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Hypoxia reduces MAX expression in endothelial cells by unproductive splicing
Author(s) -
Kemmerer Katrin,
Weigand Julia E.
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.11.011
Subject(s) - gene isoform , alternative splicing , microbiology and biotechnology , rna splicing , nonsense mediated decay , downregulation and upregulation , hypoxia (environmental) , biology , heterologous , chemistry , biochemistry , gene , rna , organic chemistry , oxygen
The MYC–MAX–MXD network is involved in the regulation of cell differentiation and proliferation. Hypoxia affects the expression levels of several members of this network, but changes specific to MAX expression have so far not been shown. We found that in endothelial cells, hypoxia induces alternative splicing of MAX , thereby increasing the expression of two MAX isoforms that differ from the wild type in their 3′ end. Isoform C is degraded by nonsense‐mediated decay and isoform E encodes a highly unstable protein. The instability of isoform E is conferred by 36 isoform‐specific amino acids, which have the capacity to destabilize heterologous proteins. Both splicing events are therefore unproductive and serve the purpose to downregulate the wild type protein.