Prof. Korenblit Sivan

Associate Professor
Prof. Sivan Korenblit


  1. Levi-Ferber M, Gian H, Dudkevich R, Henis-Korenblit S (2015) Transdifferentiation mediated tumor suppression by the endoplasmic reticulum stress sensor IRE-1 in C. elegans. Elife. doi: 10.7554/eLife.08005.

  2. Levi-Ferber M, Salzberg Y, Safra M, Haviv-Chesner A, Bülow HE, Henis-Korenblit S (2014) It's All in Your Mind: Determining Germ Cell Fate by Neuronal IRE-1 in C. elegans. PLoS Genet. 10(10):e1004747. doi: 10.1371/journal.pgen.1004747.

  3. Safra M, Fickentscher R, Levi-Ferber M, Danino YM, Haviv-Chesner A, Hansen M, Juven-Gershon T, Weiss M and Henis-Korenblit S (2014)The FOXO Transcription Factor DAF-16  Bypasses ire-1 Requirement to Promote Endoplasmic Reticulum Homeostasis.  Cell Metabolism 20(5):870-881.

  4. Safra M, Henis-Korenblit S (2014) A new tool in C. elegans reveals changes in secretory protein metabolism in ire-1-deficient animals. Worm:e27733. doi: 10.4161/worm.27733.

  5. Safra M, Ben-Hamo S, Kenyon C and Henis-Korenblit S. (2013) The ire-1 ER Stress-Response Pathway is Required for Normal Secretory-Protein Metabolism in C. elegans. J. Cell Sci. 126(Pt 18):4136-46. doi: 10.1242/jcs.123000.

  6. Henis-Korenblit S, Zhang P, Hansen M, McCormick M, Lee SJ, Cary M and Cynthia Kenyon (2010) Insulin/IGF-1 Signaling Mutants Reprogram ER-stress Response Regulators to Promote Longevity. Proc Natl Acad Sci USA.107(21):9730-35.

  7. Ghazi A., Henis-Korenblit S. and Cynthia Kenyon (2009) A transcription elongation factor that links signals from the reproductive system to lifespan extension in Caenorhabditis elegans. PLoS Genet. 5(9):e1000639.

  8. Marash L., Liberman N., Henis-Korenblit S., Sivan G., Reem E., Elroy-Stein O. and Kimchi A. (2008) DAP5 promotes cap-independent translation of Bcl-2 and CDK1 to facilitate cell survival during mitosis. Mol. Cell 30(4):447-59.

  9. Ghazi A.*,Henis-Korenblit S.* and Kenyon C. (2007) Control of C. elegans lifespan by a proteasomal E3-ligase complex. Proc Natl Acad Sci USA. 104(14):5947-52.  *Co-first authorship, these authors contributed equally to the paper.

  10. Henis-Korenblit S., Shani G., Sines T., Marash L., Shohat G. and Kimchi A. (2002) The caspase cleaved DAP5 protein supports internal ribosome entry site mediated translation of death proteins.Proc Natl Acad Sci USA. 99(8):5400-5.

  11. Shani G., Henis-Korenblit S, Jona G., Gileadi O.,Eisenstein M., Kimchi A. (2001). Autophosphorylation restrains the apoptotic activity of DRP-1kinase by controlling dimerization and CaM binding. EMBO J. 20(5):1099-113.

  12. Henis-Korenblit S*, Strumpf NL*, Goldstaub D, Kimchi A (2000). A novel form of DAP5 protein accumulates in apoptotic cells as a result of caspase cleavage and internal ribosome entry site-mediated translation. Mol. Cell Biol. 20(2):496-506.   *Co-first authorship, these authors contributed equally to the paper.

  13. Tzahar E, Pinkas-Kramarski R, Moyer JD, Klapper LN, Alroy I, Levkowitz G, Shelly M, Henis S, Eisenstein M, Ratzkin BJ, Sela M, Andrews GC, Yarden Y (1997). Bivalence of EGF-like ligands drives the ErbB signaling network. EMBO J. 16(16):4938-50.

  14. Andres C, Beeri R, Friedman A, Lev-Lehman E, Henis S, Timberg R, Shani M, Soreq H (1997). Acetylcholinesterase-transgenic mice display embryonic modulations in spinal cord choline acetyltransferase and neurexin Ibeta gene expression followed by late-onset neuromotor deterioration. Proc Natl Acad Sci USA. 94(15):8173-8.


Human aging is accompanied by an overall decline in physiological function and an increase in the incidence of age-related diseases. My main research interest is to identify what, at the molecular level, delays aging and links aging to age-related disease. In particular, I am interested in the link between aging, age-related disease and ER stress response.The long-term goal of my future lab will be to learn how to control the rate of aging and the efficiency of the ER stress response as means to treat age-related diseases. To achieve this I will study how reducing insulin/IGF-1 signaling controls aging and ER stress response and, in turn, how do these affect age-related disease models. I propose to explore these questions utilizing the model organism C. elegans, by following these specific aims:

1) Explore and delineate important molecular mechanisms that underlie each of these processes (i.e. what genes/pathways control the rate of aging, what genes/pathways improve ER stress response).

2)  Study how aging pathways and ER stress pathways interact and impact each other.

3) Study how manipulation of aging pathways and ER stress pathways affect age-related disease models.


“Basic Cell Biology ” for 1st year undergraduate students

“Introduction to Biology Laboratory course” for 1st year undergraduate students, 

“Cellular stress responses” for 3rd year undergraduate and graduate students, 

Graduate and undergraduate seminar courses, 

Advanced lab project - Mentoring undergraduate students in a practical lab project