Affiliation: The Hebrew University
- AP-1 as a regulator of cell life and deathEitan Shaulian
Department of Experimental Medicine and Cancer Research, School of Medicine, The Hebrew University, Jerusalem, 91120, Israel
Nat Cell Biol 4:E131-6. 2002..Mostly, c-Jun is a positive regulator of cell proliferation, whereas JunB has the converse effect. The intricate relationships between the different Jun proteins, their activities and the mechanisms that mediate them will be discussed...
- Jun proteins are starvation-regulated inhibitors of autophagyOrli Yogev
Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel Canada, Hebrew University Hadassah Medical School, Jerusalem, Israel
Cancer Res 70:2318-27. 2010..Most importantly, inhibition of autophagy in starved HeLa cells by JunB enhances apoptotic cell death. We suggest that JunB and c-Jun are regulators of autophagy whose expression responds to autophagy-inducing signals...
- AP-1--The Jun proteins: Oncogenes or tumor suppressors in disguise?Eitan Shaulian
Department of Biochemistry and Molecular Biology, The Institute for Medical Research Israel Canada, The Hebrew University Hadassah Medical School, Jerusalem, Israel
Cell Signal 22:894-9. 2010..These recent findings suggest that the role of each Jun protein in neoplasia as well as in cellular survival should be examined in a context-dependent manner...
- DNA damage-dependent translocation of B23 and p19 ARF is regulated by the Jun N-terminal kinase pathwayOrli Yogev
Department of Experimental Medicine and Cancer Research, Hebrew University Medical School, Jerusalem, Israel
Cancer Res 68:1398-406. 2008..In senescent cells, JNK activity and c-Jun levels are reduced concomitantly with ARF nucleolar accumulation, and UV radiation does not cause the translocation of ARF...
- Fumarase: a mitochondrial metabolic enzyme and a cytosolic/nuclear component of the DNA damage responseOhad Yogev
Department of Microbiology and Molecular Genetics, IMRIC, Faculty of Medicine, Hebrew University, Jerusalem, Israel
PLoS Biol 8:e1000328. 2010..This study shows an exciting crosstalk between primary metabolism and the DNA damage response, thereby providing a scenario for metabolic control of tumor propagation...
- Transcriptional repression of c-Jun's E3 ubiquitin ligases contributes to c-Jun induction by UVShira Anzi
Department of Experimental Medicine and Cancer Research, Hebrew University Medical School, Ein Kerem, Jerusalem, Israel
Cell Signal 20:862-71. 2008....
- Metalloprotease type III effectors that specifically cleave JNK and NF-κBKobi Baruch
Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University of Jerusalem, Faculty of Medicine, Jerusalem, Israel
EMBO J 30:221-31. 2011..This is a remarkable example of a pathogen using multiple effectors to manipulate systematically the host inflammatory response signalling network...
- Jun proteins inhibit autophagy and induce cell deathOrli Yogev
Department of Biochemistry and Molecular Biology, IMRIC, Hebrew University Hadassah Medical School, Jerusalem, Israel
Autophagy 6:566-7. 2010..Deregulation of JunB expression when autophagy is specifically required, tilts the fate of starved cells to apoptosis...
- Induction of transcriptionally active Jun proteins regulates drug-induced senescenceOrli Yogev
Department of Experimental Medicine and Cancer Research, Hebrew University Medical School, Hadassah Ein Kerem, Jerusalem 91120, Israel
J Biol Chem 281:34475-83. 2006..The effect of HU treatment, which regulates the intricate web of AP-1 transcription, depends on the balance between c-Jun and JunB activities...