Difference between revisions of "NONHSAT011777"

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Please input one-sentence summary here.
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''PRINS'' Psoriasis associated non-protein coding RNA induced by stress is involved in psoriasis susceptibility, plays a role in cellular stress response and regulation of apoptosis <ref name="ref2" />.
  
 
==Annotated Information==
 
==Annotated Information==
 
===Name===
 
===Name===
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PRINS: Psoriasis susceptibility-related RNA Gene Induced by Stress.
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PRINS: Psoriasis associated non-protein coding RNA induced by stress (HGNC).
  
 
===Characteristics===
 
===Characteristics===
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~3.6 kb, transcribed by RNA Polymerase II; spliced (2 exons) and polyadenylated [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))].
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[[File:PRINS.jpg|right|thumb|400px|'''Structure of the full-length ''PRINS'' transcript in HaCaT keratinocytes''' <ref name="ref1" />]]
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''PRINS'' is ~3.6 kb long noncoding RNA and located at human Chromosome 10p12.1 (HGNC) <ref name="ref1" />.''PRINS'' contains two Alu elements, as well as also contains a heatshock element that displays approximately 70% similarity to ''G8'', a cytoplasmic noncoding RNA in ''Tetrahymena thermophila'', that is responsible for developing thermotolerance <ref name="ref1" />.  
  
 
===Function===
 
===Function===
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siRNA knock-down shows that PRINS is required for cell viability after serum starvation [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))], and also alters cell morphology and gene expression [http://www.ncbi.nlm.nih.gov/pubmed/20377629 (Szegedi (2010))]. Elevated PRINS expression in the epidermis is suggested to contribute to psoriasis susceptibility [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))]. In keratinocytes PRINS regulates the expression of the G1P3 gene, an anti-apoptotic protein that is overexpressed in psoriasis [http://www.ncbi.nlm.nih.gov/pubmed/20377629 (Szegedi (2010))], although the mechanism is unknown.
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siRNA knock-down shows that PRINS is required for cell viability after serum starvation and also alters cell morphology and gene expression <ref name="ref1" /><ref name="ref4" />.  
  
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===Expression===
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Elevated PRINS expression in the epidermis is suggested to contribute to psoriasis susceptibility by disrupting the signal transduction events mediating the genes involved in apoptosis regulation such as G1P3 <ref name="ref1" /><ref name="ref3" />. In keratinocytes PRINS regulates the expression of the G1P3 gene, an anti-apoptotic protein that is overexpressed in psoriasis <ref name="ref4" />.
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Elevated expression in psoriatic epidermis. Regulated by the proliferation and differentiation state of keratinocytes [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))]. Expressed at different levels in various human tissues, with highest levels detected in veins [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))]. Several stress signals such as ultraviolet-B (UV-B) irradiation, viral infection (herpes simplex virus), and translational inhibition increased the RNA level of PRINS [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))], as well as HaCaT keratinocyte cell treatment with microbial agents such as bacteria peptidoglycan, lipopolysaccharide (LPS) and wall extract [http://www.ncbi.nlm.nih.gov/pubmed/21750967 (Bari (2011))].  
 
  
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===Conservation===
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''PRINS'' is essential for the survival of keratinocytes under stress conditions <ref name="ref3" />.
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Please input conservation information here.
 
  
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===Disease===
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===Expression===
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psoriasis
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''PRINS'' is expressed in various human tissues with great variability in the level of expression. Interestingly, the level of expression differed to a great extent in different organs. The lowest level of PRINS RNA was detected in cardiac muscle, whereas the highest level was seen in veins. The level of expression was 18-fold higher in veins than in cardiac muscle <ref name="ref1" />.
  
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===Misc===
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''PRINS'' is overexpressed in psoriatic epidermis. Regulated by the proliferation and differentiation state of keratinocytes  <ref name="ref1" />. Several stress signals such as ultraviolet-B (UV-B) irradiation, viral infection (herpes simplex virus), and translational inhibition increased the RNA level of PRINS as well as HaCaT keratinocyte cell treatment with microbial agents such as bacteria peptidoglycan, lipopolysaccharide (LPS) and wall extract <ref name="ref1" /><ref name="ref3" />.
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PRINS RNA contains contains two Alu elements, as well as a short sequence stretch with ~70% similarity to an element in a small cytoplasmic noncoding RNA, named G8, from Tetrahymena thermophila, whose expression responds to heat shock and is involved in thermotolerance [http://www.ncbi.nlm.nih.gov/pubmed/15855153 (Sonkoly (2005))].
 
