Difference between revisions of "NONHSAT017465"

From LncRNAWiki
Jump to: navigation, search
(→‎Disease)
 
(2 intermediate revisions by 2 users not shown)
Line 1: Line 1:
 +
''H19'', imprinted maternally expressed transcript
 
==Annotated Information==
 
==Annotated Information==
−
===Name===
+
===Approved Symbol===
−
H19:  imprinted maternally expressed transcript (non-protein coding)
+
''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"
 
ASM, ASM1, D11S813E, LINC00008, "long intergenic non-protein coding RNA 8", NCRNA00008, "non-protein coding RNA 8"
  
−
=== Cellular Localization===
+
===Characteristics===
−
H19 RNA is cytoplasmic but not associated with the translational machinery.<ref name="ref1" />
+
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" />.
−
 
+
''H19'' RNA is cytoplasmic but not associated with the translational machinery.<ref name="ref1" />
 
Instead, it is located in a particle with a sedimentation coefficient of approximately 28S. <ref name="ref1" />
 
Instead, it is located in a particle with a sedimentation coefficient of approximately 28S. <ref name="ref1" />
−
 
−
===Conservation===
 
−
The H19 gene is conserved in chicken. <ref name="ref1" />
 
−
 
−
Conserved and imprinted in therians (eutherians and marsupials). Both the miRNA and the  H19 lncRNA exon structure are conserved.<ref name="ref2" />
 
  
 
===Function===
 
===Function===
−
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" />
+
''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" />
−
 
+
''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" />
−
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" />
+
''H19'' contributes to cardiac fibroblast proliferation and fibrosis, which act in part through repression of DUSP5/ERK1/2.<ref name="ref5" />
−
 
+
The overexpression of ''H19'' might potentially serve as a reliable biomarker for poor prognosis in different types of cancers.<ref name="ref6" />
−
H19 contributes to cardiac fibroblast proliferation and fibrosis, which act in part through repression of DUSP5/ERK1/2.<ref name="ref5" />
+
''H19'' long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.<ref name="ref7" />
−
 
+
''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" />
−
The overexpression of H19 might potentially serve as a reliable biomarker for poor prognosis in different types of cancers.<ref name="ref6" />
+
''H19'' interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression.<ref name="ref9" />
−
 
+
''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" />
−
H19 long noncoding RNA alters trophoblast cell migration and invasion by regulating TβR3 in placentae with fetal growth restriction.<ref name="ref7" />
 
−
 
 
−
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" />
 
−
 
 
−
H19 interference in GBC suppressed tumor cell invasion and promoted mesenchymal-epithelial transition (MET) via suppressing Twist expression.<ref name="ref9" />
 
−
 
 
−
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" />
 
−
 
 
−
===Expression===
 
−
[[File: Overexpression of H19 gave rise to miR-675-5p and miR-675-3p while miR-675-5p downregulated the expression of H19.jpg|right|thumb|200px|'''Overexpression of H19 gave rise to miR-675-5p and miR-675-3p while miR-675-5p downregulated the expression of H19.''' <ref name="ref10" />.]]
 
−
 
 
−
{| class='wikitable' style="text-align:center"
 
−
|-
 
−
! | Primer
 
−
! | Forward primer
 
−
! | Reverse primer
 
−
|-
 
−
| rowspan="1"|RT-PCR
 
−
| | 5'-CCTCAAGATGAAAGAAATGGTGCTA-3'
 
−
| | 5'-TCCATCTCCCTTGCTGTATC -3' <ref name="ref10" />
 
−
|-
 
−
| rowspan="1"|ChIP PCR primer sequences
 
−
| | 5'-CCAAAAGTAACCGGGATGAA-3'
 
−
| | 5'-CTGGAGTCTGGCAGGAATGT -3' <ref name="ref10" />
 
−
|-
 
−
| rowspan="1"|T7 PCR primer sequences
 
−
| | 5'-TAATACGACTCACTATAGGGCTTCTTTTTCATCCTT-3'
 
−
| | 5'-CAAATGACTTAGTGCAAATTAAATTCAGAAGGGAC-3'<ref name="ref10" />
 
−
|}
 
−
 
 
−
 
 
  
 
===Regulation===
 
===Regulation===
−
H19 is negatively regulated by miR-675-5p. <ref name="ref10" />
+
''H19'' is negatively regulated by miR-675-5p. <ref name="ref10" />
−
 
 
−
===Allelic Information and Variation===
 
−
Please input allelic information and variation information here.
 
