Difference between revisions of "NONHSAT017465"

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Please input one-sentence summary here.
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''H19'', imprinted maternally expressed transcript
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==Annotated Information==
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===Approved Symbol===
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''H19''
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===Approved Name===
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''H19'' imprinted maternally expressed transcript (non-protein coding)
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ASM, ASM1, D11S813E, LINC00008, "long intergenic non-protein coding RNA 8", NCRNA00008, "non-protein coding RNA 8"
  
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==Annotated Information==
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===Characteristics===
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===Transcriptomic Nomeclature===
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The ''H19'' gene, located at human chromosome 11p15.5, encodes an imprinted lncRNA. ''H19'' is transcribed exclusively from the maternal allele, and the gene also generates an oncofetal RNA that is expressed in the developing embryo and in certain types of tumor <ref name="ref11" />.
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Please input transcriptomic nomeclature information here.
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''H19'' RNA is cytoplasmic but not associated with the translational machinery.<ref name="ref1" />
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Instead, it is located in a particle with a sedimentation coefficient of approximately 28S. <ref name="ref1" />
  
 
===Function===
 
===Function===
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Please input function information here.
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''H19'' knockdown activates SAHH, leading to increased DNMT3B-mediated methylation of an lncRNA-encoding gene Nctc1 within the Igf2-H19-Nctc1 locus.<ref name="ref3" />
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''H19'' acts as an oncogene and promotes ESCC cell proliferation and metastasis, which may infer ''H19'' as a potential therapeutic target for treating ESC patients.<ref name="ref4" />
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''H19'' contributes to cardiac fibroblast proliferation and fibrosis, which act in part through repression of DUSP5/ERK1/2.<ref name="ref5" />
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The overexpression of ''H19'' might potentially serve as a reliable biomarker for poor prognosis in different types of cancers.<ref name="ref6" />
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''H19'' long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.<ref name="ref7" />
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''H19'' competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer, whose mechanism contributes to a better understanding of thyroid cancer pathogenesis. <ref name="ref8" />
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''H19'' interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression.<ref name="ref9" />
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''H19'' potentiated Wnt/β-catenin pathway by serving as a molecular sponge for miR-141 and miR-22, leading to the promotion of osteoblast differentiation. <ref name="ref10" />
  
 
===Regulation===
 
===Regulation===
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Please input regulation information here.
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''H19'' is negatively regulated by miR-675-5p. <ref name="ref10" />
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===Disease===
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*Esophageal squamous cell carcinoma
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*Gallbladder carcinoma<ref name="ref9" />
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*Thyroid cancer<ref name="ref8" />   
  
 
===Expression===
 
===Expression===
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Please input expression information here.
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''H19'' shows expression in PNAC and PDAC cells.<ref name="ref11" />
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===Allelic Information and Variation===
 
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Please input allelic information and variation information here.
 
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===Evolution===
 
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You can also add sub-section(s) at will.
 
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
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Please input related labs here.
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*Howard Hughes Medical Institute, Princeton University New Jersey 08544.<ref name="ref1" />
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*The Babraham Institute, Laboratory of Developmental Genetics and Imprinting, Cambridge CB22 3AT, UK.<ref name="ref2" />
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*Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut 06510, USA. <ref name="ref3" />
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*Department of Cardiothoracic Surgery, Southwest Hospital. <ref name="ref4" />
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*Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei 230601, China.<ref name="ref5" />
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*The Second Clinical Medical College of Nanjing Medical University, Nanjing, China<ref name="ref6" />
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*Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA<ref name="ref7" />
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*Department of Nuclear Medicine, Shanghai Tenth people's hospital, Tongji university, Shanghai, China. <ref name="ref8" />
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*Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200000, China. <ref name="ref9" />
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*School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China. <ref name="ref10" />
 
