Genomic structure, chromosome location, and alternative splicing of the humanNKG2A gene

1996 ◽  
Vol 44 (4) ◽  
pp. 286-291 ◽  
Author(s):  
Béatrice Plougastel ◽  
Tania Jones ◽  
John Trowsdale
1996 ◽  
Vol 44 (4) ◽  
pp. 286-291 ◽  
Author(s):  
Tania Jones ◽  
B�atrice Plougastel ◽  
John Trowsdale

1998 ◽  
Vol 18 (10) ◽  
pp. 5930-5941 ◽  
Author(s):  
Martyn V. Bell ◽  
Alison E. Cowper ◽  
Marie-Paule Lefranc ◽  
John I. Bell ◽  
Gavin R. Screaton

ABSTRACT Although the splicing of transcripts from most eukaryotic genes occurs in a constitutive fashion, some genes can undergo a process of alternative splicing. This is a genetically economical process which allows a single gene to give rise to several protein isoforms by the inclusion or exclusion of sequences into or from the mature mRNA. CD44 provides a unique example; more than 1,000 possible isoforms can be produced by the inclusion or exclusion of a central tandem array of 10 alternatively spliced exons. Certain alternatively spliced exons have been ascribed specific functions; however, independent regulation of the inclusion or skipping of each of these exons would clearly demand an extremely complex regulatory network. Such a network would involve the interaction of many exon-specific trans-acting factors with the pre-mRNA. Therefore, to assess whether the exons are indeed independently regulated, we have examined the alternative exon content of a large number of individual CD44 cDNA isoforms. This analysis shows that the downstream alternatively spliced exons are favored over those lying upstream and that alternative exons are often included in blocks rather than singly. Using a novel in vivo alternative splicing assay, we show that intron length has a major influence upon the alternative splicing of CD44. We propose a kinetic model in which short introns may overcome the poor recognition of alternatively spliced exons. These observations suggest that for CD44, intron length has been exploited in the evolution of the genomic structure to enable tissue-specific patterns of splicing to be maintained.


Genomics ◽  
1994 ◽  
Vol 24 (3) ◽  
pp. 485-490 ◽  
Author(s):  
Masato Furuichi ◽  
Michihiro C. Yoshida ◽  
Hisanobu Oda ◽  
Tatsurou Tajiri ◽  
Yusaku Nakabeppu ◽  
...  

2003 ◽  
Vol 374 (1) ◽  
pp. 175-184 ◽  
Author(s):  
Daesung SHIN ◽  
Sangjin PARK ◽  
Chankyu PARK

The expression of glutamine synthetase (GS), catalysing the ATP-dependent conversion of glutamate and ammonia into glutamine, is transcriptionally and post-transcriptionally regulated. The genomic structure of dog GS shown in the present study is basically similar to that of other mammals in that it is composed of seven exons and six introns. Using 5′-cRACE (where cRACE stands for circular rapid amplification of cDNA ends) and reverse transcriptase–PCR, we identified an additional exon (120 bp) in the first intron, designated in the present study as exon 1′. By means of alternative splicing, the GS gene produces an altered form of GS transcript with 5′-untranslated region (UTR) containing the exon 1′. This alternative transcript is abundantly expressed in brain, whereas it is found at lower levels in other tissues. In the human and mouse GS genes, extra exons are also found at the corresponding site of the intron 1 but with different sizes. An exon-trapping experiment for the GS gene in COS-7, Madin–Darby canine kidney and SK-N-SH cells revealed that the pattern of alternative splicing is variable in different cell types. The propensity of forming a secondary structure is predicted to be considerably higher in the presence of extra 5′-UTR, suggesting the possibility of a translational effect. To test this, we performed a reporter assay for fusions with different 5′-UTRs, demonstrating that the long form with extra 5′-UTR was translated 20- and 10-fold less than the short one in SK-N-SH and Neuro-2A cells respectively. Similarly, translations of human and mouse transcripts with extra 5′-UTRs were less efficient, showing 6–8-fold reductions in SK-N-SH cells. Furthermore, when we mutated an ATG sequence contained in the exon 1′, the suppression of translation was partially relieved, suggesting that the negative regulation by an extra 5′-UTR is, to some extent, due to an abortive translation from the upstream ATG.


2000 ◽  
Vol 89 (1-2) ◽  
pp. 129-132 ◽  
Author(s):  
E.R. Lemmer ◽  
J.L. Welch ◽  
T. Tsai ◽  
C.L. Keck-Waggoner ◽  
C.-G. Huh ◽  
...  

2003 ◽  
Vol 371 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Gui-Ying NIE ◽  
Anne HAMPTON ◽  
Ying LI ◽  
Jock K. FINDLAY ◽  
Lois A. SALAMONSEN

In the present study, we identified an additional member of the human high-temperature requirement factor A (HtrA) protein family, called pregnancy-related serine protease or HtrA3, which was most highly expressed in the heart and placenta. We cloned the full-length sequences of two forms (long and short) of human HtrA3 mRNA, located the gene on chromosome 4p16.1, determined its genomic structure and revealed how the two mRNA variants are produced through alternative splicing. The alternative splicing was also verified by Northern blotting. Four distinct domains were found for the long form HtrA3 protein: (i) an insulin/insulin-like growth factor binding domain, (ii) a Kazal-type S protease-inhibitor domain, (iii) a trypsin protease domain and (iv) a PDZ domain. The short form is identical to the long form except it lacks the PDZ domain. Comparison of all members of human HtrA proteins, including their isoforms, suggests that both isoforms of HtrA3 represent active serine proteases, that they may have different substrate specificities and that HtrA3 may have similar functions to HtrA1. All three HtrA family members showed very different mRNA-expression patterns in 76 human tissues, indicating a specific function for each. Interestingly, both HtrA1 and HtrA3 are highly expressed in the placenta. Identification of the tissue-specific function of each HtrA family member is clearly of importance.


2000 ◽  
Vol 89 (3-4) ◽  
pp. 264-267 ◽  
Author(s):  
D.S. Holt ◽  
M.B. Powell ◽  
N.K. Rushmere ◽  
B.P. Morgan

2001 ◽  
Vol 93 (3-4) ◽  
pp. 234-238 ◽  
Author(s):  
J. Bolívar ◽  
F.J. García-Cozar ◽  
A. Astola ◽  
C. Iglesias ◽  
C. Pendón ◽  
...  

1998 ◽  
Vol 9 (7) ◽  
pp. 571-576 ◽  
Author(s):  
Tracey M. Reed ◽  
James E. Browning ◽  
Ruthann I. Blough ◽  
Charles V. Vorhees ◽  
David R. Repaske

2009 ◽  
Vol 33 (10) ◽  
pp. 1070-1076 ◽  
Author(s):  
Huan Zhang ◽  
Lingling Wang ◽  
Linsheng Song ◽  
Jianmin Zhao ◽  
Limei Qiu ◽  
...  

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