A5031715730- Cancer Cells and Metastasis
- Immune Response and Inflammation
- Reproductive tract infections research
- Cannabis and Cannabinoid Research
- Cell death mechanisms and regulation
- Prostate Cancer Treatment and Research
- Protease and Inhibitor Mechanisms
- Adipose Tissue and Metabolism
- Cancer, Stress, Anesthesia, and Immune Response
- Peroxisome Proliferator-Activated Receptors
- Cancer-related Molecular Pathways
- Hepatitis B Virus Studies
- Lipid metabolism and biosynthesis
- Reproductive Physiology in Livestock
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Atherosclerosis and Cardiovascular Diseases
- Gout, Hyperuricemia, Uric Acid
- Chemokine receptors and signaling
- Air Quality and Health Impacts
- Nanoparticles: synthesis and applications
- Immunotherapy and Immune Responses
- Immune cells in cancer
- Mesenchymal stem cell research
- Berberine and alkaloids research
- Adipokines, Inflammation, and Metabolic Diseases
Rambam Health Care Campus
2021-2023
University of Haifa
2017
Technion – Israel Institute of Technology
2014
Rappaport Family Institute for Research in the Medical Sciences
2012-2014
Weizmann Institute of Science
2009
Max Planck Institute for Infection Biology
2006-2008
Charité - Universitätsmedizin Berlin
2008
Max Planck Society
2006
We describe a mechanism by which the anti-apoptotic B cell lymphoma 2 (Bcl-2) protein is downregulated to induce apoptosis. ARTS (Sept4_i2) tumor suppressor that promotes death through specifically antagonizing XIAP (X-linked inhibitor of apoptosis). and Bcl-2 reside at outer mitochondrial membrane in living cells. Upon apoptotic induction, brings into ternary complex, allowing promote ubiquitylation degradation Bcl-2. binding involves BH3 domain Lysine 17 serves as main acceptor for...
Host cells infected with obligate intracellular bacteria Chlamydia trachomatis are profoundly resistant to diverse apoptotic stimuli. The molecular mechanisms underlying the block in signaling of is not well understood. Here we investigated mechanism by which apoptosis induced via tumor necrosis factor (TNF) receptor prevented epithelial cells. Infection C. leads up-regulation cellular inhibitor (cIAP)-2, and interfering cIAP-2 sensitized for TNF-induced apoptosis. Interestingly, besides...
It is well accepted that tumor microenvironment essential for cells survival, cancer progression and metastasis. However, the mechanisms by which interact with their surrounding at early stages of development are largely unidentified. The aim this study was to identify specific molecules involved in stromal–epithelial interactions might contribute prostate formation. Here, we show conditioned medium (CM) from immortalized non-transformed epithelial stimulated stromal express cancer-related...
The prostate is composed of a number different cell populations. interaction between them crucial for the development and proper function prostate. However, effect molecular cross talk these cells in course carcinogenesis still unclear. Employing an approach wherein immortalized epithelial human fibroblasts were cocultured, we show that normal associated (NAF) cancer-associated (CAF) differentially influenced growth proliferation cells. Whereas NAFs inhibited but promoted metastatic PC-3...
Nanoparticle research has focused on their toxicity in general, while increasing evidence points to additional specific adverse effects atherosclerosis development. Arterial macrophage cholesterol and triglyceride (TG) accumulation foam cell formation are the hallmark of early atherogenesis, leading cardiovascular events. To investigate vitro atherogenic silicon dioxide (SiO2 ), J774.1 cultured macrophages (murine line) were incubated with SiO2 nanoparticle (SP, d = 12 nm, 0-20 µg/mL),...
Infection with Chlamydophila pneumoniae (Cpn) renders host cells resistant to apoptosis induced by a variety of stimuli. While modulation has been extensively studied in acutely infected Cpn, very little is known on how persistent chlamydial infection influences cell survival. Here we show that epithelial persistently Cpn resist TNFalpha or staurosporine. the activation nuclear factor kappa B (NF-kappaB) and inhibition NF-kappaB chemical inhibitor silencing expression p65 subunit sensitized...
The obligate intracellular human pathogenic bacterium Chlamydia trachomatis has evolved multiple mechanisms to circumvent the host immune system. Infected cells exhibit a profound resistance induction of apoptosis and down-regulate expression major histocompatibility complex class I II molecules evade cytotoxic effect effector cells. Here we demonstrate down-regulation tumor necrosis factor receptor 1 (TNFR1) on surface infected Interestingly, other members TNFR family such as TNFR2 CD95...
Abstract The aim of this study was to analyze the effect and mechanism action macrophage triglyceride accumulation on cellular PON2 expression. Incubation J774A.1 (murine macrophages) with VLDL (0–75 μg protein/mL) significantly dose‐dependently increased mass, reactive oxygen species (ROS) formation, by up 3.3‐ or 1.8‐fold, respectively. expression (mRNA, protein, activity) in cells treated (50 higher 2‐ 3‐fold, as compared control cells. Similar effects were noted upon using THP‐1 (human...
Supplementary Data from Differential Influence of Normal and Cancer-Associated Fibroblasts on the Growth Human Epithelial Cells in an <i>In vitro</i> Cocultivation Model Prostate Cancer
<div>Abstract<p>The prostate is composed of a number different cell populations. The interaction between them crucial for the development and proper function prostate. However, effect molecular cross talk these cells in course carcinogenesis still unclear. Employing an approach wherein immortalized epithelial human fibroblasts were cocultured, we show that normal associated (NAF) cancer-associated (CAF) differentially influenced growth proliferation cells. Whereas NAFs inhibited...
<div>Abstract<p>The prostate is composed of a number different cell populations. The interaction between them crucial for the development and proper function prostate. However, effect molecular cross talk these cells in course carcinogenesis still unclear. Employing an approach wherein immortalized epithelial human fibroblasts were cocultured, we show that normal associated (NAF) cancer-associated (CAF) differentially influenced growth proliferation cells. Whereas NAFs inhibited...
Supplementary Data from Differential Influence of Normal and Cancer-Associated Fibroblasts on the Growth Human Epithelial Cells in an <i>In vitro</i> Cocultivation Model Prostate Cancer