Difference between revisions of "LINC00336"

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(Created page with "==Annotated Information== ===Name=== Approved symbol: LINC00336 Approved name: long intergenic non-protein coding RNA 336 HGNC ID: HGNC:33813 Previous names: chromosome 6...")
 
 
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===Characteristics ===
 
===Characteristics ===
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[[File:Functional domains of 7SK RNA..png|right|thumb|Functional domains of 7SK RNA([https://www.ncbi.nlm.nih.gov/pubmed/19246988 (Diribarne 2009)])]]
 
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~330 nt in vertebrates*. Transcribed by RNAP III, GC-rich sequence forming conserved secondary structures (especially 3' and 5' stem-loop motifs).
 
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The 7SK gene is located on chromosome 6, and chromosome 6 is the sole human chromosome that produces 7SK RNA ([https://www.ncbi.nlm.nih.gov/pubmed/8139910 (Driscoll 1994)])
 
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7SK RNA is capped at its 5' end by BCDIN3, a specific methylase methylphosphate capping enzyme (MePCE) ([http://www.ncbi.nlm.nih.gov/pubmed/17643375 (Jeronimo 2007)]).
 
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RNAP II was recently found to bind near 7SK promoter, as well as many other known Pol III genes, suggesting that RNAP II may also play a role in regulating their transcription ([http://www.ncbi.nlm.nih.gov/pubmed/20139302 (Raha 2010)]).
 
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In invertebrates, 7SK homologs may have different sizes (such as >400 nt and ~130 nt in drosophilids and nematodes, respectively). ([http://www.ncbi.nlm.nih.gov/pubmed/20139302 (Gruber 2008)]) ([http://www.ncbi.nlm.nih.gov/pubmed/18566019 (Marz 2009)])
 
  
 
===Expression===
 
===Expression===
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Nuclear, highly abundant (one of the most abundant small RNAs in vertebrate cells), first isolated from HeLa nuclear extracts, but ubiquitously expressed.
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Upregulated in lung cancer ([https://www.ncbi.nlm.nih.gov/pubmed/30787392 (Wang M 2019)]).
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RNA sequencing from 11 humans tissues confirmed ubiquitous high expression of 7SK with expression in some tissues being higher than any mRNA ([http://www.ncbi.nlm.nih.gov/pubmed/20668672 (Castle 2010)]).
 
  
 
===Regulation===
 
===Regulation===
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In the 7SK ribonucleoprotein, Larp7 binds directly to 3′ terminus of 7SK RNA ([https://www.ncbi.nlm.nih.gov/pubmed/18281698 (Krueger 2008)]) ([https://www.ncbi.nlm.nih.gov/pubmed/18483487 (Markert 2008)]), and prevents degradation of 7SK in vivo ([https://www.ncbi.nlm.nih.gov/pubmed/18281698 (Krueger 2008)]).
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ELAVL1 increased LINC00336 expression by stabilizing its posttranscriptional level([https://www.ncbi.nlm.nih.gov/pubmed/30787392 (Wang M 2019)]).
  
 
===Function===
 
===Function===
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[[File:Model of hLarp7 recognition of the 7SK.png|right|thumb|Model of hLarp7 recognition of the 7SK 3′end and mechanism of assembly of core 7SK RNP([https://www.ncbi.nlm.nih.gov/pubmed/29946027 (Eichhorn 2018)])]]
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Functions as an oncogene by acting as a competing endogenous RNA (ceRNAs) to inhibit ferroptosis in lung cancer([https://www.ncbi.nlm.nih.gov/pubmed/30787392 (Wang M 2019)]).
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7SK snRNA functions in transcriptional regulation by interacting with PTEF-B complex ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), BAF chromatin-remodeling complex ([https://www.ncbi.nlm.nih.gov/pubmed/26878240 (Flynn 2016)]), or hnRNP R ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]). Consistently, it has been found highly enriched in isolated chromatin fractions, which may be related to its role in transcriptional regulation ([http://www.ncbi.nlm.nih.gov/pubmed/20404130 (Mondal 2010)]). In addition to its critical role for controlling transcription, 7SK snRNA is also involved in alternative splicing ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]) and the localization of protein in nucleolus ([http://www.ncbi.nlm.nih.gov/pubmed/17381310 (He 2007)]). Therefore, 7SK snRNA has a variety of functions in the nuclear, playing important roles in cell growth and differentiation ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), axon maintenance ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]) and vertebrate development ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).
 