==References==
 
==References==
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Please input cited references here.
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<references>
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<ref name="ref1">Brannan CI, Dees EC, Ingram RS, Tilghman SM. The product of the H19 gene may function as an RNA[J]. Molecular and cellular biology. 1990,10(1):28-36. </ref>
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{{basic|
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<ref name="ref2">Smits G, Mungall AJ, Griffiths-Jones S, Smith P, Beury D, Matthews L, et al. Conservation of the H19 noncoding RNA and H19-IGF2 imprinting mechanism in therians[J]. Nature genetics. 2008,40(8):971-6. </ref>
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tID = NONHSAT017465|
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<ref name="ref3">Zhou J, Yang L, Zhong T, Mueller M, Men Y, Zhang N, et al. H19 lncRNA alters DNA methylation genome wide by regulating S-adenosylhomocysteine hydrolase[J]. Nature communications. 2015,6:10221.</ref>
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source = NONCODE4.0|
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<ref name="ref4">Tan D, Wu Y, Hu L, He P, Xiong G, Bai Y, et al. Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis[J]. Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus / ISDE. 2016. </ref>
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same = ,|
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<ref name="ref5">Tao H, Cao W, Yang JJ, Shi KH, Zhou X, Liu LP, et al. Long noncoding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis[J]. Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. 2016,25(5):381-9.</ref>
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classification = intergenic|
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<ref name="ref6">Chen T, Yang P, He ZY. Long non-coding RNA H19 can predict a poor prognosis and lymph node metastasis: a meta-analysis in human cancer[J]. Minerva medica. 2016,107(4):251-8. </ref>
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length = 2322 nt|
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<ref name="ref7">Zuckerwise L, Li J, Lu L, Men Y, Geng T, Buhimschi CS, et al. H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TbetaR3 in placentae with fetal growth restriction[J]. Oncotarget. 2016.</ref>
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location = chr11-:2016406..2019105|
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<ref name="ref8">Liu L, Yang J, Zhu X, Li D, Lv Z, Zhang X. Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer[J]. The FEBS journal. 2016,283(12):2326-39. </ref>
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number = 5|
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<ref name="ref9">Wang SH, Wu XC, Zhang MD, Weng MZ, Zhou D, Quan ZW. Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition[J]. American journal of cancer research. 2016,6(1):15-26. </ref>
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exons = 2016406..2017024,2017106..2017228,2017309..2017421,2017517..2017651,2017748..2019105|
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<ref name="ref10">Liang WC, Fu WM, Wang YB, Sun YX, Xu LL, Wong CW, et al. H19 activates Wnt signaling and promotes osteoblast differentiation by functioning as a competing endogenous RNA[J]. Scientific reports. 2016,6:20121. </ref>(10)
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context = <html><div align="center">
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<ref name="ref11">Sasaki N, Toyoda M, Yoshimura H, Matsuda Y, Arai T, Takubo K et al. H19 long non-coding RNA contributes to sphere formation and invasion through regulation of CD24 and integrin expression in pancreatic cancer cells[J]. Oncotarget. 2018, 9(78):34719 </ref>(11)
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<iframe src="http://lncrna.big.ac.cn/view/?data=species/human&loc=chr11:2016406..2019105&tracklist=0&overview=0&tracks=DNA,RefGene,lncRNA" style=" border-width:0 " width="100%" height="250" scrolling="yes"></iframe>
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</references>
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</div></html>|
 