  
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===Transcriptomic Nomeclature===
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{| class='wikitable' style="text-align:center"
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Please input transcriptomic nomeclature information here.
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|-
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! | Experiment
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! | Forward primer
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! | Reverse primer
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|-
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| rowspan="1"|RT-PCR
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| | 5-GCATCTTCCCTTGGCAAA-3'
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| | 5-GCCTAAAGGACATTTCGGTAT-3'<ref name="ref3" />
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|}
  
 
===Regulation===
 
===Regulation===
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Please input regulation information here.
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''PRINS'' is regulated by the proliferation and differentiation state of keratinocytes <ref name="ref1" />.
  
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===Allelic Information and Variation===
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===Disease===
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Please input allelic information and variation information here.
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* Psoriasis
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===Evolution===
 
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Please input evolution information here.
 
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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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* Department of Pathology, University of Szeged, Szeged, Hungary. <ref name="ref1" />
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* Dermatological Research Group of the Hungarian Academy of Sciences, University of Szeged, Szeged, Hungary. <ref name="ref1" />
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* Department of Dermatology and Allergology, University of Szeged, Szeged, Koranyi fasor 6, 6720, Hungary. <ref name="ref1" /><ref name="ref3" />
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* Dermatological Research Group of the Hungarian Academy of Sciences, University of Szeged, Szeged 6720, Hungary. <ref name="ref3" />
  
 
==References==
 
==References==
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[http://www.lncrnadb.org/PRINS/ Annotation originally sourced from lncRNAdb.]
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<references>
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<ref name="ref1"> Sonkoly E, Bata-Csorgo Z, Pivarcsi A, Polyanka H, Kenderessy-Szabo A, Molnar G et al. Identification and characterization of a novel, psoriasis susceptibility-related noncoding RNA gene, PRINS[J]. Journal of Biological Chemistry. 2005, 280(25):24159-24167.
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</ref>(1)
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<ref name="ref2"> Hombach S & Kretz M. The non‐coding skin: Exploring the roles of long non‐coding RNA s in epidermal homeostasis and disease[J]. Bioessays. 2013, 35(12):1093-1100.
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</ref>(2)
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<ref name="ref3"> Bari L, Bacsa S, Sonkoly E, Bata-Csörgő Z, Kemény L, Dobozy A et al. Comparison of stress-induced PRINS gene expression in normal human keratinocytes and HaCaT cells[J]. Archives of dermatological research. 2011, 303(10):745-752.
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</ref>(3)
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<ref name="ref4"> Szegedi K, Sonkoly E, Nagy N, Németh IB, Bata‐Csörgő Z, Kemény L et al. The anti‐apoptotic protein G1P3 is overexpressed in psoriasis and regulated by the non‐coding RNA, PRINS[J]. Experimental dermatology. 2010, 19(3):269-278.
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</ref>(4)
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</references>
  