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7SK snRNA controls RNAP II activity by inhibiting P-TEFb elongation factor, which is a cdk-cyclin kinase that functions as both a general and an HIV-1 Tat-specific transcription factor ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]) ([http://www.ncbi.nlm.nih.gov/pubmed/11713532 (Yang 2001)]), with an impact on cell growth and differentiation. Specifically, 7SK snRNA functions as the central scaffold that coordinates protein-protein interactions and, by inhibiting P-TEFb kinase-mediated CTD phosphorylation, regulates RNAP II elongation ([http://www.ncbi.nlm.nih.gov/pubmed/11713533 (Nguyen 2001)]).
 
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At an early stage of the HIV transcription cycle, elongation is prevented as P-TEFb is recruited to the HIV-1 promoter in a catalytically inactive state bound to the 7SK snRNP and also the Tat trans-activator of transcription protein. The inhibitory 7SK snRNP may be displaced by the nascent TAR HIV RNA that also binds Tat protein, activating P-TEFb kinase and transcriptional elongation ([http://www.ncbi.nlm.nih.gov/pubmed/20562857 (D'Orso 2010)]). Displacement of 7SK may also be performed by cellular RNAs, as indicated by the 3'-untranslated region (~300-nt) of HIC mRNA, which forms complexes with P-TEFb and is necessary and sufficient for stimulation of P-TEFb-dependent transcription of the HIV promoter ([http://www.ncbi.nlm.nih.gov/pubmed/17925858 (Young 2007)]).
 
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7SK snRNA inhibits enhancer transcription by modulating nucleosome position. 7SK physically interacts with the BAF chromatin-remodeling complex, recruits BAF to enhancers and inhibits enhancer transcription by modulating chromatin structure ([https://www.ncbi.nlm.nih.gov/pubmed/26878240 (Flynn 2016)]).
 
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In axons, 7SK snRNA interacts with hnRNP R to regulate its function in axon maintenance ([https://www.ncbi.nlm.nih.gov/pubmed/29507242 (Briese 2018)]).
 
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7SK snRNP (composed of 7SK snRNA, Hexim1, Larp7/Pip7S, and the P-TEFb subunits CycT1 and Cdk9) is not only critical for controlling transcription, but also for regulating alternative splicing coupled to transcription elongation ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).  7SK snRNP disintegration promotes inclusion of an alternative exon via the increased occupancy of P-TEFb, Ser2-phosphorylated (Ser2-P) RNAPII, and the splicing factor SF2/ASF at the minigene ([http://www.ncbi.nlm.nih.gov/pubmed/19416841 (Barboric 2009)]).
 
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7SK snRNA also inhibits APOBEC3C deaminase activity and sequesters it to the nucleolus, suggesting broader role for 7SK RNA in regulating key nuclear functions ([http://www.ncbi.nlm.nih.gov/pubmed/17381310 (He 2007)]).
 
  
 
===Disease===
 
===Disease===
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colon adenocarcinoma <ref name="ref1" />
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lung cancer ([https://www.ncbi.nlm.nih.gov/pubmed/30787392 (Wang M 2019)])
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===Evolution===
 
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Please input evolution information here.
 
  
 
==Labs working on this lncRNA==
 
==Labs working on this lncRNA==
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Please input related labs here.
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* Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
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* Department of Histology and Embryology, School of Basic Medicine, Central South University, Changsha, Hunan, 410013, China.
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==References==
 
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<references>
 
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<ref name="ref1"> Shahriyari L. Effect of normalization methods on the performance of supervised
 
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learning algorithms applied to HTSeq-FPKM-UQ data sets: 7SK RNA expression as a
 
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predictor of survival in patients with colon adenocarcinoma. Brief Bioinform.
 
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2017 Nov 3. doi: 10.1093/bib/bbx153.
 
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</ref>(1)
 
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</references>
 
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[http://www.lncrnadb.org/7SK/ Annotation originally sourced from lncRNAdb].
 
