EST comparison indicates 38% of human mRNAs contain possible alternative splice forms

被引：237

作者：

Brett, D

Hanke, J

Lehmann, G

Haase, S

Delbrück, S

Krueger, S

Reich, J

Bork, P

机构：

[1] Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany

[2] AGOWA GmbH, D-12489 Berlin, Germany

[3] European Mol Biol Lab, D-69012 Heidelberg, Germany

[4] GenProfile AG, D-13125 Berlin, Germany

来源：

FEBS LETTERS | 2000年 / 474卷 / 01期

关键词：

alternative splicing; disease gene; database;

D O I：

10.1016/S0014-5793(00)01581-7

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Expressed sequence tag (EST) databases represent a large volume of information on expressed genes including tissue type, expression profile and exon structure. In this study we create an extensive data set of human alternative splicing. We report the analysis of 7867 non-redundant mRNAs, 3011 of which contained alternative splice forms (38% of all mRNAs analysed). From a total of 12572 ESTs 4560 different possible alternative splice forms were detected. Interestingly, 70% of the alternative splice forms correspond to exon deletion events with only 30% exonic insertions. We experimentally verified 19 different splice forms from 16 genes in a total subset of 20 studied; all of the respective genes are of medical relevance. (C) 2000 Federation of European Biochemical Societies.

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页码：83 / 86

页数：4

相关论文

共 16 条

[1] Gapped BLAST and PSI-BLAST: a new generation of protein database search programs [J].

Altschul, SF ;

Madden, TL ;

Schaffer, AA ;

Zhang, JH ;

Zhang, Z ;

Miller, W ;

Lipman, DJ .

NUCLEIC ACIDS RESEARCH, 1997, 25 (17) :3389-3402

[2]

HANKE J, 1999, TRENDS GENET, P15

[3] Frasier syndrome is caused by defective alternative splicing of WT1 leading to an altered ratio of WT1 +/-KTS splice isoforms [J].

Klamt, B ;

Koziell, A ;

Poulat, F ;

Wieacker, P ;

Scambler, P ;

Berta, P ;

Gessler, M .

HUMAN MOLECULAR GENETICS, 1998, 7 (04) :709-714

[4] Frequent alternative splicing of human genes [J].

Mironov, AA ;

Fickett, JW ;

Gelfand, MS .

GENOME RESEARCH, 1999, 9 (12) :1288-1293

[5] Constitutive skipping of alternatively spliced exon 10 in the ATP7A gene abolishes Golgi localization of the Menkes protein and produces the occipital horn syndrome [J].

Qi, M ;

Byers, PH .

HUMAN MOLECULAR GENETICS, 1998, 7 (03) :465-469

[6] SPLIT GENES AND RNA SPLICING [J].

SHARP, PA .

CELL, 1994, 77 (06) :805-815

[7] Association of a human G-protein β3 subunit variant with hypertension [J].

Siffert, W ;

Rosskopf, D ;

Siffert, G ;

Busch, S ;

Moritz, A ;

Erbel, R ;

Sharma, AM ;

Ritz, E ;

Wichmann, HE ;

Jakobs, KH ;

Horsthemke, B .

NATURE GENETICS, 1998, 18 (01) :45-48

[8] CDNA CLONING AND SEQUENCE-ANALYSIS OF BETA-IG-H3, A NOVEL GENE INDUCED IN A HUMAN ADENOCARCINOMA CELL-LINE AFTER TREATMENT WITH TRANSFORMING GROWTH-FACTOR-BETA [J].

SKONIER, J ;

NEUBAUER, M ;

MADISEN, L ;

BENNETT, K ;

PLOWMAN, GD ;

PURCHIO, AF .

DNA AND CELL BIOLOGY, 1992, 11 (07) :511-522

[9] A mutation within exon 14 of the TGFBI (BIGH3) gene on chromosome 5q31 causes an asymmetric, late onset form of lattice corneal dystrophy [J].

Stewart, H ;

Black, GCM ;

Donnai, D ;

Bonshek, RE ;

McCarthy, J ;

Morgan, S ;

Dixon, MJ ;

Ridgway, AAE .

OPHTHALMOLOGY, 1999, 106 (05) :964-970

[10] Individual variation in protein-coding sequences of human genome [J].

Sunyaev, S ;

Hanke, J ;

Brett, D ;

Aydin, A ;

Zastrow, I ;

Lathe, W ;

Bork, P ;

Reich, J .

ADVANCES IN PROTEIN CHEMISTRY, VOL 54: ANALYSIS OF AMINO ACID SEQUENCES, 2000, 54 :409-437