the corneal epithelial specific miR 184 can interfere with the ability of miR 205 to suppress SHIP2 levels The mechanism by which miR 184 negatively regulates miR 205 appears to be unique and is the first example of a miRNA negatively regulating another to maintain levels of a target protein miR 184 does not directly affect SHIP2 translation but instead prevents miR 205 from interacting with SHIP2 mRNA Interfering with miR 205 function by using a synthetic antagomir or by the ectopic expression of miR 184 is thought to lead to a coordinated damping of the Akt signaling pathway via SHIP2 induction 14 R Weitzel et al showed that miR 184 mediates NFAT1 translational regulation in umbilical cord blood UCB graft CD4 T cells leading to blunted allogenic responses 15 J Roberts et al found that miR 184 repressed the expression of Argonaute 2 in epidermal keratinocytes 16 Similarly Tattikota et al showed miR 184 reduced Argonaute 2 levels in the MIN6 mouse pancreatic beta islet cell line 17 Furthermore miR 184 has multiple roles in Drosophila female germline development 18 Finally a recent study identified miR 184 as essential for embryonic corneal commitment of pluripotent stem cells 19 Disease relevance edit A single base mutation in the seed region of miR 184 causes EDICT syndrome a hereditary eye disease 20 A mutation altering the miR 184 seed region causes familial keratoconus with cataract 21 Rett syndrome 7 Several forms of cancer see below including elevation of miR 184 levels in squamous cell carcinoma of the tongue 22 All trans retinoic acid induces miR 184 expression in neuroblastoma cell line and ectopic miR 184 causes apoptosis 23 miR 184 has been implicated in ischemia induced retinal neovascularization 24 Angiogenesis and cancer edit Dysregulation of miRNA expression is thought to play a part in abnormal gene expression in cancer cells and miR 184 has been implicated in several forms of cancer 22 25 MYCN has been found to contribute to tumorigenesis in part by repressing miR 184 leading to increased levels of the serine threonine kinase AKT2 AKT2 is a major effector of the phosphatidylinositol 3 kinase PI3K pathways one of the most potent survival pathways in cancer and is a direct target of miR 184 It has been suggested that MYCN provides a tumourigenic effect in part by protecting AKT2 mRNA from degradation by miR 184 permitting the PI3K pathway to remain functional 26 miR 184 has been found to be significantly increased in the tumor cells in comparison with the normal epithelial cells of the tongue High miR 184 levels were not only detected in the tumor tissues but also in the plasma of patients with tongue squamous cell carcinoma SCC Decreased plasma levels of miR 184 were observed in patients after surgical removal of the primary tumor suggesting that it is a potential oncogenic miRNA in tongue SCC Inhibiting miR 184 promotes apoptosis as well as hindering cell proliferation in cultured tongue SCC cells 27 Furthermore over expression of miR 184 in neuroblastoma cell lines results in apoptosis 23 SND1 expression is regulated by miR 184 in gliomas 28 See also editMicroRNAReferences edit Cullen BR December 2004 Transcription and processing of human microRNA precursors Mol Cell 16 6 861 5 doi 10 1016 j molcel 2004 12 002 PMID 15610730 a b Li P Peng J Hu J Xu Z Xie W Yuan L March 2010 Localized expression pattern of miR 184 in Drosophila Mol Biol Rep 38 1 355 8 doi 10 1007 s11033 010 0115 1 PMID 20339929 S2CID 2939105 Hutvagner G Zamore PD April 2002 RNAi nature abhors a double strand Curr Opin Genet Dev 12 2 225 32 doi 10 1016 S0959 437X 02 00290 3 PMID 11893497 Hutvagner G Zamore PD September 2002 A microRNA in a multiple turnover RNAi enzyme complex Science 297 5589 2056 60 Bibcode 2002Sci 297 2056H doi 10 1126 science 1073827 PMID 12154197 S2CID 16969059 a b Aboobaker AA Tomancak P Patel N Rubin GM Lai EC December 2005 Drosophila microRNAs exhibit diverse spatial expression patterns during embryonic development Proc Natl Acad Sci U S A 102 50 18017 22 Bibcode 2005PNAS 10218017A doi 10 1073 pnas 0508823102 PMC 1306796 PMID 16330759 Weitzel RP Lesniewski ML Greco NJ Laughlin MJ October 2010 Reduced methyl CpG protein binding contributing to miR 184 expression in umbilical cord blood CD4 T cells Leukemia 25 1 169 72 doi 10 1038 leu 2010 227 PMID 20927133 a b c d e f Nomura T Kimura M Horii T et al April 2008 MeCP2 dependent repression of an imprinted miR 184 released by depolarization Hum Mol Genet 17 8 1192 9 doi 10 1093 hmg ddn011 PMID 18203756 Jorgensen HF Ben Porath I Bird AP April 2004 Mbd1 is recruited to both methylated and nonmethylated CpGs via distinct DNA binding domains Mol Cell Biol 24 8 3387 95 doi 10 1128 mcb 24 8 3387 3395 2004 PMC 381685 PMID 15060159 a b Ryan DG Oliveira Fernandes M Lavker RM 2006 MicroRNAs of the mammalian