Available Positions

OPEN PhD and Post-Doc positions: Applicants with a strong research background at the intersection of molecular biology, biochemistry, imaging and/or biophysics are encouraged to apply. Experience in microbiology, molecular genetics (including CRISPR/Cas9), advanced imaging platforms (including image analysis) or advanced protein chemistry is advantageous. This is a full-time position available from September 2020 for a period of two years with a possibility of a further extension subject to funding availability. Candidate should send a cover letter and CV (includes a publication list) to Dr. Neta Regev-Rudzki. For any informal inquiries please contact us by email at neta.regev-rudzki@weizmann.ac.il

Size matters, especially in neurons. Differentiated cells in higher eukaryotes exhibit a wide variety of shapes and sizes, while maintaining defined size ranges within cell subtypes. How do they do that? Genome expression must be matched to different cell sizes, with rapidly growing cells likely requiring higher transcriptional and translational output than cells in slow growth or maintenance phase. Neurons exhibit the greatest size differences of any class of cells, with process lengths ranging from a few microns in central interneurons to a meter in human peripheral neurons, and even longer in larger mammals. We are working on mechanisms of cell length and size sensing in neurons and other large cells, and how these mechanisms control growth and regeneration. People can integrate to a range of projects within this theme. For general information on our research please see the group home page at http://www.weizmann.ac.il/Biomolecular_Sciences/Fainzilber/ . Please note that research in our group requires work in animal models (mice, rats).

Position available from March 1, 2021

Size matters, especially in neurons. Differentiated cells in higher eukaryotes exhibit a wide variety of shapes and sizes, while maintaining defined size ranges within cell subtypes. How do they do that? Genome expression must be matched to different cell sizes, with rapidly growing cells likely requiring higher transcriptional and translational output than cells in slow growth or maintenance phase. Neurons exhibit the greatest size differences of any class of cells, with process lengths ranging from a few microns in central interneurons to a meter in human peripheral neurons, and even longer in larger mammals. We are working on mechanisms of cell length and size sensing in neurons and other large cells, and how these mechanisms control growth and regeneration. People can integrate to a range of projects within this theme. For general information on our research please see the group home page at http://www.weizmann.ac.il/Biomolecular_Sciences/Fainzilber/ . Please note that research in our group requires work in animal models (mice, rats).

Position available from March 1, 2021

See my lab web page

See my web page

See short description 

See short description 

See my web page for more details of our work http://www.weizmann.ac.il/Biological_Chemistry/scientist/futerman/ We are an active lab with at least one opening for a rotation/MSC student

Motivated and creative students with background in molecular biology are invited to join our studies of the mechanisms by which signaling by the TNF family contributes to immune defense, to chronic inflammatory and autoimmune diseases and to cancer, and our attempts to derive from this knowledge new ways of therapy. See our website and list of publications for the range of research subjects that we are exploring and for the range of experimental approaches that we are applying. (https://www.weizmann.ac.il/Biomolecular_Sciences/Wallach/home)

Caspase-8, a cysteine protease discovered in our laboratory, is the main proximal signaling enzyme in the activation of the extrinsic cell-death pathway by receptors of the TNF/NGF family. In certain cells it also participates in the regulation of cell growth, differentiation and survival. A number of different human tumors, including small cell lung carcinoma, neuroblastoma, hepatocellular carcinoma, and others, are frequently deficient of caspase-8. This deficiency occurs by several different mechanisms, indicating that it is not a consequence of the oncogenic transformation but is rather causal to it. Applying molecular approaches, cell-culture and animal models we explore the mechanisms accounting for the tumor suppressor role of caspase-8 and the functional consequences of its deletion in cancer cells.

Transgenic and conditional-knockout mouse models are applied to gain better knowledge of the physiological and pathophysiological function of the following signaling proteins that were discovered in our laboratory: (a) Caspase-8, a cysteine protease that we have initially found to serve as the main proximal signaling protein in the initiation of death induction by the receptors (the extrinsic cell-death pathway), yet has more recently found also to serve various non-apoptotic roles. We are mainly interested in further exploring its function in the cross-talk between the epidermal and dermal layers of the skin, in the liver, and in the insulin-producing beta Langerhans cells. (b) NIK, a protein kinase (a MAP3K) that signals for activation of transcription factors of the NF kappa B family, specifically by receptors that, through activation of NF kappa B, control adaptive immunity and lymph-node generation. (c) CYLD, a deubiquitination enzyme that acts specifically to reverse K63-linked ubiquitination and thus serves to arrest initiation of several signaling cascades. (d) IREN, a member of the sorting-nexins family that mediates trafficking of signaling proteins activated by the receptors of the TNF/NGF family.

Type I interferons (IFNs) are proteins produced and secreted in all higher vertebrates as a result of viral and bacterial attacks. Secreted IFNs bind cell surface receptors initiating a cascade of signals that activate cellular protection machineries against pathogens. In addition, specific immune cells are activated to establish long-term defense of the organism. These properties have been successfully exploited for IFNs to serve as a drug for a variety of complex diseases including viral infections, cancer and multiple sclerosis. Despite the proven success of IFN therapies, their use is currently limited because of their severe side effects. Better understanding of the fundamental principles that determine how IFNs induce their responses in a multicellular context will enable to optimize their use. To this end, we will take advantage of polarized epithelial cell layers and spheroids that mimic the intestine tissue. We will generate genetically engineered cell lines to incorporate a range of fluorescence reporters that monitor IFN signaling at the level of receptor engagement, effector activation and feedback regulation. In collaboration with a German partner we will apply these reporters for volumetric imaging of IFN signaling in the multicellular context using highly advanced microscopy techniques that resolve signaling at the single cell level with utmost spatial and temporal resolution. This highly defined and controlled approach will allow us to unravel the rules of IFN signal activation in tissues upon systemic and local stimulation by IFNs and viruses. Next to a fundamental understanding of signal integration in tissues, this work will also have potential medical implications for improving therapeutic application of IFNs.