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sequence = <dnaseq>GGGAGGGGGTGGGATGGGTGGGGGGTAACGGGGGAAACTGGGGAAGTGGGGAACCGAGGGGCAACCAGGGGAAGATGGGGTGCTGGAGGAGAGCTTGTGGGAGCCAAGGAGCACCTTGGACATCTGGAGTCTGGCAGGAGTGATGACGGGTGGAGGGGCTAGCTCGAGGCAGGGCTGGTGGGGCCTGAGGCCAGTGAGGAGTGTGGAGTAGGCGCCCAGGCATCGTGCAGACAGGGCGACATCAGCTGGGGACGATGGGCCTGAGCTAGGGCTGGAAAGAAGGGGGAGCCAGGCATTCATCCCGGTCACTTTTGGTTACAGGACGTGGCAGCTGGTTGGACGAGGGGAGCTGGTGGGCAGGGTTTGATCCCAGGGCCTGGGCAACGGAGGTGTAGCTGGCAGCAGCGGGCAGGTGAGGACCCCATCTGCCGGGCAGGTGAGTCCCTTCCCTCCCCAGGCCTCGCTTCCCCAGCCTTCTGAAAGAAGGAGGTTTAGGGGATCGAGGGCTGGCGGGGAGAAGCAGACACCCTCCCAGCAGAGGGGCAGGATGGGGGCAGGAGAGTTAGCAAAGGTGACATCTTCTCGGGGGGAGCCGAGACTGCGCAAGGCTGGGGGGTTATGGGCCCGTTCCAGGCAGAAAGAGCAAGAGGGCAGGGAGGGAGCACAGGGGTGGCCAGCGTAGGGTCCAGCACGTGGGGTGGTACCCCAGGCCTGGGTCAGACAGGGACATGGCAGGGGACACAGGACAGAGGGGTCCCCAGCTGCCACCTCACCCACCGCAATTCATTTAGTAGCAGGCACAGGGGCAGCTCCGGCACGGCTTTCTCAGGCCTATGCCGGAGCCTCGAGGGCTGGAGAGCGGGAAGACAGGCAGTGCTCGGGGAGTTGCAGCAGGACGTCACCAGGAGGGCGAAGCGGCCACGGGAGGGGGGCCCCGGGACATTGCGCAGCAAGGAGGCTGCAGGGGCTCGGCCTGCGGGCGCCGGTCCCACGAGGCACTGCGGCCCAGGGTCTGGTGCGGAGAGGGCCCACAGTGGACTTGGTGACGCTGTATGCCCTCACCGCTCAGCCCCTGGGGCTGGCTTGGCAGACAGTACAGCATCCAGGGGAGTCAAGGGCATGGGGCGAGACCAGACTAGGCGAGGCGGGCGGGGCGGAGTGAATGAGCTCTCAGGAGGGAGGATGGTGCAGGCAGGGGTGAGGAGCGCAGCGGGCGGCGAGCGGGAGGCACTGGCCTCCAGAGCCCGTGGCCAAGGCGGGCCTCGCGGGCGGCGACGGAGCCGGGATCGGTGCCTCAGCGTTCGGGCTGGAGACGAGGCCAGGTCTCCAGCTGGGGTGGACGTGCCCACCAGCTGCCGAAGGCCAAGACGCCAGGTCCGGTGGACGTGACAAGCAGGACATGACATGGTCCGGTGTGACGGCGAGGACAGAGGAGGCGCGTCCGGCCTTCCTGAACACCTTAGGCTGGTGGGGCTGCGGCAAGAAGCGGGTCTGTTTCTTTACTTCCTCCACGGAGTCGGCACACTATGGCTGCCCTCTGGGCTCCCAGAACCCACAACATGAAAGAAATGGTGCTACCCAGCTCAAGCCTGGGCCTTTGAATCCGGACACAAAACCCTCTAGCTTGGAAATGAATATGCTGCACTTTACAACCACTGCACTACCTGACTCAGGAATCGGCTCTGGAAGGTGAAGCTAGAGGAACCAGACCTCATCAGCCCAACATCAAAGACACCATCGGAACAGCAGCGCCCGCAGCACCCACCCCGCACCGGCGACTCCATCTTCATGGCCACCCCCTGCGGCGGACGGTTGACCACCAGCCACCACATCATCCCAGAGCTGAGCTCCTCCAGCGGGATGACGCCGTCCCCACCACCTCCCTCTTCTTCTTTTTCATCCTTCTGTCTCTTTGTTTCTGAGCTTTCCTGTCTTTCCTTTTTTCTGAGAGATTCAAAGCCTCCACGACTCTGTTTCCCCCGTCCCTTCTGAATTTAATTTGCACTAAGTCATTTGCACTGGTTGGAGTTGTGGAGACGGCCTTGAGTCTCAGTACGAGTGTGCGTGAGTGTGAGCCACCTTGGCAAGTGCCTGTGCAGGGCCCGGCCGCCCTCCATCTGGGCCGGGTGACTGGGCGCCGGCTGTGTGCCCGAGGCCTCACCCTGCCCTCGCCTAGTCTGGAAGCTCCGACCGACATCACGGAGCAGCCTTCAAGCATTCCATTACGCCCCATCTCGCTCTGTGCCCCTCCCCACCAGGGCTTCAGCAGGAGCCCTGGACTCATCATCAATAAACACTGTTACAGCAAAAAAAAAAAAAAAA</dnaseq>|
 
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}}
 
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[[Category:Intergenic]]
 
