Difference between pages "Recurring Mutations Found by Full length Sequencing of an Acute Myeloid Leukemia Genome (AML)" and "ATAD5 -YJ code:309ir"

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(Difference between pages)
imported>Larasmithe
 
imported>Yeong Jae Kim
 
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<strong><font size="4">Recurring Mutations Found by Sequencing an Acute Myeloid Leukemia Genome.&nbsp;<br />
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<h1><span style="font-size:12px">1. ATAD5&nbsp;ATPase family, AAA domain containing 5 [&nbsp;<em>Homo sapiens</em>&nbsp;(human) ]</span></h1>
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Mardis ER, Ding L, Dooling DJ, Larson DE, McLellan MD, Chen K, Koboldt DC, Fulton RS, Delehaunty KD, McGrath SD, Fulton LA, Locke DP, Magrini VJ, Abbott RM, Vickery TL, Reed JS, Robinson JS, Wylie T, Smith SM, Carmichael L, Eldred JM, Harris CC, Walker J, Peck JB, Du F, Dukes AF, Sanderson GE, Brummett AM, Clark E, McMichael JF, Meyer RJ, Schindler JK, Pohl CS, Wallis JW, Shi X, Lin L, Schmidt H, Tang Y, Haipek C, Wiechert ME, Ivy JV, Kalicki J, Elliott G, Ries RE, Payton JE, Westervelt P, Tomasson MH, Watson MA, Baty J, Heath S, Shannon WD, Nagarajan R, Link DC, Walter MJ, Graubert TA, Dipersio JF, Wilson RK, Ley TJ.&nbsp;<br />
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<p><span style="font-size:12px">Gene ID: 79915, updated on 26-May-2016</span></p>
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From the Departments of Genetics (E.R.M., L.D., V.J.M., R.K.W., T.J.L.), Medicine (R.E.R., P.W., M.H.T., S.H., W.D.S., D.C.L., M.J.W., T.A.G., J.F.D., T.J.L.), and Pathology and Immunology (J.E.P., M.A.W., R.N.); the Genome Center (E.R.M., L.D., D.J.D., D.E.L., M.D.M., K.C., D.C.K., R.S.F., K.D.D., S.D.M., L.A.F., D.P.L., V.J.M., R.M.A., T.L.V., J.S. Reed, J.S. Robinson, T.W., S.M.S., L.C., J.M.E., C.C.H., J.W., J.B.P., F.D., A.F.D., G.E.S., A.M.B., E.C., J.F.M., R.J.M., J.K.S., C.S.P., J.W.W., X.S., L.L., H.S., Y.T., C.H., M.E.W., J.V.I., J.K., G.E., M.A.W., R.K.W., T.J.L.); Siteman Cancer Center (P.W., M.H.T., M.A.W., S.H., W.D.S., R.N., D.C.L., M.J.W., T.A.G., J.F.D., R.K.W., T.J.L.); and the Division of Biostatistics (J.B.) - all at Washington University, St. Louis. This article (10.1056/NEJMoa0903840) was published on August 5, 2009, at NEJM.org. <br />
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<p><span style="font-size:12px">&lt;i want to understand about PCNA and ATAD5 role. so pick that&gt;</span></p>
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<strong>BACKGROUND</strong>: The full complement of DNA mutations that are responsible for the pathogenesis of acute myeloid leukemia (AML) is not yet known.&nbsp;<br />
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<p><span style="font-size:12px">source comes from. http://www.ncbi.nlm.nih.gov/protein/26080431?report=fasta</span></p>
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<strong>METHODS</strong>: We used massively parallel DNA sequencing to obtain a very high level of coverage (approximately 98%) of a primary, cytogenetically normal, de novo genome for AML with minimal maturation (AML-M1) and a matched normal skin genome.&nbsp;<br />
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<strong>RESULTS</strong>: We identified 12 acquired (somatic) mutations within the coding sequences of genes and 52 somatic point mutations in conserved or regulatory portions of the genome.&nbsp;<br />
