Difference between revisions of "ENST00000513868.2"
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| − | ''PVT1'', plasmacytoma variant translocation 1 gene that | + | ''PVT1'', plasmacytoma variant translocation 1 gene that has been identified as a candidate oncogene. |
==Annotated Information== | ==Annotated Information== | ||
===Name=== | ===Name=== | ||
| − | + | Approved symbol: PVT1 | |
| − | + | Approved name: Pvt1 oncogene | |
| + | |||
| + | HGNC ID: HGNC:9709 | ||
| + | |||
| + | Previous names: pvt-1 (murine) oncogene homolog, MYC activator; Pvt1 oncogene homolog (mouse) ; Pvt1 oncogene (non-protein coding) | ||
| + | |||
| + | Alias symbols: NCRNA00079; LINC00079; onco-lncRNA-100; MIR1204HG | ||
| + | |||
| + | Alias names: non-protein coding RNA 79<ref name="ref1" />; long intergenic non-protein coding RNA 79; MIR1204, MIR1205, MIR1206 and MIR1207 host gene | ||
| + | |||
| + | RefSeq ID: NR_003367 | ||
| + | |||
| + | LncBook ID: [https://bigd.big.ac.cn/lncbook/transcript?transid=HSALNT0289225 HSALNT0289225] | ||
===Characteristics=== | ===Characteristics=== | ||
| Line 15: | Line 27: | ||
[[File: PVT1.jpg|right|thumb|400px|'''Schematic representation of ''PVT1'' involvement in ECM deposition.''' . Hyperglycemia causes an excessive accumulation of extracellular matrix (ECM) in the glomerular mesangium which constitutes the major pathological feature of the glomerulosclerosis | [[File: PVT1.jpg|right|thumb|400px|'''Schematic representation of ''PVT1'' involvement in ECM deposition.''' . Hyperglycemia causes an excessive accumulation of extracellular matrix (ECM) in the glomerular mesangium which constitutes the major pathological feature of the glomerulosclerosis | ||
or glomerular fibrosis. Hyperglycemic conditions induce an increase in ''PVT1'' expression in MC which contributes to the increase of the two main ECM components, ''FN1'' and ''COL4A1'', as well as the two main regulators of ECM accumulation in the glomerule, ''PAI-1'' and ''TGFB1''. <ref name="ref2" />.]] | or glomerular fibrosis. Hyperglycemic conditions induce an increase in ''PVT1'' expression in MC which contributes to the increase of the two main ECM components, ''FN1'' and ''COL4A1'', as well as the two main regulators of ECM accumulation in the glomerule, ''PAI-1'' and ''TGFB1''. <ref name="ref2" />.]] | ||
| + | ''PVT'' is involved in diabetic neuropathy and tumorigenesis by affecting the protein stability of the MYC proto-oncogene <ref name="ref1" /><ref name="ref2" />. | ||
''PVT1'' is a downstream target of both c-Myc and N-Myc genes <ref name="ref1" />. | ''PVT1'' is a downstream target of both c-Myc and N-Myc genes <ref name="ref1" />. | ||
| Line 25: | Line 38: | ||
''PVT1'' regulates prostate cancer cell growth by inducing the methylation of miR-146a <ref name="ref4" /> | ''PVT1'' regulates prostate cancer cell growth by inducing the methylation of miR-146a <ref name="ref4" /> | ||
| + | |||
| + | ''C-MYC'' and ''PVT1'' CNG promotes a malignant phenotype of malignant pleural mesothelioma (MPM), with C-MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis <ref name="ref5" />. | ||
| + | |||
| + | ''PVT1'' promotes cell proliferation in gastric cancer by epigenetically regulating p15 and p16 <ref name="ref10" /> | ||