−
 
 
−
===Evolution===
 
−
Please input evolution information here.
 
  
 
===Disease===
 
===Disease===
 +
*Esophageal squamous cell carcinoma
 +
*Gallbladder carcinoma<ref name="ref9" />
 +
*Thyroid cancer<ref name="ref8" />   
  
−
gallbladder carcinoma<ref name="ref9" />
+
===Expression===
−
   
+
''H19'' shows expression in PNAC and PDAC cells.<ref name="ref11" />
−
esophageal squamous cell carcinoma<ref name="ref4" /> 
 
−
 
 
−
thyroid cancer<ref name="ref8" />      
 
−
 
 
−
 
 
−
You can also add sub-section(s) at will.
 
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
Line 98: Line 55:
 
<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>
 
<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>
 
<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>
 
<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>
−
<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>
+
<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)
 +
<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)
 
</references>
 
</references>
  
−
{{basic|
+
===Sequence===
−
tID = NONHSAT017465|
+
>gi|283120|ref|NR_002196.2|Homo sapiens H19, imprinted maternally expressed transcript (H19), transcript variant 1, long non-coding RNA
−
source = NONCODE4.0|
+
<dnaseq>GGGAGGGGGTGGGATGGGTGGGGGGTAACGGGGGAAACTGGGGAAGTGGGGAACCGAGGGGCAACCAGGGGAAGATGGGGTGCTGGAGGAGAGCTTGTGGGAGCCAAGGAGCACCTTGGACATCTGGAGTCTGGCAGGAGTGATGACGGGTGGAGGGGCTAGCTCGAGGCAGGGCTGGTGGGGCCTGAGGCCAGTGAGGAGTGTGGAGTAGGCGCCCAGGCATCGTGCAGACAGGGCGACATCAGCTGGGGACGATGGGCCTGAGCTAGGGCTGGAAAGAAGGGGGAGCCAGGCATTCATCCCGGTCACTTTTGGTTACAGGACGTGGCAGCTGGTTGGACGAGGGGAGCTGGTGGGCAGGGTTTGATCCCAGGGCCTGGGCAACGGAGGTGTAGCTGGCAGCAGCGGGCAGGTGAGGACCCCATCTGCCGGGCAGGTGAGTCCCTTCCCTCCCCAGGCCTCGCTTCCCCAGCCTTCTGAAAGAAGGAGGTTTAGGGGATCGAGGGCTGGCGGGGAGAAGCAGACACCCTCCCAGCAGAGGGGCAGGATGGGGGCAGGAGAGTTAGCAAAGGTGACATCTTCTCGGGGGGAGCCGAGACTGCGCAAGGCTGGGGGGTTATGGGCCCGTTCCAGGCAGAAAGAGCAAGAGGGCAGGGAGGGAGCACAGGGGTGGCCAGCGTAGGGTCCAGCACGTGGGGTGGTACCCCAGGCCTGGGTCAGACAGGGACATGGCAGGGGACACAGGACAGAGGGGTCCCCAGCTGCCACCTCACCCACCGCAATTCATTTAGTAGCAGGCACAGGGGCAGCTCCGGCACGGCTTTCTCAGGCCTATGCCGGAGCCTCGAGGGCTGGAGAGCGGGAAGACAGGCAGTGCTCGGGGAGTTGCAGCAGGACGTCACCAGGAGGGCGAAGCGGCCACGGGAGGGGGGCCCCGGGACATTGCGCAGCAAGGAGGCTGCAGGGGCTCGGCCTGCGGGCGCCGGTCCCACGAGGCACTGCGGCCCAGGGTCTGGTGCGGAGAGGGCCCACAGTGGACTTGGTGACGCTGTATGCCCTCACCGCTCAGCCCCTGGGGCTGGCTTGGCAGACAGTACAGCATCCAGGGGAGTCAAGGGCATGGGGCGAGACCAGACTAGGCGAGGCGGGCGGGGCGGAGTGAATGAGCTCTCAGGAGGGAGGATGGTGCAGGCAGGGGTGAGGAGCGCAGCGGGCGGCGAGCGGGAGGCACTGGCCTCCAGAGCCCGTGGCCAAGGCGGGCCTCGCGGGCGGCGACGGAGCCGGGATCGGTGCCTCAGCGTTCGGGCTGGAGACGAGGCCAGGTCTCCAGCTGGGGTGGACGTGCCCACCAGCTGCCGAAGGCCAAGACGCCAGGTCCGGTGGACGTGACAAGCAGGACATGACATGGTCCGGTGTGACGGCGAGGACAGAGGAGGCGCGTCCGGCCTTCCTGAACACCTTAGGCTGGTGGGGCTGCGGCAAGAAGCGGGTCTGTTTCTTTACTTCCTCCACGGAGTCGGCACACTATGGCTGCCCTCTGGGCTCCCAGAACCCACAACATGAAAGAAATGGTGCTACCCAGCTCAAGCCTGGGCCTTTGAATCCGGACACAAAACCCTCTAGCTTGGAAATGAATATGCTGCACTTTACAACCACTGCACTACCTGACTCAGGAATCGGCTCTGGAAGGTGAAGCTAGAGGAACCAGACCTCATCAGCCCAACATCAAAGACACCATCGGAACAGCAGCGCCCGCAGCACCCACCCCGCACCGGCGACTCCATCTTCATGGCCACCCCCTGCGGCGGACGGTTGACCACCAGCCACCACATCATCCCAGAGCTGAGCTCCTCCAGCGGGATGACGCCGTCCCCACCACCTCCCTCTTCTTCTTTTTCATCCTTCTGTCTCTTTGTTTCTGAGCTTTCCTGTCTTTCCTTTTTTCTGAGAGATTCAAAGCCTCCACGACTCTGTTTCCCCCGTCCCTTCTGAATTTAATTTGCACTAAGTCATTTGCACTGGTTGGAGTTGTGGAGACGGCCTTGAGTCTCAGTACGAGTGTGCGTGAGTGTGAGCCACCTTGGCAAGTGCCTGTGCAGGGCCCGGCCGCCCTCCATCTGGGCCGGGTGACTGGGCGCCGGCTGTGTGCCCGAGGCCTCACCCTGCCCTCGCCTAGTCTGGAAGCTCCGACCGACATCACGGAGCAGCCTTCAAGCATTCCATTACGCCCCATCTCGCTCTGTGCCCCTCCCCACCAGGGCTTCAGCAGGAGCCCTGGACTCATCATCAATAAACACTGTTACAGCAAAAAAAAAAAAAAAA</dnaseq>|
−
same = ,|
 