  
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{{basic|
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===Sequence===
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tID = NONHSAT113149|
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>NR_027908.1 Homo sapiens long intergenic non-protein coding RNA 336 (LINC00336), long non-coding RNA
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source = NONCODE4.0|
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<dnaseq>AGATGCGAGCGCCTGCGCAGGTACGCACGCTCCGCTGGAGCCTGGGGTGGCCTGGCAGTCGTGGCCGAGA
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same = ,|
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CGTGTTTGCTGCACTTCGGTGCGCACAGGCACTGCGGTGCCAACCTCTTGGTTCCGCCCTCCCCCCGCAG
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classification = intergenic|
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GCGCCCACGCGTGACCTCGGCCGCCCACAGGCCTTCGACTCTTCCCGGACTCCAGGTCCCAGGCCGCCCC
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length = 332 nt|
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GCTCCACCCTGCGGATGATGGAGACAAAGTCCCCCACAAGCCCCTCATATGGGGCAAGGGGGAAGGTACC
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location = chr6+:52860418..52860749|
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ACCTGGGGCGGGGCCTGGCTCCCCACTGAGCAGAGGTGCTGGCCAAGGCGCTCCCCTTAGTGAGACAAGG
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number = 1|
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TTTCACCATGTTGCCCAGGCTTTTCTCAAACTCCTGAGCTCAAGCAATCCGCCCACCTCAGCCTCCGAAA
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exons = 52860418..52860749|
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GTGCTAGGATTATAGGCGTGAGCCACTGCACCCAGCCCCAGGTGGCAAGTCTTTCTGATAGGCACTGCTC
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context = <html><div align="center">
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CAAAGTGAATCACACTGTGCTAAGCCCCCGCAAGGGAGTGCCTTTGCAGCTTACAGCTGCACACTCGTCA
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<iframe src="http://lncrna.big.ac.cn/view/?data=species/human&loc=chr6:52860418..52860749&tracklist=0&overview=0&tracks=DNA,RefGene,lncRNA" style=" border-width:0 " width="100%" height="250" scrolling="yes"></iframe>
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TCTCAGGAGGTCCTTGCAACAGTCCCCTTTCACGGGTAAAGAAACTGAGGCCTCTACTCAACCTCACAGA
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</div></html>|
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GCAAGCTAATGCCAGACTAAAACCTCTGGCCTCCAAACCCCATGCCCTTTCTTTTTGTAAGCTACACAGA