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{{basic|
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===sequence===  
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tID = NONHSAT011777|
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>gi|392973718|ref| AK022045.1| Homo sapiens psoriasis associated non-protein coding RNA induced by stress (PRINS), long non-coding RNA
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source = NONCODE4.0|
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<dnaseq>GGCCTTTTTTTTTTTTTTTTTCAAATGCCCCTTTCATTATGAAACTCTTTTTTAACTTTTAATTTAAGTTCAGGGGTATGTGTGCAGATTTGTTACATAGGTAAACTTGTGTCATGGGGCTTTGTTGTACAGGTTGTTTCATCACCCAGGTATTATTTTATTTTCATTTTAGTTTTTTAAATTTCTTTTTAGAGGCGGGGTCTCACTGTGTTTTGCCCAGGCTGGTCTCGAACTCCTCCTGGTCTCAAGCAATCCTCTCGCCTCTGCCTCCCCAAGTGTTGGGATTATAGGCATGAGCTACTGCACTCAGCCCACCATTTGTTTTAAAAAGGGTGGATCCTATTTGTATAAAAAGCCATGTGCATTTTCTGTGTACTTGTCTACACATTAATTTCCAGGCTGGGCGTGGTGGCTCACGCTTGTAATCCCAGCACTTTGGGAGGCCAAGGGGAGGCAGATCATGAGGTTAGGAGATCGAAACCATCCTGGCTAACACGGTGAAACCCCGTCTCTACTAAAAATACAAAAACAAAATTAGCAGGGTGTTGTGGCGGGCGCCTGTAGTCCCAGCTACTCAGGAGGCTGAGGCAGGAGAATGGCATGAACCCGGGAGGTGGAGCTTGCAGTGAGCTGAGATTGCGCCACTGCCCTCCAGCCTGGACAACAGAGTGAGGCTCCGTCTTAAAGGAAAAAAATTTCTGGAATGATGTCCAATAAATCAGAGAGAGGGACTAGAAGACTAATGAGGACAGAAGCTTTTATTCTTAACACCTATATTTTGCTACCATTTATATTGTCATCATATGCATATAACATTTTAACATTTAAAAACTAGTTTAAACAGAAATGGTTGCCCTGGAATGTGGCCTGTGTTCTTTCAAGGGAGGCCAGCAGTTTCTACAGTGGCTGAGATGGTACCTTCATCTCACACACCTACGCAGGCGTGCATTTGTGCTTTGATGTGGTTGTCCCTTGAAGAAGGAAGCAGTTCTCTTTTTCTTTTTTCCCTTTTCCATTATAGGATCAGTCACTTCTTGGGGCATTAGTAGTCTCATTTCCAGTGGCATCTTCCCTTGGCAAAAGGAATCCCAGATAGGACCTCATCTTTCTAAACAAATGCTGTTTTGGGTCCTAACCATCCCATGTTTGCTTTGAATATGTTTAAGTTGCCTGGAATTATCAACAAAAGAATTAAATTTATTGTAGGTCAGGGCATCTTTTGACTCATTGTATAAAACATTCACTTTAAATGTATACCGAAATGTCCTTTAGGCTGGGATTACAGGCATGAGCCATGACACCCGGCCTGTAATTTTCTTTAAAGACTGCCACTGGGTGGAACCCACTGGGCCCAGTGAGAACTACGGAAAAGAGACCCATTCTTGCCCTCATTGTTAGTGTCCACATCCGGATTTACCTAAACCCCACCCAGGTGGCATTTGCATAGTAATGAAAAACCGGTATTTTCTAGCTGTGAATCACACTTCAAATCCTGAGCGGCTGACTGTCAGGGGTGCGTCAGGCCTGCTTGCTGGGAGAATGGACGAGCTGGTTGTGGAGCGGGCGGGTCCCGCCACCCGTGGGCTCAGCACTGGACTGCTCCCAGAACATTAAAGGTCTGGCTGATGTTCCATGCCACATCTGGACATGAAGACCCATGTCTGCCCTTCTGTAGAAGGGCCAAAGAAGAAAGGAGGCATCACATGTTTCTGCTGTGGGGGGCCCTTCCGAGCAGCAGACAGGAGCAAGGTACAGGAGTGGCCTGATTCTGGGGTTTCCCTGCCCCCCCTGGGGTCCCTAAACTGCTGTGTGATATGTTTCTAACTATCTGGACAGCTCACCCAAGAGTCAGTTGTTCCCAGTCGCTTCTTGCTGAGGATAAGCCAAAAGAGGGCCGGGGGCCAATCTGGTTTCTTTCAAGTGAAATTATGCTTCTCAAGCAGAGAATGATTGCCCACAGCAGTTAAACCTTGTTTAATGGTAATTAAATTGCTTTTCTTCACTTTGAAAAATCTCTTAATTTTCTGTACAAAGGCAGGAAGCATTTTTCTTTGATTCTACAGGATGTTTCTAAGTATGGTGTAATCAGTTCATCTTACCTTGCCGGGCTCTGAAAGAATGAGTGTGTGGGATCAGATTTAGAAATGCCTCAAAGGTTAGAAAGCCGAGTGCTGCCGATTAACTCAAGCTCAGATGACC</dnaseq>
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same = ,|
 