−
classification = intergenic|
 
−
length = 2322 nt|
 
−
location = chr11-:2016406..2019105|
 
−
number = 5|
 
−
exons = 2016406..2017024,2017106..2017228,2017309..2017421,2017517..2017651,2017748..2019105|
 
−
context = <html><div align="center">
 
−
<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>
 
−
</div></html>|
 
−
sequence = <dnaseq>GGGAGGGGGTGGGATGGGTGGGGGGTAACGGGGGAAACTGGGGAAGTGGGGAACCGAGGGGCAACCAGGGGAAGATGGGGTGCTGGAGGAGAGCTTGTGGGAGCCAAGGAGCACCTTGGACATCTGGAGTCTGGCAGGAGTGATGACGGGTGGAGGGGCTAGCTCGAGGCAGGGCTGGTGGGGCCTGAGGCCAGTGAGGAGTGTGGAGTAGGCGCCCAGGCATCGTGCAGACAGGGCGACATCAGCTGGGGACGATGGGCCTGAGCTAGGGCTGGAAAGAAGGGGGAGCCAGGCATTCATCCCGGTCACTTTTGGTTACAGGACGTGGCAGCTGGTTGGACGAGGGGAGCTGGTGGGCAGGGTTTGATCCCAGGGCCTGGGCAACGGAGGTGTAGCTGGCAGCAGCGGGCAGGTGAGGACCCCATCTGCCGGGCAGGTGAGTCCCTTCCCTCCCCAGGCCTCGCTTCCCCAGCCTTCTGAAAGAAGGAGGTTTAGGGGATCGAGGGCTGGCGGGGAGAAGCAGACACCCTCCCAGCAGAGGGGCAGGATGGGGGCAGGAGAGTTAGCAAAGGTGACATCTTCTCGGGGGGAGCCGAGACTGCGCAAGGCTGGGGGGTTATGGGCCCGTTCCAGGCAGAAAGAGCAAGAGGGCAGGGAGGGAGCACAGGGGTGGCCAGCGTAGGGTCCAGCACGTGGGGTGGTACCCCAGGCCTGGGTCAGACAGGGACATGGCAGGGGACACAGGACAGAGGGGTCCCCAGCTGCCACCTCACCCACCGCAATTCATTTAGTAGCAGGCACAGGGGCAGCTCCGGCACGGCTTTCTCAGGCCTATGCCGGAGCCTCGAGGGCTGGAGAGCGGGAAGACAGGCAGTGCTCGGGGAGTTGCAGCAGGACGTCACCAGGAGGGCGAAGCGGCCACGGGAGGGGGGCCCCGGGACATTGCGCAGCAAGGAGGCTGCAGGGGCTCGGCCTGCGGGCGCCGGTCCCACGAGGCACTGCGGCCCAGGGTCTGGTGCGGAGAGGGCCCACAGTGGACTTGGTGACGCTGTATGCCCTCACCGCTCAGCCCCTGGGGCTGGCTTGGCAGACAGTACAGCATCCAGGGGAGTCAAGGGCATGGGGCGAGACCAGACTAGGCGAGGCGGGCGGGGCGGAGTGAATGAGCTCTCAGGAGGGAGGATGGTGCAGGCAGGGGTGAGGAGCGCAGCGGGCGGCGAGCGGGAGGCACTGGCCTCCAGAGCCCGTGGCCAAGGCGGGCCTCGCGGGCGGCGACGGAGCCGGGATCGGTGCCTCAGCGTTCGGGCTGGAGACGAGGCCAGGTCTCCAGCTGGGGTGGACGTGCCCACCAGCTGCCGAAGGCCAAGACGCCAGGTCCGGTGGACGTGACAAGCAGGACATGACATGGTCCGGTGTGACGGCGAGGACAGAGGAGGCGCGTCCGGCCTTCCTGAACACCTTAGGCTGGTGGGGCTGCGGCAAGAAGCGGGTCTGTTTCTTTACTTCCTCCACGGAGTCGGCACACTATGGCTGCCCTCTGGGCTCCCAGAACCCACAACATGAAAGAAATGGTGCTACCCAGCTCAAGCCTGGGCCTTTGAATCCGGACACAAAACCCTCTAGCTTGGAAATGAATATGCTGCACTTTACAACCACTGCACTACCTGACTCAGGAATCGGCTCTGGAAGGTGAAGCTAGAGGAACCAGACCTCATCAGCCCAACATCAAAGACACCATCGGAACAGCAGCGCCCGCAGCACCCACCCCGCACCGGCGACTCCATCTTCATGGCCACCCCCTGCGGCGGACGGTTGACCACCAGCCACCACATCATCCCAGAGCTGAGCTCCTCCAGCGGGATGACGCCGTCCCCACCACCTCCCTCTTCTTCTTTTTCATCCTTCTGTCTCTTTGTTTCTGAGCTTTCCTGTCTTTCCTTTTTTCTGAGAGATTCAAAGCCTCCACGACTCTGTTTCCCCCGTCCCTTCTGAATTTAATTTGCACTAAGTCATTTGCACTGGTTGGAGTTGTGGAGACGGCCTTGAGTCTCAGTACGAGTGTGCGTGAGTGTGAGCCACCTTGGCAAGTGCCTGTGCAGGGCCCGGCCGCCCTCCATCTGGGCCGGGTGACTGGGCGCCGGCTGTGTGCCCGAGGCCTCACCCTGCCCTCGCCTAGTCTGGAAGCTCCGACCGACATCACGGAGCAGCCTTCAAGCATTCCATTACGCCCCATCTCGCTCTGTGCCCCTCCCCACCAGGGCTTCAGCAGGAGCCCTGGACTCATCATCAATAAACACTGTTACAGCAAAAAAAAAAAAAAAA</dnaseq>|
 
−
}}
 
−
[[Category:Intergenic]][[Category:NONHSAG007409]][[Category:Transcripts]][[Category:Transcripts]]
 

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 GGCCCCGG