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sequence = <dnaseq>GGATGTGAGGGCGATCTGGCTGCGACATCTGTCACCCCATTGATCGCCAGGGTTGATTCGGCTGATCTGGCTGGCTAGGCGGGTGTCCCCTTCCTCCCTCACCGCTCCATGTGCGTCCCTCCCGAAGCTGCGCGCTCGGTCGAAGAGGACGACCATCCCCGATAGAGGAGGACCGGTCTTCGGTCAAGGGTATACGAGTAGCTGCGCTCCCCTGCTAGAACCTCCAAACAAGCTCTCAAGGTCCATTTGTAGGAGAACGTAGGGTAGTCAAGCTTCCAAGACTCCAGACACATCCAAATGAGGCGCTGCATGTGGCAGTCTGCCTTTCTTTT</dnaseq>|
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CTGTCAGGGCAAATGTCCACTGGATAAAAGCATGAGATGATGAATGGACGGAAATTAACCAAAAAGGTCA
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}}
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TCAACACATTTTCAACAGATCCATCAATGTGCACTCAAAGAAGCTGAGACAGGCCTAACCTTTAAAGGCT
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[[Category:Intergenic]][[Category:NONHSAG043942]][[Category:Transcripts]]
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GATGTCAAGGAAGGGGAGCAGCAGGATGGTACTCGGTCTGACCCAGGGGGGTCGCTCCCCTGAGCCTATG
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TGTGTTTGGAGTGGACGAGAATGGGAGAGAGATTAGAAAAACAGCAGCATCATGTGAATTACAGATGCAC
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AGGAAAGCTTACAGCCTGTCTAGACAAATTCACTTATGTTACAGATGAGGAAACTGAGGCTCAGAAAGAG
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GAAGGGACTTGCCCAAGGCCACATAGCAAAGGAATAGCAAAGTTGAGACAAAAATAATGGACATTGTGAC
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TCTGAGTCAAGTGAGAAACAGAGAGACTGATGGAGAAGTGTGTGTGTGTGTGTGTGTGTGTGTGTGTTTA
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TGTGCATGCAGTGTGCACTCACTCAGGGGGCCAGGGTCCTGAATTTAGAAACACTACCACCAAGAAGGCA
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TTATGCCTACCCTACCCAGGCAGTGGGGGCTGGAGCCAGGGCCTGGGGGCTGGAACCAGGGCCCAGGGCC
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TGGAGGGGATGGTAAGCCTCCAGCCCCACCTTCTCCAGGAAGGGGTTGGTGGTCTGGCACGGGCCAAGCG
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TACCTGGCCATCCACAATGCTCACCTCCACCACGGTGATCTCTGGCCGGGTAAGCAGCTCTCGGCCCTCT
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TGGCTGCCTAGCTTCCAGAGGCGGGACTCTTGCTGCATTCCCAGAAGCTTCTTCAACTCCGACTCCAGGA
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AACCTGAGAGCCAGAGAGATGGCAAGGGACAGGGAGATGGCAGGGAACAGGCAGGAGTAGGATGGAGCAG
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CCCACTGGGAACCCAAGGACCCGGAGGTGCAACCGCTCCCTGAGCCTCATCCCAGCTCTGTGTGGTTCCT
 +
GCTCACCCTCAGCCACAGCCCTCTCTTCTTCCAGGACGTAGAGCCAGCCAGGTACCACCCCTCCTTCGCC
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CTGCCTTCCCCAGGAAGCTCACTCTTTGAGGGCCTTCTCTGGCAGCGGCAGCATGAGAGCCTGCGTCTTC
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ACCCACTGGGGACAGCATGCAAGGGGCAGGTATTTGCCCCCACCACCAACCAACTCAAGAGCCTGGATCT
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GGAACCCAAACTGCCTGCACTCAAGTCCCAGCTCTGCCCATCACTAGCTGTGTGACATCGGGCAAGTTCT
 +
CACTGTGAACTGGAGATGGCAATAGGACCTACCTCAGAGTCGTAAAATGCAGGATTTTATGAAAAGTGCT
 +
TAAAGAGGGTCTGCCCCATTAATGGCTATGTAAATGTGAACCACGATTTTCATCATATTATGTATGCTAT
 +
CACCACT</dnaseq>