  
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{{lncrnadb|
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===Sequence===
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tID = NONHSAT017465|
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>gi|283120|ref|NR_002196.2|Homo sapiens H19, imprinted maternally expressed transcript (H19), transcript variant 1, long non-coding RNA
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ltID = H19|
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<dnaseq>GGGAGGGGGTGGGATGGGTGGGGGGTAACGGGGGAAACTGGGGAAGTGGGGAACCGAGGGGCAACCAGGGGAAGATGGGGTGCTGGAGGAGAGCTTGTGGGAGCCAAGGAGCACCTTGGACATCTGGAGTCTGGCAGGAGTGATGACGGGTGGAGGGGCTAGCTCGAGGCAGGGCTGGTGGGGCCTGAGGCCAGTGAGGAGTGTGGAGTAGGCGCCCAGGCATCGTGCAGACAGGGCGACATCAGCTGGGGACGATGGGCCTGAGCTAGGGCTGGAAAGAAGGGGGAGCCAGGCATTCATCCCGGTCACTTTTGGTTACAGGACGTGGCAGCTGGTTGGACGAGGGGAGCTGGTGGGCAGGGTTTGATCCCAGGGCCTGGGCAACGGAGGTGTAGCTGGCAGCAGCGGGCAGGTGAGGACCCCATCTGCCGGGCAGGTGAGTCCCTTCCCTCCCCAGGCCTCGCTTCCCCAGCCTTCTGAAAGAAGGAGGTTTAGGGGATCGAGGGCTGGCGGGGAGAAGCAGACACCCTCCCAGCAGAGGGGCAGGATGGGGGCAGGAGAGTTAGCAAAGGTGACATCTTCTCGGGGGGAGCCGAGACTGCGCAAGGCTGGGGGGTTATGGGCCCGTTCCAGGCAGAAAGAGCAAGAGGGCAGGGAGGGAGCACAGGGGTGGCCAGCGTAGGGTCCAGCACGTGGGGTGGTACCCCAGGCCTGGGTCAGACAGGGACATGGCAGGGGACACAGGACAGAGGGGTCCCCAGCTGCCACCTCACCCACCGCAATTCATTTAGTAGCAGGCACAGGGGCAGCTCCGGCACGGCTTTCTCAGGCCTATGCCGGAGCCTCGAGGGCTGGAGAGCGGGAAGACAGGCAGTGCTCGGGGAGTTGCAGCAGGACGTCACCAGGAGGGCGAAGCGGCCACGGGAGGGGGGCCCCGGGACATTGCGCAGCAAGGAGGCTGCAGGGGCTCGGCCTGCGGGCGCCGGTCCCACGAGGCACTGCGGCCCAGGGTCTGGTGCGGAGAGGGCCCACAGTGGACTTGGTGACGCTGTATGCCCTCACCGCTCAGCCCCTGGGGCTGGCTTGGCAGACAGTACAGCATCCAGGGGAGTCAAGGGCATGGGGCGAGACCAGACTAGGCGAGGCGGGCGGGGCGGAGTGAATGAGCTCTCAGGAGGGAGGATGGTGCAGGCAGGGGTGAGGAGCGCAGCGGGCGGCGAGCGGGAGGCACTGGCCTCCAGAGCCCGTGGCCAAGGCGGGCCTCGCGGGCGGCGACGGAGCCGGGATCGGTGCCTCAGCGTTCGGGCTGGAGACGAGGCCAGGTCTCCAGCTGGGGTGGACGTGCCCACCAGCTGCCGAAGGCCAAGACGCCAGGTCCGGTGGACGTGACAAGCAGGACATGACATGGTCCGGTGTGACGGCGAGGACAGAGGAGGCGCGTCCGGCCTTCCTGAACACCTTAGGCTGGTGGGGCTGCGGCAAGAAGCGGGTCTGTTTCTTTACTTCCTCCACGGAGTCGGCACACTATGGCTGCCCTCTGGGCTCCCAGAACCCACAACATGAAAGAAATGGTGCTACCCAGCTCAAGCCTGGGCCTTTGAATCCGGACACAAAACCCTCTAGCTTGGAAATGAATATGCTGCACTTTACAACCACTGCACTACCTGACTCAGGAATCGGCTCTGGAAGGTGAAGCTAGAGGAACCAGACCTCATCAGCCCAACATCAAAGACACCATCGGAACAGCAGCGCCCGCAGCACCCACCCCGCACCGGCGACTCCATCTTCATGGCCACCCCCTGCGGCGGACGGTTGACCACCAGCCACCACATCATCCCAGAGCTGAGCTCCTCCAGCGGGATGACGCCGTCCCCACCACCTCCCTCTTCTTCTTTTTCATCCTTCTGTCTCTTTGTTTCTGAGCTTTCCTGTCTTTCCTTTTTTCTGAGAGATTCAAAGCCTCCACGACTCTGTTTCCCCCGTCCCTTCTGAATTTAATTTGCACTAAGTCATTTGCACTGGTTGGAGTTGTGGAGACGGCCTTGAGTCTCAGTACGAGTGTGCGTGAGTGTGAGCCACCTTGGCAAGTGCCTGTGCAGGGCCCGGCCGCCCTCCATCTGGGCCGGGTGACTGGGCGCCGGCTGTGTGCCCGAGGCCTCACCCTGCCCTCGCCTAGTCTGGAAGCTCCGACCGACATCACGGAGCAGCCTTCAAGCATTCCATTACGCCCCATCTCGCTCTGTGCCCCTCCCCACCAGGGCTTCAGCAGGAGCCCTGGACTCATCATCAATAAACACTGTTACAGCAAAAAAAAAAAAAAAA</dnaseq>|
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ann = <tab class=wikitable sep=tab head=top>
 
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Section Description
 
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ID H19
 
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Characteristics 2.3 kb. Imprinted at the Igf2 locus ([http://www.ncbi.nlm.nih.gov/pubmed/1709450 Bartolomei (1991)], [http://www.ncbi.nlm.nih.gov/pubmed/1303252 Zemel (1992)]).<br /> Also contains a microRNA (miR-675) in exon one [http://www.ncbi.nlm.nih.gov/pubmed/17237358 (Cai (2007))].
 
