Difference between revisions of "NONHSAT001953"

Latest revision as of 07:06, 1 August 2019

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Annotated Information

Name

SNHG3: Small nucleolar RNA host gene 3

Previous symbols: RNU17C

Alias symbols: U17HG; U17HG-A; NCRNA00014

HGNC ID : HGNC:10118

RefSeq ID: NR_002909.1

Disease

Alzheimer's disease

Glioma(Fei (2018))

Characteristics

Upstream from the RCC1 protein-coding gene. Multiple SNHG3 splice isoforms exist, minority join RCC1, majority do not. Isoforms range from ~0.9kb to ~2.6kb in human.

Contain U17a and U17b snoRNAs in introns.

SNHG3 contains a number of exonic Alu elements.

Transcriptional start site has characteristics of 5' TOP gene family.

Cell fractionation experiments indicated that U17HG RNA is enriched in the cytoplasm(Pelczar (1998)).

Function

Involved in maintaining pluripotency in ESCs (Guttman (2011)).

Knockdown in mECSs lead to down-regulation of Nanog, Sox2, Klf4 and Oct4 expression as well as changes to ESC morphology (Guttman (2011)).

Snhg3 was found to interact with a number of chromatin binding proteins/complexes in mESCs including PRC1, PRC2, JARID1B and SUV39H1, with the general pattern being interaction with repressors of gene expression (Guttman (2011)).

The up-regulation of SNHG3 promoted cell proliferation, accelerate cell cycle progress, and repressed cell apoptosis. Mechanically, SNHG3 facilitated the malignant progression of glioma through epigenetically repressing KLF2 and p21 via recruiting enhancer of zeste homolog 2 to the promoter of KLF2 and p21(Fei (2018)).

Expression

The expression pattern of SNHG3 in glioma tissues and normal tissues(Fei (2018)).

Localised to cytoplasm. Unlike SNHG1 it was not stabilised by translation inhibitors or associated with translating ribosomes and was unaffected by translation inhibitors.

Identified as expressed in mouse embryonic stem cells (Guttman (2011)).

Transcript found to be unstable with a half-life <2 hr in mouse N2A (neuroblastoma) cells and human B cells (Friedel (2009), Clark (2012)).

SNHG3 was more highly expressed in glioma tissues, especially in tissues with advanced tumor grade, and cell lines(Fei (2018)).

Experiment	Forward primer	Reverse primer
Quantitative real-time PCR	5'-TTCAAGCGATTCTCGTGCC- 3'	5'-AAGATTGTCAAACCCTCCCTGT- 3'(Fei (2018))

Conservation

Not highly conserved, ~40-50% identity between mouse and human exons.

Misc

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Transcriptomic Nomeclature

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Regulation

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Allelic Information and Variation

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Evolution

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You can also add sub-section(s) at will.