eye display distinct and overlapping tissue specificity Mol Vis 12 1175 84 PMID 17102797 Wienholds E Kloosterman WP Miska E et al July 2005 MicroRNA expression in zebrafish embryonic development Science 309 5732 310 1 Bibcode 2005Sci 309 310W doi 10 1126 science 1114519 PMID 15919954 S2CID 38939571 a b Liu C Teng ZQ Santistevan NJ et al May 2010 Epigenetic regulation of miR 184 by MBD1 governs neural stem cell proliferation and differentiation Cell Stem Cell 6 5 433 44 doi 10 1016 j stem 2010 02 017 PMC 2867837 PMID 20452318 Li HS Wang D Shen Q et al December 2003 Inactivation of Numb and Numblike in embryonic dorsal forebrain impairs neurogenesis and disrupts cortical morphogenesis Neuron 40 6 1105 18 doi 10 1016 S0896 6273 03 00755 4 PMID 14687546 Petersen PH Zou K Hwang JK Jan YN Zhong W October 2002 Progenitor cell maintenance requires numb and numblike during mouse neurogenesis Nature 419 6910 929 34 Bibcode 2002Natur 419 929P doi 10 1038 nature01124 PMID 12410312 S2CID 4412567 Yu J Ryan DG Getsios S Oliveira Fernandes M Fatima A Lavker RM December 2008 MicroRNA 184 antagonizes microRNA 205 to maintain SHIP2 levels in epithelia Proc Natl Acad Sci U S A 105 49 19300 5 Bibcode 2008PNAS 10519300Y doi 10 1073 pnas 0803992105 PMC 2587229 PMID 19033458 Weitzel RP Lesniewski ML Haviernik P et al June 2009 microRNA 184 regulates expression of NFAT1 in umbilical cord blood CD4 T cells Blood 113 26 6648 57 doi 10 1182 blood 2008 09 181156 PMC 2710921 PMID 19286996 Roberts JC Warren RB Griffiths CE Ross K 2013 Expression of microRNA 184 in keratinocytes represses argonaute 2 J Cell Physiol 228 12 2314 23 doi 10 1002 jcp 24401 PMID 23696368 S2CID 206052733 Tattikota SG Rathjen T McAnulty SJ Wessels HH Akerman I van de Bunt M Hausser J Esguerra JL Musahl A Pandey AK You X Chen W Herrera PL Johnson PR O Carroll D Eliasson L Zavolan M Gloyn AL Ferrer J Shalom Feuerstein R Aberdam D Poy MN 2014 Argonaute2 mediates compensatory expansion of the pancreatic b cell Cell Metab 19 1 122 34 doi 10 1016 j cmet 2013 11 015 PMC 3945818 PMID 24361012 Iovino N Pane A Gaul U July 2009 miR 184 has multiple roles in Drosophila female germline development Dev Cell 17 1 123 33 doi 10 1016 j devcel 2009 06 008 hdl 21 11116 0000 0007 F64E D PMID 19619497 Shalom Feuerstein R Serror L De La Forest Divonne S Petit I Aberdam E Camargo L Damour O Vigouroux C Solomon A Gaggioli C Itskovitz Eldor J Ahmad S Aberdam D May 2012 Pluripotent stem cell model reveals essential roles for miR 450b 5p and miR 184 in embryonic corneal lineage specification Stem Cells 30 5 898 909 doi 10 1002 stem 1068 PMID 22367714 Iliff BW Riazuddin SA Gottsch JD January 2012 A Single Base Substitution in the Seed Region of miR 184 Causes EDICT Syndrome Invest Ophthalmol Vis Sci 53 1 348 53 doi 10 1167 iovs 11 8783 PMC 3292370 PMID 22131394 Hughes AE Bradley DT Campbell M Lechner J Dash DP Simpson DA Willoughby CE 2011 Mutation Altering the miR 184 Seed Region Causes Familial Keratoconus with Cataract American Journal of Human Genetics 89 5 628 33 doi 10 1016 j ajhg 2011 09 014 PMC 3213395 PMID 21996275 a b Wong TS Liu XB Wong BY Ng RW Yuen AP Wei WI May 2008 Mature miR 184 as Potential Oncogenic microRNA of Squamous Cell Carcinoma of Tongue Clin Cancer Res 14 9 2588 92 doi 10 1158 1078 0432 CCR 07 0666 PMID 18451220 a b Chen Y Stallings RL February 2007 Differential patterns of microRNA expression in neuroblastoma are correlated with prognosis differentiation and apoptosis Cancer Res 67 3 976 83 doi 10 1158 0008 5472 CAN 06 3667 PMID 17283129 Shen J Yang X Xie B et al July 2008 MicroRNAs regulate ocular neovascularization Mol Ther 16 7 1208 16 doi 10 1038 mt 2008 104 PMC 3033219 PMID 18500251 Hayashita Y Osada H Tatematsu Y et al November 2005 A polycistronic microRNA cluster miR 17 92 is overexpressed in human lung cancers and enhances cell proliferation Cancer Res 65 21 9628 32 doi 10 1158 0008 5472 CAN 05 2352 PMID 16266980 Foley NH Bray IM Tivnan A et al 2010 MicroRNA 184 inhibits neuroblastoma cell survival through targeting the serine threonine kinase AKT2 Mol Cancer 9 83 doi 10 1186 1476 4598 9 83 PMC 2864218 PMID 20409325 Wong TS Ho WK Chan JY Ng RW Wei WI 2009 Mature miR 184 and squamous cell carcinoma of the tongue ScientificWorldJournal 9 130 2 doi 10 1100 tsw 2009 12 PMC 5823126 PMID 19219377 Emdad L Janjic A Alzubi MA Hu B Santhekadur PK Menezes ME Shen XN Das SK Sarkar D Fisher PB 2015 Suppression of miR 184 in malignant gliomas upregulates SND1 and promotes tumor aggressiveness Neuro Oncology 17 3 419 29 doi 10 1093 neuonc nou220 PMC 4483100 PMID 25216670 External links editPage for mir 184 microRNA precursor family at Rfam Retrieved from https en wikipedia org w index php title Mir 184 amp oldid 1184076952, wikipedia, wiki, book, books, library,

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