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Expression Expressed from the maternal allele, while the neighbouring Igf2 gene is transcribed from the paternal allele [http://www.ncbi.nlm.nih.gov/pubmed/1709450 (Bartolomei (1991))].<br /> In mice, H19 is activated in extra-embryonic cell types at the time of implantation. Strongly expressed during embryogenesis, down-regulated after birth with strong expression only retained in skeletal muscle and cartilage ([http://www.ncbi.nlm.nih.gov/pubmed/6206499 Pachnis (1984)], [http://www.ncbi.nlm.nih.gov/pubmed/3396539 Pachnis (1988)], [http://www.ncbi.nlm.nih.gov/pubmed/1811930 Poirier (1991)], [http://www.ncbi.nlm.nih.gov/pubmed/20668672 Castle (2010)], [http://www.ncbi.nlm.nih.gov/pubmed/20529846 Dudek (2010)]); upregulated in various tumors [http://www.ncbi.nlm.nih.gov/pubmed/17786216 (Matouk (2007))].<br /> Can be found in both the nucleus and the cytoplasm ([http://www.ncbi.nlm.nih.gov/pubmed/10875929 Runge (2000)], [http://www.ncbi.nlm.nih.gov/pubmed/17948025 Schoenfelder (2007)], [http://www.ncbi.nlm.nih.gov/pubmed/1688465 Brannan (1990)]).
 
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Function Complex functions: <br />Influences growth via control of Igf2 expression, with a H19 knockout showing an overgrowth phenotype due in part to bi-allelic expression of Igf2 [http://www.ncbi.nlm.nih.gov/pubmed/9203585 (Ripoche (1997))].<br /> Can also function in trans to downregulate the expression of a number of imprinted genes in the hypothesised Imprinted Gene Network (IGN) including Igf2r, Dlk1 etc. Allowing H19 to regulate growth during development [http://www.ncbi.nlm.nih.gov/pubmed/19762426 (Gabory (2009))].<br /> Implicated as both a tumor suppressor ([http://www.ncbi.nlm.nih.gov/pubmed/7692308 Hao (1993)], [http://www.ncbi.nlm.nih.gov/pubmed/18719115 Yoshimizu (2008)]) and an oncogene upregulated by c-myc and hypoxia ([http://www.ncbi.nlm.nih.gov/pubmed/17786216 Matouk (2007)], [http://www.ncbi.nlm.nih.gov/pubmed/16707459 Barsyte-Lovejoy (2006)] and references therein). A number of reports have also shown upregulation / reactivation of H19 in various cancers although the functional significance (if any) is unclear in many cases ([http://www.ncbi.nlm.nih.gov/pubmed/20486133 Gabory (2010)], [http://www.ncbi.nlm.nih.gov/pubmed/9811352 Adriaenssens (1998)]).<br /> The mode of action by which H19 functions is still unclear: . Focusing on its regulation of Igf2, H19 has been hypothesised to act at the level of transcription since an H19 knockout lead to methylation changes and loss of imprinting of Igf2 ([http://www.ncbi.nlm.nih.gov/pubmed/9203585 Ripoche (1997)], [http://www.ncbi.nlm.nih.gov/pubmed/9294195 Forn®¶ (1997)]). However, H19 can bind Igf2 mRNA binding-protein (IMP) family members [http://www.ncbi.nlm.nih.gov/pubmed/10875929 (Runge (2000))], which appear to act to promote translation of Igf2 ([http://www.ncbi.nlm.nih.gov/pubmed/15121863 Hansen (2004)], [http://www.ncbi.nlm.nih.gov/pubmed/15753088 Liao (2005)]), therefore competition between Igf2 and H19 for IMP1 binding may allow H19 to regulate Igf2 post-transcriptionally.<br /> Both sense and antisense transcripts from the H19 locus were identified as binding to the PRC2 chromatin modification complex in mouse embryonic stem cells, suggesting a potential function for H19 RNA [http://www.ncbi.nlm.nih.gov/pubmed/21172659 (Zhao (2010))].<br /> miR-675 may be responsible for the oncogenic activity of H19 as it was found to down-regulate the tumour suppressor retinoblastoma (RB) in human colorectal cancer, causing increased tumour cell growth [http://www.ncbi.nlm.nih.gov/pubmed/19926638 (Tsang (2010))]. Also, in adult human chondrocytes, expression of H19 (and subsequently miR-675) is driven by SOX9 with miR-675 acting to positively regulate COL2A1 which encodes a collagen protein important to the cartilage matrix [http://www.ncbi.nlm.nih.gov/pubmed/20529846 (Dudek (2010))].<br /> H19 appears to be a bi-functional RNA acting as both a miRNA and a lncRNA. Such properties may help to explain the conflicting reports that it is both a tumour suppressor and an oncogene [http://www.ncbi.nlm.nih.gov/pubmed/18587395 (Smits (2008))]. Additionally its effect on tumour development may be heavily context dependent [http://www.ncbi.nlm.nih.gov/pubmed/20486133 (Gabory (2010))].
 