Latest revision as of 05:07, 13 September 2019

Annotated Information

Name

Approved symbol: LINC00336

Approved name: long intergenic non-protein coding RNA 336

HGNC ID: HGNC:33813

Previous names: chromosome 6 open reading frame 227, non-protein coding RNA 336

Alias symbols: FLJ43752, C6orf227, NCRNA00336

RefSeq ID: NR_027908

Characteristics

Expression

Upregulated in lung cancer ((Wang M 2019)).

Regulation

ELAVL1 increased LINC00336 expression by stabilizing its posttranscriptional level((Wang M 2019)).

Function

Functions as an oncogene by acting as a competing endogenous RNA (ceRNAs) to inhibit ferroptosis in lung cancer((Wang M 2019)).

Disease

lung cancer ((Wang M 2019))

Labs working on this lncRNA

  • Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, 410078, China.
  • Department of Histology and Embryology, School of Basic Medicine, Central South University, Changsha, Hunan, 410013, China.

Sequence

>NR_027908.1 Homo sapiens long intergenic non-protein coding RNA 336 (LINC00336), long non-coding RNA

000001 AGATGCGAGC GCCTGCGCAG GTACGCACGC TCCGCTGGAG CCTGGGGTGG CCTGGCAGTC GTGGCCGAGA CGTGTTTGCT 000080
000081 GCACTTCGGT GCGCACAGGC ACTGCGGTGC CAACCTCTTG GTTCCGCCCT CCCCCCGCAG GCGCCCACGC GTGACCTCGG 000160
000161 CCGCCCACAG GCCTTCGACT CTTCCCGGAC TCCAGGTCCC AGGCCGCCCC GCTCCACCCT GCGGATGATG GAGACAAAGT 000240
000241 CCCCCACAAG CCCCTCATAT GGGGCAAGGG GGAAGGTACC ACCTGGGGCG GGGCCTGGCT CCCCACTGAG CAGAGGTGCT 000320
000321 GGCCAAGGCG CTCCCCTTAG TGAGACAAGG TTTCACCATG TTGCCCAGGC TTTTCTCAAA CTCCTGAGCT CAAGCAATCC 000400
000401 GCCCACCTCA GCCTCCGAAA GTGCTAGGAT TATAGGCGTG AGCCACTGCA CCCAGCCCCA GGTGGCAAGT CTTTCTGATA 000480
000481 GGCACTGCTC CAAAGTGAAT CACACTGTGC TAAGCCCCCG CAAGGGAGTG CCTTTGCAGC TTACAGCTGC ACACTCGTCA 000560
000561 TCTCAGGAGG TCCTTGCAAC AGTCCCCTTT CACGGGTAAA GAAACTGAGG CCTCTACTCA ACCTCACAGA GCAAGCTAAT 000640
000641 GCCAGACTAA AACCTCTGGC CTCCAAACCC CATGCCCTTT CTTTTTGTAA GCTACACAGA CTGTCAGGGC AAATGTCCAC 000720
000721 TGGATAAAAG CATGAGATGA TGAATGGACG GAAATTAACC AAAAAGGTCA TCAACACATT TTCAACAGAT CCATCAATGT 000800
000801 GCACTCAAAG AAGCTGAGAC AGGCCTAACC TTTAAAGGCT GATGTCAAGG AAGGGGAGCA GCAGGATGGT ACTCGGTCTG 000880
000881 ACCCAGGGGG GTCGCTCCCC TGAGCCTATG TGTGTTTGGA GTGGACGAGA ATGGGAGAGA GATTAGAAAA ACAGCAGCAT 000960
000961 CATGTGAATT ACAGATGCAC AGGAAAGCTT ACAGCCTGTC TAGACAAATT CACTTATGTT ACAGATGAGG AAACTGAGGC 001040
001041 TCAGAAAGAG GAAGGGACTT GCCCAAGGCC ACATAGCAAA GGAATAGCAA AGTTGAGACA AAAATAATGG ACATTGTGAC 001120
001121 TCTGAGTCAA GTGAGAAACA GAGAGACTGA TGGAGAAGTG TGTGTGTGTG TGTGTGTGTG TGTGTGTTTA TGTGCATGCA 001200
001201 GTGTGCACTC ACTCAGGGGG CCAGGGTCCT GAATTTAGAA ACACTACCAC CAAGAAGGCA TTATGCCTAC CCTACCCAGG 001280
001281 CAGTGGGGGC TGGAGCCAGG GCCTGGGGGC TGGAACCAGG GCCCAGGGCC TGGAGGGGAT GGTAAGCCTC CAGCCCCACC 001360
001361 TTCTCCAGGA AGGGGTTGGT GGTCTGGCAC GGGCCAAGCG TACCTGGCCA TCCACAATGC TCACCTCCAC CACGGTGATC 001440
001441 TCTGGCCGGG TAAGCAGCTC TCGGCCCTCT TGGCTGCCTA GCTTCCAGAG GCGGGACTCT TGCTGCATTC CCAGAAGCTT 001520
001521 CTTCAACTCC GACTCCAGGA AACCTGAGAG CCAGAGAGAT GGCAAGGGAC AGGGAGATGG CAGGGAACAG GCAGGAGTAG 001600
001601 GATGGAGCAG CCCACTGGGA ACCCAAGGAC CCGGAGGTGC AACCGCTCCC TGAGCCTCAT CCCAGCTCTG TGTGGTTCCT 001680
001681 GCTCACCCTC AGCCACAGCC CTCTCTTCTT CCAGGACGTA GAGCCAGCCA GGTACCACCC CTCCTTCGCC CTGCCTTCCC 001760
001761 CAGGAAGCTC ACTCTTTGAG GGCCTTCTCT GGCAGCGGCA GCATGAGAGC CTGCGTCTTC ACCCACTGGG GACAGCATGC 001840
001841 AAGGGGCAGG TATTTGCCCC CACCACCAAC CAACTCAAGA GCCTGGATCT GGAACCCAAA CTGCCTGCAC TCAAGTCCCA 001920
001921 GCTCTGCCCA TCACTAGCTG TGTGACATCG GGCAAGTTCT CACTGTGAAC TGGAGATGGC AATAGGACCT ACCTCAGAGT 002000
002001 CGTAAAATGC AGGATTTTAT GAAAAGTGCT TAAAGAGGGT CTGCCCCATT AATGGCTATG TAAATGTGAA CCACGATTTT 002080
002081 CATCATATTA TGTATGCTAT CACCACT
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