===Expression=== | ===Expression=== | ||
| + | ''PVT1'' is upregulated in gastric cancer.<ref name="ref11" /> | ||
| + | |||
''PVT1'' expression was significantly upregulated by glucose treatment in human mesangial cells <ref name="ref2" />. | ''PVT1'' expression was significantly upregulated by glucose treatment in human mesangial cells <ref name="ref2" />. | ||
''PVT1'' is upregulated in thyroid tissues compared with that in adjacent tissues and was up-regulated in IHH-4, FTC-133, and 8505C cell lines compared to controls <ref name="ref3" />. | ''PVT1'' is upregulated in thyroid tissues compared with that in adjacent tissues and was up-regulated in IHH-4, FTC-133, and 8505C cell lines compared to controls <ref name="ref3" />. | ||
| − | ''PVT1'' is overexpressed in prostate cancer <ref name="ref4" />. | + | ''PVT1'' is overexpressed in prostate cancer, non small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) <ref name="ref4" /><ref name="ref8" /><ref name="ref9" />. |
| + | |||
| + | ''PVT1'' is significantly upregulated in pancreatic cancer tissues (PCT) and overexpression of ''PVT1'' is associated with poor prognosis in pancreatic cancer patients <ref name="ref6" /><ref name="ref7" /> | ||
{|class='wikitable' style="text-align:center" | {|class='wikitable' style="text-align:center" | ||
| Line 51: | Line 72: | ||
| | 5′-TGAGAACTGTCCTTACGTGACC-3′ | | | 5′-TGAGAACTGTCCTTACGTGACC-3′ | ||
| | 5′-AGAGCACCAAGACTGGCTCT-3′<ref name="ref3" /> | | | 5′-AGAGCACCAAGACTGGCTCT-3′<ref name="ref3" /> | ||
| + | |- | ||
| + | | | qRT PCR | ||
| + | | | 5′-TTACAGGCGTGTGCCACAAAGC-3′ | ||
| + | | | 5′-GCCTGTAATCCCAGCACGTTGA-3′<ref name="ref5" /> | ||
|} | |} | ||
| Line 58: | Line 83: | ||
===Disease=== | ===Disease=== | ||
| − | * | + | * Diabetic nephropathy <ref name="ref2" /> |
| + | * Gastric cancer <ref name="ref10" /><ref name="ref11" /> | ||
| + | * Malignant pleural mesothelioma (MPM) <ref name="ref5" /> | ||
| + | * Non-small cell lung cancer (NSCLC) <ref name="ref8" /> | ||
| + | * Pancreatic ductal adenocarcinoma (PDAC) <ref name="ref7" /> | ||
* Prostate cancer <ref name="ref4" /> | * Prostate cancer <ref name="ref4" /> | ||
| + | * Thyroid cancer <ref name="ref3" /> | ||
==Labs working on this lncRNA== | ==Labs working on this lncRNA== | ||
| Line 66: | Line 96: | ||
* Department of Head and Neck Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, #145 Shandong Road, Huangpu District, Shanghai 200001, China.<ref name="ref3" /> | * Department of Head and Neck Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, #145 Shandong Road, Huangpu District, Shanghai 200001, China.<ref name="ref3" /> | ||
* Department of Pathology, Qian-fo-shan Hospital Affiliated to Shandong University, No. 16766 Jingshi Road, Jinan, Shandong 250014, China.<ref name="ref4" /> | * Department of Pathology, Qian-fo-shan Hospital Affiliated to Shandong University, No. 16766 Jingshi Road, Jinan, Shandong 250014, China.<ref name="ref4" /> | ||
| + | * Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang 310003, P.R. China.<ref name="ref9" /> | ||
| + | * Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Hangzhou, Zhejiang 310003, P.R. China.<ref name="ref9" /> | ||
| + | * Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, Jiangsu Province, China.<ref name="ref11" /> | ||
==References== | ==References== | ||
| Line 76: | Line 109: | ||
<ref name="ref4"> Liu Ht, Fang L, Cheng Yx & Sun Q. LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR‐146a[J]. Cancer medicine. 2016, 5(12):3512-3519. | <ref name="ref4"> Liu Ht, Fang L, Cheng Yx & Sun Q. LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR‐146a[J]. Cancer medicine. 2016, 5(12):3512-3519. | ||
</ref>(4) | </ref>(4) | ||
| + | <ref name="ref5"> Riquelme E, Suraokar MB, Rodriguez J, Mino B, Lin HY, Rice DC et al. Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma[J]. Journal of Thoracic Oncology. 2014, 9(7):998-1007. | ||
| + | </ref>(5) | ||
| + | <ref name="ref6"> Xie ZJ, Chen XL, Li JZ, Guo YW, Li HJ, Pan XM et al. Salivary HOTAIR and PVT1 as novel biomarkers for early pancreatic cancer[J]. Oncotarget. 2016, 7(18):25408-25419. | ||
| + | </ref>(6) | ||
| + | <ref name="ref7"> Huang C, Yu W, Wang Q, Cui H, Wang Y, Zhang L et al. Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients[J]. Minerva Med. 2015, 106(3):143-149. | ||
| + | </ref>(7) | ||
| + | <ref name="ref8"> Yang YR, Zang SZ, Zhong CL, Li YX, Zhao SS & Feng XJ. Increased expression of the lncRNA PVT1 promotes tumorigenesis in non-small cell lung cancer[J]. Int J Clin Exp Pathol. 2014, 7(10):6929-6935. | ||
| + | </ref>(8) | ||
| + | <ref name="ref9"> Ding CF, Yang Z, Lv Z, Du CL, Xiao H, Peng CH et al. Long non-coding RNA PVT1 is associated with tumor progression and predicts recurrence in hepatocellular carcinoma patients[J]. Oncol Lett. 2015, 9(2):955-963. | ||
| + | </ref>(9) | ||
| + | <ref name="ref10"> Kong R, Zhang EB, Yin DD, You LH, Xu TP, Chen WM et al. Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16[J]. Mol Cancer. 2015, 14. | ||
| + | </ref>(10) | ||
| + | |||
| + | <ref name="ref11">Cao WJ, Wu HL, He BS, et al. Analysis of long non-coding RNA expression profiles in gastric cancer[J]. World J Gastroenterol, 2013, 19: 3658-3664.</ref>(11) | ||
| + | |||
</references> | </references> | ||
Latest revision as of 02:29, 11 August 2019
PVT1, plasmacytoma variant translocation 1 gene that has been identified as a candidate oncogene.
Contents
Annotated Information
Name
Approved symbol: PVT1
Approved name: Pvt1 oncogene
HGNC ID: HGNC:9709
Previous names: pvt-1 (murine) oncogene homolog, MYC activator; Pvt1 oncogene homolog (mouse) ; Pvt1 oncogene (non-protein coding)
Alias symbols: NCRNA00079; LINC00079; onco-lncRNA-100; MIR1204HG
Alias names: non-protein coding RNA 79[1]; long intergenic non-protein coding RNA 79; MIR1204, MIR1205, MIR1206 and MIR1207 host gene
RefSeq ID: NR_003367
LncBook ID: HSALNT0289225
Characteristics
PVT1 gene is 1957 bp long intergenic non-coding RNA and harbors nine exons (GenBank), located on human chromosome 8q24.21 telomeric to the c-Myc gene and it is frequently involved in the translocations occurring in variant Burkitt's lymphomas and murine plasmacytomas[1].
PVT1 gene contains two non canonical Myc-binding sites (E-box CACGCG) in the promoter region proximal to the transcriptional start site (−155/−95) the consensus and the surrounding sequences are conserved in the homologous mouse and rat genes[1].