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Conservation Conserved and imprinted in therians (eutherians and marsupials). Both the miRNA and the  H19 lncRNA exon structure are conserved [http://www.ncbi.nlm.nih.gov/pubmed/18587395 (Smits (2008))].
 
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Misc First long noncoding RNA described in mammalian cells [http://www.ncbi.nlm.nih.gov/pubmed/1688465 (Brannan (1990))]. Gabory 2010 provides a useful review of some of the extensive literature on H19 [http://www.ncbi.nlm.nih.gov/pubmed/20486133 (Gabory (2010))].
 
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</tab>|
 
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}}
 

Latest revision as of 07:27, 21 November 2018

H19, imprinted maternally expressed transcript

Annotated Information

Approved Symbol

H19

Approved Name

H19 imprinted maternally expressed transcript (non-protein coding) ASM, ASM1, D11S813E, LINC00008, "long intergenic non-protein coding RNA 8", NCRNA00008, "non-protein coding RNA 8"

Characteristics

The H19 gene, located at human chromosome 11p15.5, encodes an imprinted lncRNA. H19 is transcribed exclusively from the maternal allele, and the gene also generates an oncofetal RNA that is expressed in the developing embryo and in certain types of tumor [1]. H19 RNA is cytoplasmic but not associated with the translational machinery.[2] Instead, it is located in a particle with a sedimentation coefficient of approximately 28S. [2]

Function

H19 knockdown activates SAHH, leading to increased DNMT3B-mediated methylation of an lncRNA-encoding gene Nctc1 within the Igf2-H19-Nctc1 locus.[3] H19 acts as an oncogene and promotes ESCC cell proliferation and metastasis, which may infer H19 as a potential therapeutic target for treating ESC patients.[4] H19 contributes to cardiac fibroblast proliferation and fibrosis, which act in part through repression of DUSP5/ERK1/2.[5] The overexpression of H19 might potentially serve as a reliable biomarker for poor prognosis in different types of cancers.[6] H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.[7] H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer, whose mechanism contributes to a better understanding of thyroid cancer pathogenesis. [8] H19 interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression.[9] H19 potentiated Wnt/β-catenin pathway by serving as a molecular sponge for miR-141 and miR-22, leading to the promotion of osteoblast differentiation. [10]

Regulation

H19 is negatively regulated by miR-675-5p. [10]

Disease

  • Esophageal squamous cell carcinoma
  • Gallbladder carcinoma[9]
  • Thyroid cancer[8]

Expression

H19 shows expression in PNAC and PDAC cells.[1]

Labs working on this lncRNA

  • Howard Hughes Medical Institute, Princeton University New Jersey 08544.[2]
  • The Babraham Institute, Laboratory of Developmental Genetics and Imprinting, Cambridge CB22 3AT, UK.[11]
  • Department of Obstetrics, Gynecology, and Reproductive Sciences, Yale School of Medicine, New Haven, Connecticut 06510, USA. [3]
  • Department of Cardiothoracic Surgery, Southwest Hospital. [4]
  • Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei 230601, China.[5]
  • The Second Clinical Medical College of Nanjing Medical University, Nanjing, China[6]
  • Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA[7]
  • Department of Nuclear Medicine, Shanghai Tenth people's hospital, Tongji university, Shanghai, China. [8]
  • Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200000, China. [9]
  • School of Biomedical Sciences, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong, P.R. China. [10]