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<h1>ATPase family AAA domain-containing protein 5 [Homo sapiens]</h1>
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All mutations appeared to be heterozygous and present in nearly all cells in the tumor sample.&nbsp;<br />
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Four of the 64 mutations occurred in at least 1 additional AML sample in 188 samples that were tested.&nbsp;<br />
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<p>NCBI Reference Sequence: NP_079133.3</p>
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Mutations in NRAS and NPM1 had been identified previously in patients with AML, but two other mutations had not been identified. One of these mutations, in the IDH1 gene, was present in 15 of 187 additional AML genomes tested and was strongly associated with normal cytogenetic status; it was present in 13 of 80 cytogenetically normal samples (16%).&nbsp;<br />
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The other was a nongenic mutation in a genomic region with regulatory potential and conservation in higher mammals; we detected it in one additional AML tumor.&nbsp;<br />
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<pre>
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The AML genome that we sequenced contains approximately 750 point mutations, of which only a small fraction are likely to be relevant to pathogenesis.&nbsp;<br />
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&gt;gi|26080431|ref|NP_079133.3| ATPase family AAA domain-containing protein 5 [Homo sapiens]
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<strong>CONCLUSIONS</strong>: By comparing the sequences of tumor and skin genomes of a patient with AML-M1, we have identified recurring mutations that may be relevant for pathogenesis.&nbsp;<br />
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MVGVLAMAAAAAPPPVKDCEIEPCKKRKKDDDTSTCKTITKYLSPLGKTRDRVFAPPKPSNILDYFRKTS
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PTNEKTQLGKECKIKSPESVPVDSNKDCTTPLEMFSNVEFKKKRKRVNLSHQLNNIKTENEAPIEISSDD
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<strong>69.9 billion base pairs were sequenced (23.3<font face="arial,helvetica">x</font> haploid coverage)</strong><br />
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SKEDYSLNNDFVESSTSVLRYKKQVEVLAENIQDTKSQPNTMTSLQNSKKVNPKQGTTKNDFKKLRKRKC
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RDVVDLSESLPLAEELNLLKKDGKDTKQMENTTSHANSRDNVTEAAQLNDSIITVSYEEFLKSHKENKVE
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Copyright 2009 Massachusetts Medical Society.&nbsp;<br />
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EIPDSTMSICVPSETVDEIVKSGYISESENSEISQQVRFKTVTVLAQVHPIPPKKTGKIPRIFLKQKQFE
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<br />
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MENSLSDPENEQTVQKRKSNVVIQEEELELAVLEAGSSEAVKPKCTLEERQQFMKAFRQPASDALKNGVK
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<a href="http://content.nejm.org/cgi/content/full/NEJMoa0903840">http://content.nejm.org/cgi/content/full/NEJMoa0903840</a><br />
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KSSDKQKDLNEKCLYEVGRDDNSKKIMENSGIQMVSKNGNLQLHTDKGSFLKEKNKKLKKKNKKTLDTGA
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IPGKNREGNTQKKETTFFLKEKQYQNRMSLRQRKTEFFKSSTLFNNESLVYEDIANDDLLKVSSLCNNNK