Labs working on this lncRNA

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References

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Basic Information

Transcript ID	NONHSAT001953
Source	NONCODE4.0
Same with	,
Classification	intergenic
Length	2346 nt
Genomic location	chr1+:28832455..28837404
Exon number	4
Exons	28832455..28832596,28832732..28832839,28834640..28834672,28835342..28837404
Genome context
Sequence	000001 GATTCTCTAA CTGCGCATGC TTCTGCGCAC GCGCAATAGA CATTCCAGGA CTTCCGGGCA CTTCGTAAGG TTTAAAAAGG 000080 000081 ATGCTTCGCG TTTTCTCTCT CCTTTTTGGA GACAGATTCG CAGTGGTCGC TTCTTCTCCT TGACGGAGTC GGTTTGTCAC 000160 000161 TCAGGCTGGA CTGCAGTGCT CGTTGCAACC TCCGCCTGCC GGGTTCAAGC GATTCTCGTG CCTCAGCCTC TCCAGCAGCT 000240 000241 GGGATTACAG GATTTGTTAA GGATTCCAAG TAACTCTTAT TTGGAGAGAA GACGATCTGC ACTTCGCATT TTGGCATTGA 000320 000321 CATTTAATTT TAGGGTCCTT TATATAGAAG GGAGAGTAGG TAAACTGATT TTTTTTTTTA ACAGGGAGGG TTTGACAATC 000400 000401 TTTGGCAGAC TTGGAGCAAA AGATTGAGGT GCATTTCATG CCTCCTTTTG AGAGTCTTGC TCTGTCGCCC AGGCTGTAGT 000480 000481 GCAGTGGCGC AATCTTGGCT GCAACCTCAG CCTCCCAAGT AGCTGGGATT ACAAACATAA GCCACCACGC CCAGCCCTCA 000560 000561 TACCTCTTTT AAAAGTCGAC CTGTTTTGCA GAAAGTCTGC TGTTTTTGTA CTAAAGGCTT TGGAATTTGG CATTTAGCTA 000640 000641 GGAATGCACA TTCTTTCACC TCATTCATAC TTTAAGAACC ACAGAAGTGA CTCTGCTTGG CCAGAAGGCA CACTGTGTTG 000720 000721 GTGGTTATAT TAAAAGTCCT TGAGTATTTT GCTTTTCATG ATCTTGCTCA CTGCAACTTC CGCCTCCCAG GTTCAGGCGA 000800 000801 TTCTCCTGCC TCAGCCTCCC AAGTAGCTGC GACTACAGGC GTGTAGCACC ACACCTGGCT AATTTTTGTA TTTTTAGTAG 000880 000881 AGATGAGGTT TCACCATATT GGCCAGGCTG TTCTCAACTC CTGACCTCGT GATCCGCCCA CCTCAGCCTC CTAAAGTGCT 000960 000961 GGGATTACAG CTGTGAGCCA CCCTGCCCGG CCACTTTTGT ATGATTTCTA ATGTATTTGT AATTTACCTA ACAAATTGCC 001040 001041 TAATCTGCTA TGTTAATGTA TTTATGAATT AAAATAAATA CGACTGCATG TTTGTGGTTC ATTTTTGTGG AGGTGGCTGT 001120 001121 GGTGACATCA GCCAAGAATC TGAATGGTAC TGTTGAAGGA AACTAGCATG ATAGCTTCAG TTCTAAAGGC CCTGAAACCT 001200 001201 AGTCTCAGGT GGGTCCCCCT TGGGTTCACT TTATATTGGC AGTTTATTGG GAAAATGGAT ATTAGGT