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classification = intronic(S)|
 
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length = 2199 nt|
 
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location = chr10+:24536054..24544975|
 
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number = 2|
 
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exons = 24536054..24537320,24544051..24544975|
 
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context = <html><div align="center">
 
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<iframe src="http://lncrna.big.ac.cn/view/?data=species/human&loc=chr10:24536054..24544975&tracklist=0&overview=0&tracks=DNA,RefGene,lncRNA" style=" border-width:0 " width="100%" height="250" scrolling="yes"></iframe>
 
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</div></html>|
 
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sequence = <dnaseq>GGCCTTTTTTTTTTTTTTTTTCAAATGCCCCTTTCATTATGAAACTCTTTTTTAACTTTTAATTTAAGTTCAGGGGTATGTGTGCAGATTTGTTACATAGGTAAACTTGTGTCATGGGGCTTTGTTGTACAGGTTGTTTCATCACCCAGGTATTATTTTATTTTCATTTTAGTTTTTTAAATTTCTTTTTAGAGGCGGGGTCTCACTGTGTTTTGCCCAGGCTGGTCTCGAACTCCTCCTGGTCTCAAGCAATCCTCTCGCCTCTGCCTCCCCAAGTGTTGGGATTATAGGCATGAGCTACTGCACTCAGCCCACCATTTGTTTTAAAAAGGGTGGATCCTATTTGTATAAAAAGCCATGTGCATTTTCTGTGTACTTGTCTACACATTAATTTCCAGGCTGGGCGTGGTGGCTCACGCTTGTAATCCCAGCACTTTGGGAGGCCAAGGGGAGGCAGATCATGAGGTTAGGAGATCGAAACCATCCTGGCTAACACGGTGAAACCCCGTCTCTACTAAAAATACAAAAACAAAATTAGCAGGGTGTTGTGGCGGGCGCCTGTAGTCCCAGCTACTCAGGAGGCTGAGGCAGGAGAATGGCATGAACCCGGGAGGTGGAGCTTGCAGTGAGCTGAGATTGCGCCACTGCCCTCCAGCCTGGACAACAGAGTGAGGCTCCGTCTTAAAGGAAAAAAATTTCTGGAATGATGTCCAATAAATCAGAGAGAGGGACTAGAAGACTAATGAGGACAGAAGCTTTTATTCTTAACACCTATATTTTGCTACCATTTATATTGTCATCATATGCATATAACATTTTAACATTTAAAAACTAGTTTAAACAGAAATGGTTGCCCTGGAATGTGGCCTGTGTTCTTTCAAGGGAGGCCAGCAGTTTCTACAGTGGCTGAGATGGTACCTTCATCTCACACACCTACGCAGGCGTGCATTTGTGCTTTGATGTGGTTGTCCCTTGAAGAAGGAAGCAGTTCTCTTTTTCTTTTTTCCCTTTTCCATTATAGGATCAGTCACTTCTTGGGGCATTAGTAGTCTCATTTCCAGTGGCATCTTCCCTTGGCAAAAGGAATCCCAGATAGGACCTCATCTTTCTAAACAAATGCTGTTTTGGGTCCTAACCATCCCATGTTTGCTTTGAATATGTTTAAGTTGCCTGGAATTATCAACAAAAGAATTAAATTTATTGTAGGTCAGGGCATCTTTTGACTCATTGTATAAAACATTCACTTTAAATGTATACCGAAATGTCCTTTAGGCTGGGATTACAGGCATGAGCCATGACACCCGGCCTGTAATTTTCTTTAAAGACTGCCACTGGGTGGAACCCACTGGGCCCAGTGAGAACTACGGAAAAGAGACCCATTCTTGCCCTCATTGTTAGTGTCCACATCCGGATTTACCTAAACCCCACCCAGGTGGCATTTGCATAGTAATGAAAAACCGGTATTTTCTAGCTGTGAATCACACTTCAAATCCTGAGCGGCTGACTGTCAGGGGTGCGTCAGGCCTGCTTGCTGGGAGAATGGACGAGCTGGTTGTGGAGCGGGCGGGTCCCGCCACCCGTGGGCTCAGCACTGGACTGCTCCCAGAACATTAAAGGTCTGGCTGATGTTCCATGCCACATCTGGACATGAAGACCCATGTCTGCCCTTCTGTAGAAGGGCCAAAGAAGAAAGGAGGCATCACATGTTTCTGCTGTGGGGGGCCCTTCCGAGCAGCAGACAGGAGCAAGGTACAGGAGTGGCCTGATTCTGGGGTTTCCCTGCCCCCCCTGGGGTCCCTAAACTGCTGTGTGATATGTTTCTAACTATCTGGACAGCTCACCCAAGAGTCAGTTGTTCCCAGTCGCTTCTTGCTGAGGATAAGCCAAAAGAGGGCCGGGGGCCAATCTGGTTTCTTTCAAGTGAAATTATGCTTCTCAAGCAGAGAATGATTGCCCACAGCAGTTAAACCTTGTTTAATGGTAATTAAATTGCTTTTCTTCACTTTGAAAAATCTCTTAATTTTCTGTACAAAGGCAGGAAGCATTTTTCTTTGATTCTACAGGATGTTTCTAAGTATGGTGTAATCAGTTCATCTTACCTTGCCGGGCTCTGAAAGAATGAGTGTGTGGGATCAGATTTAGAAATGCCTCAAAGGTTAGAAAGCCGAGTGCTGCCGATTAACTCAAGCTCAGATGACC</dnaseq>|
 
