A putative role for human BFK in DNA damage-induced apoptosis
dc.contributor.author | Özören, Nesrin | en_US |
dc.contributor.author | Inohara, Naohiro | en_US |
dc.contributor.author | Núñez, Gabriel | en_US |
dc.date.accessioned | 2009-08-12T15:34:36Z | |
dc.date.available | 2010-09-01T19:24:05Z | en_US |
dc.date.issued | 2009-07 | en_US |
dc.identifier.citation | ÖzÖren, Nesrin; Inohara, Naohiro; NÚÑez, Gabriel (2009). "A putative role for human BFK in DNA damage-induced apoptosis." Biotechnology Journal 4(7): 1046-1054. <http://hdl.handle.net/2027.42/63538> | en_US |
dc.identifier.issn | 1860-6768 | en_US |
dc.identifier.issn | 1860-7314 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/63538 | |
dc.description.abstract | Human BFK (BCL-2 family kin) is a novel pro-apoptotic BCL-2 family member specifically expressed in the gastrointestinal tract. BFK has the characteristic BH3 domain, which was shown to be essential for the apoptosis-inducing activity of pro-apoptotic BCL-2 family members. When overexpressed, BFK interacts with BCL-XL and BCL-W but not BCL-2 or BAD in co-immunoprecipitations studies. We find that BFK exhibits striking similarity to BID in the way it is activated through cleavage during apoptosis. The endogenous and cleaved versions of BFK are readily recognized by the rabbit and mouse sera raised against human BFK. An ideal caspase 3 or 7 target sequence, DEVD (amino acids 38–41), is evident N-terminal to the BH3 domain. A recombinant version of the protein containing all residues downstream of the putative caspase cleavage site induces apoptosis in human colon cancer cells, HCT116, and in wild-type mouse embryonic fibroblasts (MEFs), which can be reversed by co-expression of BCL-XL or BCL-W. BFK becomes activated through caspase-dependent cleavage during DNA damage-induced apoptosis. The cleaved form of the protein is dependent on the presence of BAX or BAK for its ability to induce apoptosis, since BAX –/– -BAK –/– double-knockout MEFs are completely resistant to BFK-induced apoptosis. | en_US |
dc.format.extent | 1285203 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | WILEY-VCH Verlag | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Biochemistry and Biotechnology | en_US |
dc.title | A putative role for human BFK in DNA damage-induced apoptosis | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Biomedical Engineering | en_US |
dc.subject.hlbsecondlevel | Biomedical Engineering | en_US |
dc.subject.hlbtoplevel | Engineering | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationum | Department of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, USA | en_US |
dc.contributor.affiliationother | Department of Molecular Biology and Genetics, Apoptosis and Cancer Immunology Laboratory (AKIL), BoğaziÇi University, Istanbul, Turkey ; BoğaziÇi University, Department of Molecular Biology and Genetics, Apoptosis and Cancer Immunology Laboratory (AKIL), 34342 Bebek-Istanbul, Turkey, Fax: +90-212-287-2468 | en_US |
dc.identifier.pmid | 19557800 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/63538/1/1046_ftp.pdf | |
dc.identifier.doi | 10.1002/biot.200900091 | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
Files in this item
Remediation of Harmful Language
The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.
Accessibility
If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.