@@ Line 2: / Line 2: @@
 ==Annotated Information==
+===Name===
+SNHG3: Small nucleolar RNA host gene 3
+Previous symbols: RNU17C
+Alias symbols: U17HG; U17HG-A; NCRNA00014
+HGNC ID : HGNC:10118
+RefSeq ID: NR_002909.1
+===Disease===
+Alzheimer's disease
+Glioma[http://www.ncbi.nlm.nih.gov/pubmed/30042166 (Fei (2018))]
+===Characteristics===
+Upstream from the RCC1 protein-coding gene. Multiple SNHG3 splice isoforms exist, minority join RCC1, majority do not. Isoforms range from ~0.9kb to ~2.6kb in human.
+Contain U17a and U17b snoRNAs in introns.
+SNHG3 contains a number of exonic Alu elements.
+Transcriptional start site has characteristics of 5' TOP gene family.
+Cell fractionation experiments indicated that U17HG RNA is enriched in the cytoplasm[http://www.ncbi.nlm.nih.gov/pubmed/9671460 (Pelczar (1998))].
+===Function===
+* Involved in maintaining pluripotency in ESCs [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))].
+* Knockdown in mECSs lead to down-regulation of Nanog, Sox2, Klf4 and Oct4 expression as well as changes to ESC morphology [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))].
+* Snhg3 was found to interact with a number of chromatin binding proteins/complexes in mESCs including PRC1, PRC2, JARID1B and SUV39H1, with the general pattern being interaction with repressors of gene expression [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))].
+* The up-regulation of SNHG3 promoted cell proliferation, accelerate cell cycle progress, and repressed cell apoptosis. Mechanically, SNHG3 facilitated the malignant progression of glioma through epigenetically repressing KLF2 and p21 via recruiting enhancer of zeste homolog 2 to the promoter of KLF2 and p21[http://www.ncbi.nlm.nih.gov/pubmed/30042166 (Fei (2018))].
+===Expression===
+[[File:SNHG3exp.png|right|thumb|400px|The expression pattern of SNHG3 in glioma tissues and normal tissues[http://www.ncbi.nlm.nih.gov/pubmed/30042166 (Fei (2018))].]]
+Localised to cytoplasm. Unlike SNHG1 it was not stabilised by translation inhibitors or associated with translating ribosomes and was unaffected by translation inhibitors.
+Identified as expressed in mouse embryonic stem cells [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))].
+Transcript found to be unstable with a half-life <2 hr in mouse N2A (neuroblastoma) cells and human B cells ([http://www.ncbi.nlm.nih.gov/pubmed/19561200 Friedel (2009)], [http://www.ncbi.nlm.nih.gov/pubmed/22406755 Clark (2012)]).
+SNHG3 was more highly expressed in glioma tissues, especially in tissues with advanced tumor grade, and cell lines[http://www.ncbi.nlm.nih.gov/pubmed/30042166 (Fei (2018))].
+{| class='wikitable' style="text-align:center"
+|-
+! | Experiment
+! | Forward primer
+! | Reverse primer
+|-
+| rowspan="1"|Quantitative real-time PCR
+| | 5'-TTCAAGCGATTCTCGTGCC- 3'
+| | 5'-AAGATTGTCAAACCCTCCCTGT- 3'[http://www.ncbi.nlm.nih.gov/pubmed/30042166 (Fei (2018))]
+|}
+===Conservation===
+Not highly conserved, ~40-50% identity between mouse and human exons.
+===Misc===
+Please input misc information here.
 ===Transcriptomic Nomeclature===
 Please input transcriptomic nomeclature information here.
-===Function===
-Please input function information here.
 ===Regulation===
 Please input regulation information here.
-===Expression===
-Please input expression information here.
 ===Allelic Information and Variation===
@@ Line 42: / Line 97: @@