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}}
 
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[[Category:Intronic(S)]][[Category:NONHSAG005407]][[Category:Transcripts]][[Category:Transcripts]]
 

Revision as of 06:35, 15 November 2018

PRINS Psoriasis associated non-protein coding RNA induced by stress is involved in psoriasis susceptibility, plays a role in cellular stress response and regulation of apoptosis [1].

Annotated Information

Name

PRINS: Psoriasis associated non-protein coding RNA induced by stress (HGNC).

Characteristics

Structure of the full-length PRINS transcript in HaCaT keratinocytes [2]

PRINS is ~3.6 kb long noncoding RNA and located at human Chromosome 10p12.1 (HGNC) [2].PRINS contains two Alu elements, as well as also contains a heatshock element that displays approximately 70% similarity to G8, a cytoplasmic noncoding RNA in Tetrahymena thermophila, that is responsible for developing thermotolerance [2].

Function

siRNA knock-down shows that PRINS is required for cell viability after serum starvation and also alters cell morphology and gene expression [2][3].

Elevated PRINS expression in the epidermis is suggested to contribute to psoriasis susceptibility by disrupting the signal transduction events mediating the genes involved in apoptosis regulation such as G1P3 [2][4]. In keratinocytes PRINS regulates the expression of the G1P3 gene, an anti-apoptotic protein that is overexpressed in psoriasis [3].

PRINS is essential for the survival of keratinocytes under stress conditions [4].

Expression

PRINS is expressed in various human tissues with great variability in the level of expression. Interestingly, the level of expression differed to a great extent in different organs. The lowest level of PRINS RNA was detected in cardiac muscle, whereas the highest level was seen in veins. The level of expression was 18-fold higher in veins than in cardiac muscle [2].

PRINS is overexpressed in psoriatic epidermis. Regulated by the proliferation and differentiation state of keratinocytes [2]. Several stress signals such as ultraviolet-B (UV-B) irradiation, viral infection (herpes simplex virus), and translational inhibition increased the RNA level of PRINS as well as HaCaT keratinocyte cell treatment with microbial agents such as bacteria peptidoglycan, lipopolysaccharide (LPS) and wall extract [2][4].

Experiment Forward primer Reverse primer
RT-PCR 5-GCATCTTCCCTTGGCAAA-3' 5-GCCTAAAGGACATTTCGGTAT-3'[4]

Regulation

PRINS is regulated by the proliferation and differentiation state of keratinocytes [2].