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<a href="http://content.nejm.org/cgi/reprint/NEJMoa0903840v1.pdf">http://content.nejm.org/cgi/reprint/NEJMoa0903840v1.pdf</a><br />
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LSRKTSIPVKDIKLTQSKAESEASLLNVSTPKSTRRSGRISSTPTTETIRGIDSDDVQDNSQLKASTQKA
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ANLSEKHSLYTAELITVPFDSESPIRMKFTRISTPKKSKKKSNKRSEKSEATDGGFTSQIRKASNTSKNI
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<a href="http://www.ncbi.nlm.nih.gov/pubmed/19657110?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum">http://www.ncbi.nlm.nih.gov/pubmed/19657110?ordinalpos=1&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum</a>
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SKAKQLIEKAKALHISRSKVTEEIAIPLRRSSRHQTLPERKKLSETEDSVIIIDSSPTALKHPEKNQKKL
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QCLNDVLGKKLNTSTKNVPGKMKVAPLFLVRKAQKAADPVPSFDESSQDTSEKSQDCDVQCKAKRDFLMS
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GLPDLLKRQIAKKAAALDVYNAVSTSFQRVVHVQQKDDGCCLWHLKPPSCPLLTKFKELNTKVIDLSKCG
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IALGEFSTLNSKLKSGNSAAVFMRTRKEFTEEVRNLLLEEIRWSNPEFSLKKYFPLLLKKQIEHQVLSSE
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CHSKQELEADVSHKETKRKLVEAENSKSKRKKPNEYSKNLEKTNRKSEELSKRNNSSGIKLDSSKDSGTE
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DMLWTEKYQPQTASELIGNELAIKKLHSWLKDWKRRAELEERQNLKGKRDEKHEDFSGGIDFKGSSDDEE
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ESRLCNTVLITGPTGVGKTAAVYACAQELGFKIFEVNASSQRSGRQILSQLKEATQSHQVDKQGVNSQKP
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CFFNSYYIGKSPKKISSPKKVVTSPRKVPPPSPKSSGPKRALPPKTLANYFKVSPKPKNNEEIGMLLENN
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KGIKNSFEQKQITQTKSTNATNSNVKDVGAEEPSRKNATSLILFEEVDVIFDEDAGFLNAIKTFMATTKR
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PVILTTSDPTFSLMFDGCFEEIKFSTPSLLNVASYLQMICLTENFRTDVKDFVTLLTANTCDIRKSILYL
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QFWIRSGGGVLEERPLTLYRGNSRNVQLVCSEHGLDNKIYPKNTKKKRVDLPKCDSGCAETLFGLKNIFS
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PSEDLFSFLKHKITMKEEWHKFIQLLTEFQMRNVDFLYSNLEFILPLPVDTIPETKNFCGPSVTVDASAA
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TKSMNCLARKHSEREQPLKKSQKKKQKKTLVILDDSDLFDTDLDFPDQSISLSSVSSSSNAEESKTGDEE
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SKARDKGNNPETKKSIPCPPKTTAGKKCSALVSHCLNSLSEFMDNMSFLDALLTDVREQNKYGRNDFSWT
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NGKVTSGLCDEFSLESNDGWTSQSSGELKAAAEALSFTKCSSAISKALETLNSCKKLGRDPTNDLTFYVS
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QKRNNVYFSQSAANLDNAWKRISVIKSVFSSRSLLYVGNRQASIIEYLPTLRNICKTEKLKEQGKSKRRF
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LHYFEGIHLDIPKETVNTLAADFP</pre>
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<p>&nbsp;</p>
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<p>&nbsp;</p>
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<p>result :&nbsp;http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/</p>
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<p>&nbsp; &nbsp; &nbsp; &nbsp; &nbsp;&nbsp;http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/</p>
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<p>&nbsp; &nbsp; &nbsp; &nbsp; &nbsp;<a href="http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/S274747_results.tar.bz2">http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/S274747_results.tar.bz2</a></p>