Function
Schematic representation of PVT1 involvement in ECM deposition. . Hyperglycemia causes an excessive accumulation of extracellular matrix (ECM) in the glomerular mesangium which constitutes the major pathological feature of the glomerulosclerosis or glomerular fibrosis. Hyperglycemic conditions induce an increase in PVT1 expression in MC which contributes to the increase of the two main ECM components, FN1 and COL4A1, as well as the two main regulators of ECM accumulation in the glomerule, PAI-1 and TGFB1. [2].
PVT is involved in diabetic neuropathy and tumorigenesis by affecting the protein stability of the MYC proto-oncogene [1][2].
PVT1 is a downstream target of both c-Myc and N-Myc genes [1].
The E-boxes region in the PVT1 proximal promoter is important for PVT1 transcriptional regulation by Myc proteins and reveal a novel cross-talk between PVT1 and N-Myc in neuroblastoma cells [1].
PVT1 mediate the development and progression of diabetic nephropathy through mechanisms involving ECM accumulation. PVT1 knockdown significantly reduced mRNA and protein levels of the major ECM proteins, FN1 and COL4A1, and two key regulators of ECM proteins, TGFB1 and PAI-1 [2].
PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulate thyroid-stimulating hormone receptor (TSHR) [3]
PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a [4]
C-MYC and PVT1 CNG promotes a malignant phenotype of malignant pleural mesothelioma (MPM), with C-MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis [5].
PVT1 promotes cell proliferation in gastric cancer by epigenetically regulating p15 and p16 [6]
Expression
PVT1 is upregulated in gastric cancer.[7]
PVT1 expression was significantly upregulated by glucose treatment in human mesangial cells [2].
PVT1 is upregulated in thyroid tissues compared with that in adjacent tissues and was up-regulated in IHH-4, FTC-133, and 8505C cell lines compared to controls [3].
PVT1 is overexpressed in prostate cancer, non small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) [4][8][9].
PVT1 is significantly upregulated in pancreatic cancer tissues (PCT) and overexpression of PVT1 is associated with poor prognosis in pancreatic cancer patients [10][11]
| Experiment | Forward | Reverse |
|---|---|---|
| PCR | CAT GGT TCC ACC AGC GTT ATT C | TCC TTG CGG AAA GGA TGT TGG[1] |
| Knockdown | 5′-GCUUGGAGGCUGAGGAGUUTT-3′ | 5′-AACUCCUCAGCCUCCAAGCTT-3′[3] |
| Quantitative PCR | 5′-TGAGAACTGTCCTTACGTGACC-3′ | 5′-AGAGCACCAAGACTGGCTCT-3′[3] |
| qRT PCR | 5′-TTACAGGCGTGTGCCACAAAGC-3′ | 5′-GCCTGTAATCCCAGCACGTTGA-3′[5] |
Regulation
The E-boxes region in the PVT-1 proximal promoter is important for PVT-1 transcriptional regulation by Myc proteins [1].
PVT-1 transactivation by c-Myc [1].
Disease
- Diabetic nephropathy [2]
- Gastric cancer [6][7]
- Malignant pleural mesothelioma (MPM) [5]
- Non-small cell lung cancer (NSCLC) [8]
- Pancreatic ductal adenocarcinoma (PDAC) [11]
- Prostate cancer [4]
- Thyroid cancer [3]
Labs working on this lncRNA
- Dipartimento di Oncologia Sperimentale e Applicazioni Cliniche, Università di Palermo, Palermo, Italy.[1]
- Diabetes, Cardiovascular and Metabolic Diseases Center, Translational Genomics Research Institute, Phoenix, Arizona, United States of America.[2]
- Department of Head and Neck Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, #145 Shandong Road, Huangpu District, Shanghai 200001, China.[3]
- Department of Pathology, Qian-fo-shan Hospital Affiliated to Shandong University, No. 16766 Jingshi Road, Jinan, Shandong 250014, China.[4]
- Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang 310003, P.R. China.[9]
- Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Hangzhou, Zhejiang 310003, P.R. China.[9]
- Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, Jiangsu Province, China.[7]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Carramusa L, Contino F, Ferro A, Minafra L, Perconti G, Giallongo A, et al. The PVT-1 oncogene is a Myc protein target that is overexpressed in transformed cells[J]. Journal of cellular physiology. 2007,213(2):511-8.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Alvarez ML & DiStefano JK. Functional characterization of the plasmacytoma variant translocation 1 gene (PVT1) in diabetic nephropathy[J]. PloS one. 2011, 6(4):e18671.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Zhou Q, Chen J, Feng J & Wang J. Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR)[J]. Tumor Biology. 2016, 37(3):3105-3113.
