Identification of β1C-2, a novel variant of the integrin β1 subunit generated by utilization of an alternative splice acceptor site in exon C
Autor: | Staffan Johansson, Reinhard Fässler, Gunbj⊘rg Svineng |
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Rok vydání: | 1998 |
Předmět: |
Transcription
Genetic T-Lymphocytes Protein subunit Molecular Sequence Data Alu element Biology Polymerase Chain Reaction Biochemistry Cell Line Mice Exon Sequence Homology Nucleic Acid Complementary DNA Animals Humans splice Amino Acid Sequence RNA Messenger Molecular Biology Cells Cultured DNA Primers Splice site mutation Base Sequence Sequence Homology Amino Acid Integrin beta1 Alternative splicing Genetic Variation Exons Cell Biology Molecular biology Recombinant Proteins Alternative Splicing Organ Specificity RNA splicing Sequence Alignment Research Article |
Zdroj: | Biochemical Journal. 330:1255-1263 |
ISSN: | 1470-8728 0264-6021 |
DOI: | 10.1042/bj3301255 |
Popis: | A new splice variant of the human integrin subunit beta1 has been identified and designated beta1C-2. It differs from the previously reported beta1C (in this report designated beta1C-1) by 18 nucleotides, and is generated by splicing from exon 6 to an alternative splice acceptor site within exon C, causing an in-frame deletion of six amino acids of the cytoplasmic region of beta1C-1. The beta1C-2 mRNA is present in several human cell lines and tissues at low levels, similarly to beta1C-1. In peripheral T-lymphocytes, beta1C-2 is the selectively expressed isoform. Neither beta1C-1 nor beta1C-2 mRNA could be detected in mouse tissues, and Southern hybridization of a mouse genomic beta1 clone with a human exon-C-specific probe failed to identify a corresponding mouse exon. The antisense orientation of exon C is highly homologous to an Alu element. Since Alu elements are restricted to primates, the beta1C-1 and beta1C-2 variants of the integrin subunit beta1 are specific for these species. The protein coded for by the beta1C-2 cDNA can be expressed and localized to the surface of beta1 deficient mouse cells. However, while stable transformed clones expressing high levels of the beta1A were commonly found, the beta1C-1 and beta1C-2 expressing clones expressed barely detectable amounts of the beta1 protein. Hence, high levels of beta1C-2 may be incompatible with cell proliferation, as previously suggested for beta1C-1. |
Databáze: | OpenAIRE |
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