 sequence = <dnaseq>GATTCTCTAACTGCGCATGCTTCTGCGCACGCGCAATAGACATTCCAGGACTTCCGGGCACTTCGTAAGGTTTAAAAAGGATGCTTCGCGTTTTCTCTCTCCTTTTTGGAGACAGATTCGCAGTGGTCGCTTCTTCTCCTTGACGGAGTCGGTTTGTCACTCAGGCTGGACTGCAGTGCTCGTTGCAACCTCCGCCTGCCGGGTTCAAGCGATTCTCGTGCCTCAGCCTCTCCAGCAGCTGGGATTACAGGATTTGTTAAGGATTCCAAGTAACTCTTATTTGGAGAGAAGACGATCTGCACTTCGCATTTTGGCATTGACATTTAATTTTAGGGTCCTTTATATAGAAGGGAGAGTAGGTAAACTGATTTTTTTTTTTAACAGGGAGGGTTTGACAATCTTTGGCAGACTTGGAGCAAAAGATTGAGGTGCATTTCATGCCTCCTTTTGAGAGTCTTGCTCTGTCGCCCAGGCTGTAGTGCAGTGGCGCAATCTTGGCTGCAACCTCAGCCTCCCAAGTAGCTGGGATTACAAACATAAGCCACCACGCCCAGCCCTCATACCTCTTTTAAAAGTCGACCTGTTTTGCAGAAAGTCTGCTGTTTTTGTACTAAAGGCTTTGGAATTTGGCATTTAGCTAGGAATGCACATTCTTTCACCTCATTCATACTTTAAGAACCACAGAAGTGACTCTGCTTGGCCAGAAGGCACACTGTGTTGGTGGTTATATTAAAAGTCCTTGAGTATTTTGCTTTTCATGATCTTGCTCACTGCAACTTCCGCCTCCCAGGTTCAGGCGATTCTCCTGCCTCAGCCTCCCAAGTAGCTGCGACTACAGGCGTGTAGCACCACACCTGGCTAATTTTTGTATTTTTAGTAGAGATGAGGTTTCACCATATTGGCCAGGCTGTTCTCAACTCCTGACCTCGTGATCCGCCCACCTCAGCCTCCTAAAGTGCTGGGATTACAGCTGTGAGCCACCCTGCCCGGCCACTTTTGTATGATTTCTAATGTATTTGTAATTTACCTAACAAATTGCCTAATCTGCTATGTTAATGTATTTATGAATTAAAATAAATACGACTGCATGTTTGTGGTTCATTTTTGTGGAGGTGGCTGTGGTGACATCAGCCAAGAATCTGAATGGTACTGTTGAAGGAAACTAGCATGATAGCTTCAGTTCTAAAGGCCCTGAAACCTAGTCTCAGGTGGGTCCCCCTTGGGTTCACTTTATATTGGCAGTTTATTGGGAAAATGGATATTAGGTCCTGACCAATAGGACCGTAAGTCTGGGTTGAGTGCAAGATGAGTTAGACCGATTCTTTAGCTTCCTGCAGTGTAGTGGAGGAAAAATCGATGGTAGCAACGGGAGGTTGTATCCCTAGCTGATGAGTTGTATGAGCCTCTACTACCTGGCGCACCTCCGCCTGAAGATTGCCAGAATTGCTTGCCTCATGACGTGAGTCACAATGGAAACTTTGTCAAGCCCCCTGCACTGGCTGCCAACATAAATGTTCAGTACCCTGAAGGATGGGACTGAAGGGGGATCATCTAGAAGGTAAAGTTACCTACTGGCATAGGGGAGGTGGGACAGCCGTTAAGCCATTTGGAACTTGATGGAGACAGGTTTGAGGGAGGTGGGTGAGATTGGAGTTTGGTGGACTGTAGAGCTTGCTTGCCAAGGTGTTGAGGTCAGGGTTGGTTTGAGAATGGAAGCTAGTTACTAGCTATGATTGTGGGGGAACACAGCTTGATTTTTCTTACAAGCTAAGAGGAGTGAGGCAGTGTTTAAGAGGGCATGTTAAATGCAGCCAGGCTTGGTGGCTCACACCCGTAATCCCAGCACTTAGGCTAAGGCAGGCGGATCACAACATCTAGAGATCCTGGCCAACGCGGTGAAACCCTGTCTGTACTAAAAATACAAAATAACTGGGCATGGTGGTGTGCACCTGTGGGAGGCTGAGGCAGAATTGCTGGAACCCGGGAGATGGAGGTTGTACTGAGCTGAGACCTTGCCACTGCGCTCCAGCCTGGTGACAGAGTTAAGTCTCAAAAAAAAGGCATCTTCCTAAAGCAATTGTATTTGTGCTTACCTGTGCCAGGCACTGTTCTAGGTAAGCACTAAGTGGGCTTTAATACAGCATATTCCAATGGGGAATCCCAGGAACCAAAAGACTAATTGTCCAAGTCCACAACTAGAAGTGGCACCTCTGCAGAAACAAGCATCAAATTCCCTGCTCAGGAAGAAGCCAGATGAGTCAGCCCCATTCGTCTGTATGCCCAGTCCCATCCGTGTCCTGCTGTAACTACATAGATCTCACCTGAGTAAAGTGATTTTTTTCTGAA</dnaseq>|
 }}
-[[Category:Intergenic]]
+[[Category:Intergenic]][[Category:NONHSAG000835]][[Category:Transcripts]]
-{{lncrnadb|
-tID = NONHSAT001953|
-ltID = SNHG3|
-ann = <tab class=wikitable sep=tab head=top>
-Section	Description
-ID	SNHG3
-Characteristics	Upstream from the RCC1 protein coding gene. Multiple SNHG3 splice isoforms exist, minority join RCC1, majority do not. Isoforms range from ~0.9kb to ~2.6kb in human. Contain U17a and U17b snoRNAs in introns. SNHG3 contains a number of exonic Alu elements. Transcriptional start site has characteristics of 5' TOP gene family.
-Expression	Localised to cytoplasm. Unlike SNHG1 it was not stabilised by translation inhibitors or associated with translating ribosomes and was unaffected by translation inhibitors. Identified as expressed in mouse embryonic stem cells [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))]. Transcript found to be unstable with a half-life <2 hr in mouse N2A (neuroblastoma) cells and human B cells ([http://www.ncbi.nlm.nih.gov/pubmed/19561200 Friedel (2009)], [http://www.ncbi.nlm.nih.gov/pubmed/22406755 Clark (2012)]).
-Function	Involved in maintaining pluripotency in ESCs [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))]. Knockdown in mECSs lead to down-regulation of Nanog, Sox2, Klf4 and Oct4 expression as well as changes to ESC morphology [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))]. Snhg3 was found to interact with a number of chromatin binding proteins/complexes in mESCs including PRC1, PRC2, JARID1B and SUV39H1, with the general pattern being interaction with repressors of gene expression [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))].
-Conservation	Not highly conserved, ~40-50% identity between mouse and human exons.
-Name	SNHG3: Small nucleolar RNA host gene 3
-</tab>|
-}}