References

  1. ↑ 1.0 1.1 Sasaki N, Toyoda M, Yoshimura H, Matsuda Y, Arai T, Takubo K et al. H19 long non-coding RNA contributes to sphere formation and invasion through regulation of CD24 and integrin expression in pancreatic cancer cells[J]. Oncotarget. 2018, 9(78):34719
  2. ↑ 2.0 2.1 2.2 Brannan CI, Dees EC, Ingram RS, Tilghman SM. The product of the H19 gene may function as an RNA[J]. Molecular and cellular biology. 1990,10(1):28-36.
  3. ↑ 3.0 3.1 Zhou J, Yang L, Zhong T, Mueller M, Men Y, Zhang N, et al. H19 lncRNA alters DNA methylation genome wide by regulating S-adenosylhomocysteine hydrolase[J]. Nature communications. 2015,6:10221.
  4. ↑ 4.0 4.1 Tan D, Wu Y, Hu L, He P, Xiong G, Bai Y, et al. Long noncoding RNA H19 is up-regulated in esophageal squamous cell carcinoma and promotes cell proliferation and metastasis[J]. Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus / ISDE. 2016.
  5. ↑ 5.0 5.1 Tao H, Cao W, Yang JJ, Shi KH, Zhou X, Liu LP, et al. Long noncoding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis[J]. Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. 2016,25(5):381-9.
  6. ↑ 6.0 6.1 Chen T, Yang P, He ZY. Long non-coding RNA H19 can predict a poor prognosis and lymph node metastasis: a meta-analysis in human cancer[J]. Minerva medica. 2016,107(4):251-8.
  7. ↑ 7.0 7.1 Zuckerwise L, Li J, Lu L, Men Y, Geng T, Buhimschi CS, et al. H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TbetaR3 in placentae with fetal growth restriction[J]. Oncotarget. 2016.
  8. ↑ 8.0 8.1 8.2 Liu L, Yang J, Zhu X, Li D, Lv Z, Zhang X. Long noncoding RNA H19 competitively binds miR-17-5p to regulate YES1 expression in thyroid cancer[J]. The FEBS journal. 2016,283(12):2326-39.
  9. ↑ 9.0 9.1 9.2 Wang SH, Wu XC, Zhang MD, Weng MZ, Zhou D, Quan ZW. Upregulation of H19 indicates a poor prognosis in gallbladder carcinoma and promotes epithelial-mesenchymal transition[J]. American journal of cancer research. 2016,6(1):15-26.
  10. ↑ 10.0 10.1 10.2 Liang WC, Fu WM, Wang YB, Sun YX, Xu LL, Wong CW, et al. H19 activates Wnt signaling and promotes osteoblast differentiation by functioning as a competing endogenous RNA[J]. Scientific reports. 2016,6:20121.
  11. ↑ Smits G, Mungall AJ, Griffiths-Jones S, Smith P, Beury D, Matthews L, et al. Conservation of the H19 noncoding RNA and H19-IGF2 imprinting mechanism in therians[J]. Nature genetics. 2008,40(8):971-6.

Sequence

>gi|283120|ref|NR_002196.2|Homo sapiens H19, imprinted maternally expressed transcript (H19), transcript variant 1, long non-coding RNA

