Difference between revisions of "NONHSAT001953"
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===Name=== | ===Name=== | ||
SNHG3: Small nucleolar RNA host gene 3 | 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=== | ===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. | + | 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. | Contain U17a and U17b snoRNAs in introns. | ||
− | SNHG3 contains a number of exonic Alu elements | + | SNHG3 contains a number of exonic Alu elements. |
Transcriptional start site has characteristics of 5' TOP gene family. | 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=== | ===Function=== | ||
− | Involved in maintaining pluripotency in ESCs [http://www.ncbi.nlm.nih.gov/pubmed/21874018 (Guttman (2011))]. | + | * 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))]. | + | * 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))]. | + | * 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=== | ===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. | Localised to cytoplasm. Unlike SNHG1 it was not stabilised by translation inhibitors or associated with translating ribosomes and was unaffected by translation inhibitors. | ||
Line 28: | Line 46: | ||
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)]). | 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=== | ===Conservation=== | ||
Not highly conserved, ~40-50% identity between mouse and human exons. | Not highly conserved, ~40-50% identity between mouse and human exons. |
Latest revision as of 07:06, 1 August 2019
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Contents
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
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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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 ATTAGGTCCT GACCAATAGG 001280 001281 ACCGTAAGTC TGGGTTGAGT GCAAGATGAG TTAGACCGAT TCTTTAGCTT CCTGCAGTGT AGTGGAGGAA AAATCGATGG 001360 001361 TAGCAACGGG AGGTTGTATC CCTAGCTGAT GAGTTGTATG AGCCTCTACT ACCTGGCGCA CCTCCGCCTG AAGATTGCCA 001440 001441 GAATTGCTTG CCTCATGACG TGAGTCACAA TGGAAACTTT GTCAAGCCCC CTGCACTGGC TGCCAACATA AATGTTCAGT 001520 001521 ACCCTGAAGG ATGGGACTGA AGGGGGATCA TCTAGAAGGT AAAGTTACCT ACTGGCATAG GGGAGGTGGG ACAGCCGTTA 001600 001601 AGCCATTTGG AACTTGATGG AGACAGGTTT GAGGGAGGTG GGTGAGATTG GAGTTTGGTG GACTGTAGAG CTTGCTTGCC 001680 001681 AAGGTGTTGA GGTCAGGGTT GGTTTGAGAA TGGAAGCTAG TTACTAGCTA TGATTGTGGG GGAACACAGC TTGATTTTTC 001760 001761 TTACAAGCTA AGAGGAGTGA GGCAGTGTTT AAGAGGGCAT GTTAAATGCA GCCAGGCTTG GTGGCTCACA CCCGTAATCC 001840 001841 CAGCACTTAG GCTAAGGCAG GCGGATCACA ACATCTAGAG ATCCTGGCCA ACGCGGTGAA ACCCTGTCTG TACTAAAAAT 001920 001921 ACAAAATAAC TGGGCATGGT GGTGTGCACC TGTGGGAGGC TGAGGCAGAA TTGCTGGAAC CCGGGAGATG GAGGTTGTAC 002000 002001 TGAGCTGAGA CCTTGCCACT GCGCTCCAGC CTGGTGACAG AGTTAAGTCT CAAAAAAAAG GCATCTTCCT AAAGCAATTG 002080 002081 TATTTGTGCT TACCTGTGCC AGGCACTGTT CTAGGTAAGC ACTAAGTGGG CTTTAATACA GCATATTCCA ATGGGGAATC 002160 002161 CCAGGAACCA AAAGACTAAT TGTCCAAGTC CACAACTAGA AGTGGCACCT CTGCAGAAAC AAGCATCAAA TTCCCTGCTC 002240 002241 AGGAAGAAGC CAGATGAGTC AGCCCCATTC GTCTGTATGC CCAGTCCCAT CCGTGTCCTG CTGTAACTAC ATAGATCTCA 002320 002321 CCTGAGTAAA GTGATTTTTT TCTGAA |
Predicted Small Protein
Name | NONHSAT001953_smProtein_2150:2305 |
Length | 52 |
Molecular weight | 5630.549 |
Aromaticity | 0.0196078431373 |
Instability index | 77.8235294118 |
Isoelectric point | 9.69427490234 |
Runs | 9 |
Runs residual | 0.0222286934576 |
Runs probability | 0.0374688413904 |
Amino acid sequence | MGNPRNQKTNCPSPQLEVAPLQKQASNSLLRKKPDESAPFVCMPSPIRVLL |
Secondary structure | LLLLLLLLLLLLLLLLLLLLHHHHHLHHHHLLLLLLLLLEEELLLLEEEEL |
PRMN | - |
PiMo | - |