A5042195436- Cancer-related Molecular Pathways
- RNA modifications and cancer
- Cancer-related molecular mechanisms research
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- Cell death mechanisms and regulation
- Virus-based gene therapy research
- Genomics and Chromatin Dynamics
- Cancer Research and Treatments
- MicroRNA in disease regulation
- DNA Repair Mechanisms
- interferon and immune responses
- Ubiquitin and proteasome pathways
- Advanced Breast Cancer Therapies
- Microtubule and mitosis dynamics
- RNA Interference and Gene Delivery
- Molecular Biology Techniques and Applications
- Polyamine Metabolism and Applications
- Caveolin-1 and cellular processes
- Circular RNAs in diseases
- Retinoids in leukemia and cellular processes
- Autophagy in Disease and Therapy
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cancer Risks and Factors
- Wnt/β-catenin signaling in development and cancer
Bar-Ilan University
2012-2024
Weizmann Institute of Science
1990-2020
Peter MacCallum Cancer Centre
2017
The University of Melbourne
2017
Tel Aviv University
2001
Dana-Farber Cancer Institute
1994-1997
Brigham and Women's Hospital
1997
Harvard University
1996-1997
Hebrew University of Jerusalem
1983
University of Chicago
1955
The wild-type (wt) p53 protein is the product of a tumor suppressor gene that frequent target for inactivation in many types tumors. nuclear localization protein, as well additional features, suggest it may be involved regulation expression. To explore this possibility, effects overproduced wt were investigated number systems. Induction growth arrest via antiproliferative effect greatly impaired ability cells to exhibit an increase c-fos mRNA upon serum stimulation. Experiments which...
Mutations in the p53 gene are most frequent cancer. Many mutants possess transforming activity vitro. In cells transformed by such mutants, mutant protein is oligomerized with endogenous cell p53. To determine relevance of oligomerization for transformation, miniproteins containing C-terminal portions were generated. These miniproteins, although carrying no point mutation, at least as efficiently full-length Transforming was coupled ability to oligomerize wild-type p53, well abrogate...
The E2F family of transcription factors has been implicated in the regulation cell proliferation, and E2F-binding sites are present promoters several growth-regulating genes. members functionally regulated, part, by complex formation with one or more nuclear pocket protein family, RB, p107, p130. Pocket likely contributes to normal cellular growth control. While three cloned species E2F, E2F-1, E2F-2, E2F-3, known be targets RB interaction, no yet shown a specific p107 p130 target. Here, we...
The E2F1 transcription factor is a critical downstream target of the tumor suppressor pRB. retinoblastoma (RB) pathway often inactivated in human tumors, resulting deregulated E2F activity that can induce both proliferation and apoptosis. Bcl-2 homology 3 (BH3)-only proteins are pro-apoptotic members protein family trigger apoptosis response to diverse stimuli. We show here up-regulates expression BH3-only PUMA, Noxa, Bim, Hrk/DP5 through direct transcriptional mechanism. Expression E7...
Little is known of the mechanisms controlling G0/G1 transition cell cycle. The induction immediate early gene expression, thought to be important for this process, suggests that key factors preexist in quiescent cells. E2F family transcription likely play an role because DNA-binding activity exists cells, and at least some genes requires intact regulatory promoter sites. Here, we show major G0 primary human T E2F-4, stably bound p130 pocket protein association with a DP heterodimerization...
The E2F family of transcription factors plays a crucial role in cell cycle progression. activity is tightly regulated by number mechanisms, which include the timely synthesis and degradation E2F, interaction with retinoblastoma protein members (“pocket proteins”), association DP heterodimeric partner proteins, phosphorylation E2F/DP complex. Here we report that another mechanism, subcellular localization, important for regulation activity. Unlike E2F-1, -2, or -3, are constitutively nuclear,...
Abstract microRNAs (miR) are small noncoding RNA molecules that have recently emerged as critical regulators of gene expression and often deregulated in cancer. In particular, miRs encoded by the miR-15a, miR-16-1 cluster seem to act tumor suppressors. Here, we evidence related miR-15b, miR-16-2 comprise regulated E2F1, a pivotal transcription factor can induce both proliferation cell death. E2F1 is downstream target suppressor retinoblastoma (RB). The RB pathway inactivated human tumors...
Autophagy genes' expression is upregulated in visceral fat human obesity, associating with obesity-related cardio-metabolic risk. E2F1 (E2F transcription factor 1) was shown cancer cells to transcriptionally regulate autophagy. We hypothesize that regulates adipocyte autophagy endocrine/metabolic dysfunction, thereby, representing non-cell-cycle function of this factor. protein (N=69) and mRNA (N=437) were elevated obese humans, correlating increased ATG5 (autophagy-related 5), MAP1LC3B/LC3B...
LAP2beta is an integral membrane protein of the nuclear envelope involved in chromatin and architecture. Using yeast two-hybrid system, we have cloned a novel LAP2beta-binding protein, mGCL, which contains BTB/POZ domain mouse homologue Drosophila germ-cell-less (GCL) protein. In embryos, GCL was shown to be essential for germ cell formation localized envelope. Here, show that, mammalian cells, co-localized with Nuclear fractionation studies reveal that mGCL acts as matrix component not...
A temperature-sensitive mutant of p53, p53Val-135, was found to be able arrest cell proliferation when overexpressed at 32.5 degrees C. While much the protein cytoplasmic in cells proliferating 37.5 C, it became predominantly nuclear Concomitantly, p53Val-135 destabilized, although not extent seen primary fibroblasts.
Inactivation of p53 and activation telomerase occur in the majority human cancers, raising possibility a link between these two pathways. Overexpression wild-type down-regulates enzymatic activity various cancer cell lines through transcriptional repression its catalytic subunit, reverse transcriptase (hTERT). In this study, we re-evaluated role regulation using isogenic expressing physiological levels p53. We demonstrate that endogenous was able to down-regulate activity, hTERT mRNA levels,...
Abstract Background The human genome encodes thousands of unique long non-coding RNAs (lncRNAs), and these transcripts are emerging as critical regulators gene expression cell fate. However, the transcriptional regulation their is not fully understood. pivotal transcription factor E2F1 which can induce both proliferation death, a downstream target tumor suppressor, RB. retinoblastoma pathway often inactivated in tumors resulting deregulated E2F activity. Results Here, we report that lncRNA...
Despite advances in novel therapeutic approaches for the treatment of glioblastoma (GBM), median survival 12-14 months has not changed significantly. Therefore, there is an imperative need to identify molecular mechanisms that play a role patient survival. Here, we analyzed expression and functions lncRNA, TALNEC2 was identified using RNA seq E2F1-regulated lncRNAs. localized cytosol its cell-cycle dependent. highly expressed GBM with poor prognosis, specimens derived from short-term...