000001 GGGAGGGGGT GGGATGGGTG GGGGGTAACG GGGGAAACTG GGGAAGTGGG GAACCGAGGG GCAACCAGGG GAAGATGGGG 000080
000081 TGCTGGAGGA GAGCTTGTGG GAGCCAAGGA GCACCTTGGA CATCTGGAGT CTGGCAGGAG TGATGACGGG TGGAGGGGCT 000160
000161 AGCTCGAGGC AGGGCTGGTG GGGCCTGAGG CCAGTGAGGA GTGTGGAGTA GGCGCCCAGG CATCGTGCAG ACAGGGCGAC 000240
000241 ATCAGCTGGG GACGATGGGC CTGAGCTAGG GCTGGAAAGA AGGGGGAGCC AGGCATTCAT CCCGGTCACT TTTGGTTACA 000320
000321 GGACGTGGCA GCTGGTTGGA CGAGGGGAGC TGGTGGGCAG GGTTTGATCC CAGGGCCTGG GCAACGGAGG TGTAGCTGGC 000400
000401 AGCAGCGGGC AGGTGAGGAC CCCATCTGCC GGGCAGGTGA GTCCCTTCCC TCCCCAGGCC TCGCTTCCCC AGCCTTCTGA 000480
000481 AAGAAGGAGG TTTAGGGGAT CGAGGGCTGG CGGGGAGAAG CAGACACCCT CCCAGCAGAG GGGCAGGATG GGGGCAGGAG 000560
000561 AGTTAGCAAA GGTGACATCT TCTCGGGGGG AGCCGAGACT GCGCAAGGCT GGGGGGTTAT GGGCCCGTTC CAGGCAGAAA 000640
000641 GAGCAAGAGG GCAGGGAGGG AGCACAGGGG TGGCCAGCGT AGGGTCCAGC ACGTGGGGTG GTACCCCAGG CCTGGGTCAG 000720
000721 ACAGGGACAT GGCAGGGGAC ACAGGACAGA GGGGTCCCCA GCTGCCACCT CACCCACCGC AATTCATTTA GTAGCAGGCA 000800
000801 CAGGGGCAGC TCCGGCACGG CTTTCTCAGG CCTATGCCGG AGCCTCGAGG GCTGGAGAGC GGGAAGACAG GCAGTGCTCG 000880
000881 GGGAGTTGCA GCAGGACGTC ACCAGGAGGG CGAAGCGGCC ACGGGAGGGG GGCCCCGGGA CATTGCGCAG CAAGGAGGCT 000960
000961 GCAGGGGCTC GGCCTGCGGG CGCCGGTCCC ACGAGGCACT GCGGCCCAGG GTCTGGTGCG GAGAGGGCCC ACAGTGGACT 001040
001041 TGGTGACGCT GTATGCCCTC ACCGCTCAGC CCCTGGGGCT GGCTTGGCAG ACAGTACAGC ATCCAGGGGA GTCAAGGGCA 001120
001121 TGGGGCGAGA CCAGACTAGG CGAGGCGGGC GGGGCGGAGT GAATGAGCTC TCAGGAGGGA GGATGGTGCA GGCAGGGGTG 001200
001201 AGGAGCGCAG CGGGCGGCGA GCGGGAGGCA CTGGCCTCCA GAGCCCGTGG CCAAGGCGGG CCTCGCGGGC GGCGACGGAG 001280
001281 CCGGGATCGG TGCCTCAGCG TTCGGGCTGG AGACGAGGCC AGGTCTCCAG CTGGGGTGGA CGTGCCCACC AGCTGCCGAA 001360
001361 GGCCAAGACG CCAGGTCCGG TGGACGTGAC AAGCAGGACA TGACATGGTC CGGTGTGACG GCGAGGACAG AGGAGGCGCG 001440
001441 TCCGGCCTTC CTGAACACCT TAGGCTGGTG GGGCTGCGGC AAGAAGCGGG TCTGTTTCTT TACTTCCTCC ACGGAGTCGG 001520
001521 CACACTATGG CTGCCCTCTG GGCTCCCAGA ACCCACAACA TGAAAGAAAT GGTGCTACCC AGCTCAAGCC TGGGCCTTTG 001600
001601 AATCCGGACA CAAAACCCTC TAGCTTGGAA ATGAATATGC TGCACTTTAC AACCACTGCA CTACCTGACT CAGGAATCGG 001680
001681 CTCTGGAAGG TGAAGCTAGA GGAACCAGAC CTCATCAGCC CAACATCAAA GACACCATCG GAACAGCAGC GCCCGCAGCA 001760
001761 CCCACCCCGC ACCGGCGACT CCATCTTCAT GGCCACCCCC TGCGGCGGAC GGTTGACCAC CAGCCACCAC ATCATCCCAG 001840
001841 AGCTGAGCTC CTCCAGCGGG ATGACGCCGT CCCCACCACC TCCCTCTTCT TCTTTTTCAT CCTTCTGTCT CTTTGTTTCT 001920
001921 GAGCTTTCCT GTCTTTCCTT TTTTCTGAGA GATTCAAAGC CTCCACGACT CTGTTTCCCC CGTCCCTTCT GAATTTAATT 002000
002001 TGCACTAAGT CATTTGCACT GGTTGGAGTT GTGGAGACGG CCTTGAGTCT CAGTACGAGT GTGCGTGAGT GTGAGCCACC 002080
002081 TTGGCAAGTG CCTGTGCAGG GCCCGGCCGC CCTCCATCTG GGCCGGGTGA CTGGGCGCCG GCTGTGTGCC CGAGGCCTCA 002160
002161 CCCTGCCCTC GCCTAGTCTG GAAGCTCCGA CCGACATCAC GGAGCAGCCT TCAAGCATTC CATTACGCCC CATCTCGCTC 002240
002241 TGTGCCCCTC CCCACCAGGG CTTCAGCAGG AGCCCTGGAC TCATCATCAA TAAACACTGT TACAGCAAAA AAAAAAAAAA 002320
002321 AA
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