Revision as of 20:03, 11 June 2016

1. ATAD5 ATPase family, AAA domain containing 5 [ Homo sapiens (human) ]

Gene ID: 79915, updated on 26-May-2016

<i want to understand about PCNA and ATAD5 role. so pick that>

source comes from. http://www.ncbi.nlm.nih.gov/protein/26080431?report=fasta

ATPase family AAA domain-containing protein 5 [Homo sapiens]

NCBI Reference Sequence: NP_079133.3

>gi|26080431|ref|NP_079133.3| ATPase family AAA domain-containing protein 5 [Homo sapiens]
MVGVLAMAAAAAPPPVKDCEIEPCKKRKKDDDTSTCKTITKYLSPLGKTRDRVFAPPKPSNILDYFRKTS
PTNEKTQLGKECKIKSPESVPVDSNKDCTTPLEMFSNVEFKKKRKRVNLSHQLNNIKTENEAPIEISSDD
SKEDYSLNNDFVESSTSVLRYKKQVEVLAENIQDTKSQPNTMTSLQNSKKVNPKQGTTKNDFKKLRKRKC
RDVVDLSESLPLAEELNLLKKDGKDTKQMENTTSHANSRDNVTEAAQLNDSIITVSYEEFLKSHKENKVE
EIPDSTMSICVPSETVDEIVKSGYISESENSEISQQVRFKTVTVLAQVHPIPPKKTGKIPRIFLKQKQFE
MENSLSDPENEQTVQKRKSNVVIQEEELELAVLEAGSSEAVKPKCTLEERQQFMKAFRQPASDALKNGVK
KSSDKQKDLNEKCLYEVGRDDNSKKIMENSGIQMVSKNGNLQLHTDKGSFLKEKNKKLKKKNKKTLDTGA
IPGKNREGNTQKKETTFFLKEKQYQNRMSLRQRKTEFFKSSTLFNNESLVYEDIANDDLLKVSSLCNNNK
LSRKTSIPVKDIKLTQSKAESEASLLNVSTPKSTRRSGRISSTPTTETIRGIDSDDVQDNSQLKASTQKA
ANLSEKHSLYTAELITVPFDSESPIRMKFTRISTPKKSKKKSNKRSEKSEATDGGFTSQIRKASNTSKNI
SKAKQLIEKAKALHISRSKVTEEIAIPLRRSSRHQTLPERKKLSETEDSVIIIDSSPTALKHPEKNQKKL
QCLNDVLGKKLNTSTKNVPGKMKVAPLFLVRKAQKAADPVPSFDESSQDTSEKSQDCDVQCKAKRDFLMS
GLPDLLKRQIAKKAAALDVYNAVSTSFQRVVHVQQKDDGCCLWHLKPPSCPLLTKFKELNTKVIDLSKCG
IALGEFSTLNSKLKSGNSAAVFMRTRKEFTEEVRNLLLEEIRWSNPEFSLKKYFPLLLKKQIEHQVLSSE
CHSKQELEADVSHKETKRKLVEAENSKSKRKKPNEYSKNLEKTNRKSEELSKRNNSSGIKLDSSKDSGTE
DMLWTEKYQPQTASELIGNELAIKKLHSWLKDWKRRAELEERQNLKGKRDEKHEDFSGGIDFKGSSDDEE
ESRLCNTVLITGPTGVGKTAAVYACAQELGFKIFEVNASSQRSGRQILSQLKEATQSHQVDKQGVNSQKP
CFFNSYYIGKSPKKISSPKKVVTSPRKVPPPSPKSSGPKRALPPKTLANYFKVSPKPKNNEEIGMLLENN
KGIKNSFEQKQITQTKSTNATNSNVKDVGAEEPSRKNATSLILFEEVDVIFDEDAGFLNAIKTFMATTKR
PVILTTSDPTFSLMFDGCFEEIKFSTPSLLNVASYLQMICLTENFRTDVKDFVTLLTANTCDIRKSILYL
QFWIRSGGGVLEERPLTLYRGNSRNVQLVCSEHGLDNKIYPKNTKKKRVDLPKCDSGCAETLFGLKNIFS
PSEDLFSFLKHKITMKEEWHKFIQLLTEFQMRNVDFLYSNLEFILPLPVDTIPETKNFCGPSVTVDASAA
TKSMNCLARKHSEREQPLKKSQKKKQKKTLVILDDSDLFDTDLDFPDQSISLSSVSSSSNAEESKTGDEE
SKARDKGNNPETKKSIPCPPKTTAGKKCSALVSHCLNSLSEFMDNMSFLDALLTDVREQNKYGRNDFSWT
NGKVTSGLCDEFSLESNDGWTSQSSGELKAAAEALSFTKCSSAISKALETLNSCKKLGRDPTNDLTFYVS
QKRNNVYFSQSAANLDNAWKRISVIKSVFSSRSLLYVGNRQASIIEYLPTLRNICKTEKLKEQGKSKRRF
LHYFEGIHLDIPKETVNTLAADFP

 

 

result : http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/

          http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/

         http://zhanglab.ccmb.med.umich.edu/I-TASSER/output/S274747/S274747_results.tar.bz2

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