- ↑ 4.0 4.1 4.2 4.3 Liu Ht, Fang L, Cheng Yx & Sun Q. LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR‐146a[J]. Cancer medicine. 2016, 5(12):3512-3519.
- ↑ 5.0 5.1 5.2 Riquelme E, Suraokar MB, Rodriguez J, Mino B, Lin HY, Rice DC et al. Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma[J]. Journal of Thoracic Oncology. 2014, 9(7):998-1007.
- ↑ 6.0 6.1 Kong R, Zhang EB, Yin DD, You LH, Xu TP, Chen WM et al. Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16[J]. Mol Cancer. 2015, 14.
- ↑ 7.0 7.1 7.2 Cao WJ, Wu HL, He BS, et al. Analysis of long non-coding RNA expression profiles in gastric cancer[J]. World J Gastroenterol, 2013, 19: 3658-3664.
- ↑ 8.0 8.1 Yang YR, Zang SZ, Zhong CL, Li YX, Zhao SS & Feng XJ. Increased expression of the lncRNA PVT1 promotes tumorigenesis in non-small cell lung cancer[J]. Int J Clin Exp Pathol. 2014, 7(10):6929-6935.
- ↑ 9.0 9.1 9.2 Ding CF, Yang Z, Lv Z, Du CL, Xiao H, Peng CH et al. Long non-coding RNA PVT1 is associated with tumor progression and predicts recurrence in hepatocellular carcinoma patients[J]. Oncol Lett. 2015, 9(2):955-963.
- ↑ Xie ZJ, Chen XL, Li JZ, Guo YW, Li HJ, Pan XM et al. Salivary HOTAIR and PVT1 as novel biomarkers for early pancreatic cancer[J]. Oncotarget. 2016, 7(18):25408-25419.
- ↑ 11.0 11.1 Huang C, Yu W, Wang Q, Cui H, Wang Y, Zhang L et al. Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients[J]. Minerva Med. 2015, 106(3):143-149.
sequence
>gi|5820|ref|NR_003367.3| Homo sapiens Pvt1 oncogene (PVT1), long non-coding RNA
000001 CTCCGGGCAG AGCGCGTGTG GCGGCCGAGC ACATGGGCCC GCGGGCCGGG CGGGCTCGGG GCGGCCGGGA CGAGGAGGGG 000080
000081 CGACGACGAG CTGCGAGCAA AGATGTGCCC CGGGACCCCC GGCACCTTCC AGTGGATTTC CTTGCGGAAA GGATGTTGGC 000160
000161 GGTCCCTGTG ACCTGTGGAG ACACGGCCAG ATCTGCCCTC CAGCCTGATC TTTTGGCCAG AAGGAGATTA AAAAGATGCC 000240
000241 CCTCAAGATG GCTGTGCCTG TCAGCTGCAT GGAGCTTCGT TCAAGTATTT TCTGAGCCTG ATGGATTTAC AGTGATCTTC 000320
000321 AGTGGTCTGG GGAATAACGC TGGTGGAACC ATGCACTGGA ATGACACACG CCCGGCACAT TTCAGGATAC TAAAAGTGGT 000400
