Please use this identifier to cite or link to this item: https://doi.org/10.1073/pnas.1320815111/-/DCSupplemental
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dc.titleHypoxia-induced and calpain-dependent cleavage of filamin A regulates the hypoxic response
dc.contributor.authorZheng, X.
dc.contributor.authorZhou, A.-X.
dc.contributor.authorRouhi, P.
dc.contributor.authorUramoto, H.
dc.contributor.authorBorén, J.
dc.contributor.authorCao, Y.
dc.contributor.authorPereira, T.
dc.contributor.authorAkyürek, L.M.
dc.contributor.authorPoellinger, L.
dc.date.accessioned2014-12-12T07:32:10Z
dc.date.available2014-12-12T07:32:10Z
dc.date.issued2014-02-18
dc.identifier.citationZheng, X., Zhou, A.-X., Rouhi, P., Uramoto, H., Borén, J., Cao, Y., Pereira, T., Akyürek, L.M., Poellinger, L. (2014-02-18). Hypoxia-induced and calpain-dependent cleavage of filamin A regulates the hypoxic response. Proceedings of the National Academy of Sciences of the United States of America 111 (7) : 2560-2565. ScholarBank@NUS Repository. https://doi.org/10.1073/pnas.1320815111/-/DCSupplemental
dc.identifier.issn00278424
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/115763
dc.description.abstractThe cellular response to hypoxia is regulated by hypoxia-inducible factor-1a and -2a (HIF-1a and -2a). We have discovered that filamin A (FLNA), a large cytoskeletal actin-binding protein, physically interacts with HIF-1a and promotes tumor growth and angiogenesis. Hypoxia induces a calpain-dependent cleavage of FLNA to generate a naturally occurring C-terminal fragment that accumulates in the cell nucleus. This fragment interacts with the N-terminal portion of HIF-1a spanning amino acid residues 1-390 but not with HIF-2a. In hypoxia this fragment facilitates the nuclear localization of HIF-1a, is recruited to HIF-1a target gene promoters, and enhances HIF-1a function, resulting in up-regulation of HIF-1a target gene expression in a hypoxia-dependent fashion. These results unravel an important mechanism that selectively regulates the nuclear accumulation and function of HIF-1a and potentiates angiogenesis and tumor progression.
dc.sourceScopus
dc.subjectCancer
dc.subjectSignal transduction
dc.subjectSubcellular localization
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.description.doi10.1073/pnas.1320815111/-/DCSupplemental
dc.description.sourcetitleProceedings of the National Academy of Sciences of the United States of America
dc.description.volume111
dc.description.issue7
dc.description.page2560-2565
dc.description.codenPNASA
dc.identifier.isiutNOT_IN_WOS
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