Antigenic determinants encoded by alternatively spliced exons of CD45 are determined by the polypeptide but influenced by glycosylation

1994 ◽  
Vol 6 (12) ◽  
pp. 1875-1881 ◽  
Author(s):  
Jason G. Cyster ◽  
Deborah Fowell ◽  
A. Neil Barclay
Keyword(s):  
Antigenic Determinants ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons

scholarly journals Identification of the alternatively spliced exons of murine CD45 (T200) required for reactivity with B220 and other T200-restricted antibodies.

1989 ◽  
Vol 169 (3) ◽  
pp. 1179-1184 ◽  
Author(s):  
P Johnson ◽  
L Greenbaum ◽  
K Bottomly ◽  
I S Trowbridge
Keyword(s):  
Cell Lines ◽  
Antigenic Site ◽  
Antigenic Determinants ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons

Cell lines expressing specific variants of murine CD45 (T200) were established by infection with retroviral constructs of four cDNAs encoding different forms of CD45. These lines were then used to determine which sequences encoded by alternatively spliced exons of CD45 were required to generate antigenic determinants recognized by anti-CD45 mAbs. The binding of two B220 antibodies (14.8 and RA32C2) to CD45 was dependent on the expression of the first alternatively spliced exon (exon A). A third B220 antibody, RA3-6B2, did not bind to any of the forms of CD45 expressed on fibroblasts. A newly defined anti-CD45R antibody, C363.16A, reacts with an antigenic site dependent upon the expression of the second alternatively spliced exon, exon B.

scholarly journals Positive Selection in Alternatively Spliced Exons of Human Genes

2008 ◽  
Vol 83 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Vasily E. Ramensky ◽  
Ramil N. Nurtdinov ◽  
Alexei D. Neverov ◽  
Andrei A. Mironov ◽  
Mikhail S. Gelfand
Keyword(s):  
Positive Selection ◽  
Human Genes ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons

Elements regulating an alternatively spliced exon of the rat fibronectin gene

1993 ◽  
Vol 13 (9) ◽  
pp. 5301-5314 ◽  
Author(s):  
G S Huh ◽  
R O Hynes
Keyword(s):  
Splice Sites ◽  
Cell Type ◽  
Long Distance ◽  
Sequence Elements ◽  
Alternatively Spliced ◽  
A Cell ◽  
Cell Type Specific ◽  
Alternatively Spliced Exons

We have investigated the regulation of splicing of one of the alternatively spliced exons in the rat fibronectin gene, the EIIIB exon. This 273-nucleotide exon is excluded by some cells and included to various degrees by others. We find that EIIIB is intrinsically poorly spliced and that both its exon sequences and its splice sites contribute to its poor recognition. Therefore, cells which recognize the EIIIB exon must have mechanisms for improving its splicing. Furthermore, in order for EIIB to be regulated, a balance must exist between the EIIIB splice sites and those of its flanking exons. Although the intron upstream of EIIIB does not appear to play a role in the recognition of EIIIB for splicing, the intron downstream contains sequence elements which can promote EIIIB recognition in a cell-type-specific fashion. These elements are located an unusually long distance from the exon that they regulate, more than 518 nucleotides downstream from EIIIB, and may represent a novel mode of exon regulation.

scholarly journals Mutations primarily alter the inclusion of alternatively spliced exons

2020 ◽  
Author(s):  
Pablo Baeza-Centurion ◽  
Belén Miñana ◽  
Juan Valcárcel ◽  
Ben Lehner
Keyword(s):  
Genome Sequence ◽  
Sequence Variation ◽  
Common Mechanism ◽  
Genetic Analyses ◽  
Exon Inclusion ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons ◽  
Mature Mrnas

AbstractGenetic analyses and systematic mutagenesis have revealed that synonymous, non-synonymous and intronic mutations frequently alter the inclusion levels of alternatively spliced exons, consistent with the concept that altered splicing might be a common mechanism by which mutations cause disease. However, most exons expressed in any cell are highly-included in mature mRNAs. Here, by performing deep mutagenesis of highly-included exons and by analysing the association between genome sequence variation and exon inclusion across the transcriptome, we report that mutations only very rarely alter the inclusion of highly-included exons. This is true for both exonic and intronic mutations as well as for perturbations in trans. Therefore, mutations that affect splicing are not evenly distributed across primary transcripts but are focussed in and around alternatively spliced exons with intermediate inclusion levels. These results provide a resource for prioritising synonymous and other variants as disease-causing mutations.

scholarly journals Novel alternatively-spliced exons of the VRK2 gene in mouse brain and microglial cells

2020 ◽  
Vol 47 (7) ◽  
pp. 5127-5136
Author(s):  
Salsabil Almarzooq ◽  
Jaedeok Kwon ◽  
Ashleigh Willis ◽  
John Craig ◽  
Brian J. Morris
Keyword(s):  
Mouse Brain ◽  
Microglial Cells ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons

scholarly journals The gene structure and hypervariability of the complete Penaeus monodon Dscam gene

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kantamas Apitanyasai ◽  
Shiao-Wei Huang ◽  
Tze Hann Ng ◽  
Shu-Ting He ◽  
Yu-Hsun Huang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Gene Structure ◽  
Transmembrane Domain ◽  
Stop Codon ◽  
Penaeus Monodon ◽  
Cytoplasmic Tail ◽  
Extracellular Region ◽  
Alternatively Spliced ◽  
Alternatively Spliced Exons ◽  
Selection Of

Abstract Using two advanced sequencing approaches, Illumina and PacBio, we derive the entire Dscam gene from an M2 assembly of the complete Penaeus monodon genome. The P. monodon Dscam (PmDscam) gene is ~266 kbp, with a total of 44 exons, 5 of which are subject to alternative splicing. PmDscam has a conserved architectural structure consisting of an extracellular region with hypervariable Ig domains, a transmembrane domain, and a cytoplasmic tail. We show that, contrary to a previous report, there are in fact 26, 81 and 26 alternative exons in N-terminal Ig2, N-terminal Ig3 and the entirety of Ig7, respectively. We also identified two alternatively spliced exons in the cytoplasmic tail, with transmembrane domains in exon variants 32.1 and 32.2, and stop codons in exon variants 44.1 and 44.2. This means that alternative splicing is involved in the selection of the stop codon. There are also 7 non-constitutive cytoplasmic tail exons that can either be included or skipped. Alternative splicing and the non-constitutive exons together produce more than 21 million isoform combinations from one PmDscam locus in the P. monodon gene. A public-facing database that allows BLAST searches of all 175 exons in the PmDscam gene has been established at http://pmdscam.dbbs.ncku.edu.tw/.

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