Disease

  • Psoriasis

Labs working on this lncRNA

  • Department of Pathology, University of Szeged, Szeged, Hungary. [2]
  • Dermatological Research Group of the Hungarian Academy of Sciences, University of Szeged, Szeged, Hungary. [2]
  • Department of Dermatology and Allergology, University of Szeged, Szeged, Koranyi fasor 6, 6720, Hungary. [2][4]
  • Dermatological Research Group of the Hungarian Academy of Sciences, University of Szeged, Szeged 6720, Hungary. [4]

References

  1. ↑ Hombach S & Kretz M. The non‐coding skin: Exploring the roles of long non‐coding RNA s in epidermal homeostasis and disease[J]. Bioessays. 2013, 35(12):1093-1100.
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 Sonkoly E, Bata-Csorgo Z, Pivarcsi A, Polyanka H, Kenderessy-Szabo A, Molnar G et al. Identification and characterization of a novel, psoriasis susceptibility-related noncoding RNA gene, PRINS[J]. Journal of Biological Chemistry. 2005, 280(25):24159-24167.
  3. ↑ 3.0 3.1 Szegedi K, Sonkoly E, Nagy N, Németh IB, Bata‐Csörgő Z, Kemény L et al. The anti‐apoptotic protein G1P3 is overexpressed in psoriasis and regulated by the non‐coding RNA, PRINS[J]. Experimental dermatology. 2010, 19(3):269-278.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Bari L, Bacsa S, Sonkoly E, Bata-Csörgő Z, Kemény L, Dobozy A et al. Comparison of stress-induced PRINS gene expression in normal human keratinocytes and HaCaT cells[J]. Archives of dermatological research. 2011, 303(10):745-752.

sequence

>gi|392973718|ref| AK022045.1| Homo sapiens psoriasis associated non-protein coding RNA induced by stress (PRINS), long non-coding RNA

000001 GGCCTTTTTT TTTTTTTTTT TCAAATGCCC CTTTCATTAT GAAACTCTTT TTTAACTTTT AATTTAAGTT CAGGGGTATG 000080
000081 TGTGCAGATT TGTTACATAG GTAAACTTGT GTCATGGGGC TTTGTTGTAC AGGTTGTTTC ATCACCCAGG TATTATTTTA 000160
000161 TTTTCATTTT AGTTTTTTAA ATTTCTTTTT AGAGGCGGGG TCTCACTGTG TTTTGCCCAG GCTGGTCTCG AACTCCTCCT 000240
000241 GGTCTCAAGC AATCCTCTCG CCTCTGCCTC CCCAAGTGTT GGGATTATAG GCATGAGCTA CTGCACTCAG CCCACCATTT 000320
000321 GTTTTAAAAA GGGTGGATCC TATTTGTATA AAAAGCCATG TGCATTTTCT GTGTACTTGT CTACACATTA ATTTCCAGGC 000400
000401 TGGGCGTGGT GGCTCACGCT TGTAATCCCA GCACTTTGGG AGGCCAAGGG GAGGCAGATC ATGAGGTTAG GAGATCGAAA 000480
000481 CCATCCTGGC TAACACGGTG AAACCCCGTC TCTACTAAAA ATACAAAAAC AAAATTAGCA GGGTGTTGTG GCGGGCGCCT 000560
000561 GTAGTCCCAG CTACTCAGGA GGCTGAGGCA GGAGAATGGC ATGAACCCGG GAGGTGGAGC TTGCAGTGAG CTGAGATTGC 000640
000641 GCCACTGCCC TCCAGCCTGG ACAACAGAGT GAGGCTCCGT CTTAAAGGAA AAAAATTTCT GGAATGATGT CCAATAAATC 000720
000721 AGAGAGAGGG ACTAGAAGAC TAATGAGGAC AGAAGCTTTT ATTCTTAACA CCTATATTTT GCTACCATTT ATATTGTCAT 000800
000801 CATATGCATA TAACATTTTA ACATTTAAAA ACTAGTTTAA ACAGAAATGG TTGCCCTGGA ATGTGGCCTG TGTTCTTTCA 000880
000881 AGGGAGGCCA GCAGTTTCTA CAGTGGCTGA GATGGTACCT TCATCTCACA CACCTACGCA GGCGTGCATT TGTGCTTTGA 000960
000961 TGTGGTTGTC CCTTGAAGAA GGAAGCAGTT CTCTTTTTCT TTTTTCCCTT TTCCATTATA GGATCAGTCA CTTCTTGGGG 001040
001041 CATTAGTAGT CTCATTTCC