Available Positions

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See short description 

Regulation of gene expression at the transcriptional and translational levels is fundamental to all biological activities and is frequently altered in disease states. Our broad research interests are (i) to elucidate how the transcription and translation processes control the cellular response to enviromental stimuli; (ii) to reveal the connections between the transcription and translation processes and (iii) to develop tools to manipulate these processes for potential treatment of cancer, chronic inflammation and neurodegenrative diseases.

Regulation of gene expression at the transcriptional and translational levels is fundamental to all biological activities and is frequently altered in disease states. Our broad research interests are (i) to elucidate how the transcription and translation processes control the cellular response to enviromental stimuli; (ii) to reveal the connections between the transcription and translation processes and (iii) to develop tools to manipulate these processes for potential treatment of cancer, chronic inflammation and neurodegenrative diseases.

Regulation of gene expression at the transcriptional and translational levels is fundamental to all biological activities and is frequently altered in disease states. Our broad research interests are (i) to elucidate how the transcription and translation processes control the cellular response to enviromental stimuli; (ii) to reveal the connections between the transcription and translation processes and (iii) to develop tools to manipulate these processes for potential treatment of cancer, chronic inflammation and neurodegenrative diseases.

Regulation of gene expression at the transcriptional and translational levels is fundamental to all biological activities and is frequently altered in disease states. Our broad research interests are (i) to elucidate how the transcription and translation processes control the cellular response to enviromental stimuli; (ii) to reveal the connections between the transcription and translation processes and (iii) to develop tools to manipulate these processes for potential treatment of cancer, chronic inflammation and neurodegenrative diseases.

We focus on 1) the mechanisms underlying the embryonic development of beta cells both in vivo and in vitro and 2) the transcriptional and post-transcriptional mechanisms that permit beta cells to fulfill their role of releasing insulin in response to physiological needs.

We focus on 1) the mechanisms underlying the embryonic development of beta cells both in vivo and in vitro and 2) the transcriptional and post-transcriptional mechanisms that permit beta cells to fulfill their role of releasing insulin in response to physiological needs.

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.

The Yaron lab studies the regulation of neuronal wiring

• The mechanisms of axonal guidance and pruning.
• The interplay between genetics and experience.

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

Membrane proteins make up a quarter of the proteome of every living organism and participate in nearly every biological process. We are interested in the fascinating process of how these proteins get produced, fold, and assemble in cells. The questions we address are: How do proteins fold in the membranes of living cells? How do the dynamic features of unfolded proteins assist in this process? How do cellular factors recognize membrane proteins that failed to fold and need to be cleared? The lab combines biochemical, cell biology, genetic and computational tools. For more details, visit http://www.weizmann.ac.il/Biomolecular_Sciences/Fluman  

Membrane proteins make up a quarter of the proteome of every living organism and participate in nearly every biological process. We are interested in the fascinating process of how these proteins get produced, fold, and assemble in cells. The questions we address are: How do proteins fold in the membranes of living cells? How do the dynamic features of unfolded proteins assist in this process? How do cellular factors recognize membrane proteins that failed to fold and need to be cleared? The lab combines biochemical, cell biology, genetic and computational tools. For more details, visit http://www.weizmann.ac.il/Biomolecular_Sciences/Fluman  

Membrane proteins make up a quarter of the proteome of every living organism and participate in nearly every biological process. We are interested in the fascinating process of how these proteins get produced, fold, and assemble in cells. The questions we address are: How do proteins fold in the membranes of living cells? How do the dynamic features of unfolded proteins assist in this process? How do cellular factors recognize membrane proteins that failed to fold and need to be cleared? The lab combines biochemical, cell biology, genetic and computational tools. For more details, visit http://www.weizmann.ac.il/Biomolecular_Sciences/Fluman  

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