000401 TTTAAGGGAG GCTGTGGCTG AATGCCTCAT GGATTCTTAC AGCTTGGATG TCCATGGGGG ACGAAGGACT GCAGCTGGCT 000480
000481 GAGAGGGTTG AGATCTCTGT TTACTTAGAT CTCTGCCAAC TTCCTTTGGG TCTCCCTATG GAATGTAAGA CCCCGACTCT 000560
000561 TCCTGGTGAA GCATCTGATG CACGTTCCAT CCGGCGCTCA GCTGGGCTTG AGCTGACCAT ACTCCCTGGA GCCTTCTCCC 000640
000641 GAGGTGCGCG GGTGACCTTG GCACATACAG CCATCATGAT GGTACTTTAA GTGGAGGCTG AATCATCTCC CCTTTGAGCT 000720
000721 GCTTGGCACG TGGCTCCCTT GGTGTTCCCC TTTTACTGCC AGGACACTGA GATTTGGAGA GAGTCTCACT CTGTGGTCCA 000800
000801 GGCTGAAGTA CAGTGGCATG ATCCCAGGTC ACTGCAACCC CCACCTCCCG GGTTCAAGTG ATCCTCCTGC CTCAGCCTCC 000880
000881 CGAGTAGCTG GTATTACAGG CGTGTGCCAC AAAGCCTGGC TAAGTTTTGT ATTTTTAGTA GAGACGGGGT TTCACCATGT 000960
000961 TGGCCAGGTT GGTCTCGAAC TCCTGACCTC AAGTGATCCA CTCACTTTGG CCTTTCAACG T
000081 CGACGACGAG CTGCGAGCAA AGATGTGCCC CGGGACCCCC GGCACCTTCC AGTGGATTTC CTTGCGGAAA GGATGTTGGC 000160
000161 GGTCCCTGTG ACCTGTGGAG ACACGGCCAG ATCTGCCCTC CAGCCTGATC TTTTGGCCAG AAGGAGATTA AAAAGATGCC 000240
000241 CCTCAAGATG GCTGTGCCTG TCAGCTGCAT GGAGCTTCGT TCAAGTATTT TCTGAGCCTG ATGGATTTAC AGTGATCTTC 000320
000321 AGTGGTCTGG GGAATAACGC TGGTGGAACC ATGCACTGGA ATGACACACG CCCGGCACAT TTCAGGATAC TAAAAGTGGT 000400
000401 TTTAAGGGAG GCTGTGGCTG AATGCCTCAT GGATTCTTAC AGCTTGGATG TCCATGGGGG ACGAAGGACT GCAGCTGGCT 000480
000481 GAGAGGGTTG AGATCTCTGT TTACTTAGAT CTCTGCCAAC TTCCTTTGGG TCTCCCTATG GAATGTAAGA CCCCGACTCT 000560
000561 TCCTGGTGAA GCATCTGATG CACGTTCCAT CCGGCGCTCA GCTGGGCTTG AGCTGACCAT ACTCCCTGGA GCCTTCTCCC 000640
000641 GAGGTGCGCG GGTGACCTTG GCACATACAG CCATCATGAT GGTACTTTAA GTGGAGGCTG AATCATCTCC CCTTTGAGCT 000720
000721 GCTTGGCACG TGGCTCCCTT GGTGTTCCCC TTTTACTGCC AGGACACTGA GATTTGGAGA GAGTCTCACT CTGTGGTCCA 000800
000801 GGCTGAAGTA CAGTGGCATG ATCCCAGGTC ACTGCAACCC CCACCTCCCG GGTTCAAGTG ATCCTCCTGC CTCAGCCTCC 000880
000881 CGAGTAGCTG GTATTACAGG CGTGTGCCAC AAAGCCTGGC TAAGTTTTGT ATTTTTAGTA GAGACGGGGT TTCACCATGT 000960
000961 TGGCCAGGTT GGTCTCGAAC TCCTGACCTC AAGTGATCCA CTCACTTTGG CCTTTCAACG T