Publications

Joseph S; Zbidat S; Volodin A; Kasiviswanathan D; Fried A.I.; Armani A; Gilda J.E. and Cohen S. Insulin receptor turnover in fasting is dependent on β-dystroglycan deglycosylation. BioRxiv

Gilda J.E. and Cohen S. Molecular mechanisms of skeletal muscle atrophy in cancer. Springer Nature. Book chapter.

Aweida D and Cohen S. The AAA-ATPase ATAD1 and its partners promote degradation of desmin intermediate filaments in muscle. 2022. EMBO reports. 23(12):e55175.

Gilda J.E., Ko J.H., Elfassy A.Y., Tropp N., Parnis A., Ayalon B., Jhe W. and Cohen S. A semi-automated measurement of muscle fiber size using the Imaris software. 2021. AJP-Cell Physiol. 321(3):C615.

Agnetti G., Herrmann H. and Cohen S. New roles for desmin in maintenance of muscle homeostasis. 2021. FEBS J. Invited review. 289(10):2755.

Aweida D. and Cohen S. Breakdown of filamentous myofibrils by the UPS – step by step. 2021. Biomolecules. 11(1):110.

Cohen S. Role of calpains in promoting desmin filaments depolymerization and muscle atrophy. 2020. BBA Mol Cell Res. 1867(1):118788.

Kucherenko M.M., Xie Y., Yatsenko A.S., Aweida D., Urlaub H., Cohen S., Shcherbata H.R. Profiling of muscle-specific Dystroglycan complexome in Drosophila reveals interactions with the Hippo kinase signaling pathway in maintaining adult muscle size and integrity. 2020. BMC Medicine. 18(1):8.

Goldbraikh D., Neufeld D., Mutlak-Eid Y., Lasry I., Gilda JE., Parnis A. and Cohen S. USP1 deubiquitinates Akt to inhibit PI3K-Akt-FoxO signaling in muscle during prolonged starvation. 2020. EMBO reports. 21(4):e48791.

Eid -Mutlak Y., Aweida D.Volodin A.Ayalon B.Dahan N.Parnis A. and Cohen S. A signaling hub of insulin receptor, dystrophin glycoprotein complex and plakoglobin regulates muscle size. 2020. Nature Communications. 11(1):1381.

Aweida D., Rudesky I., Volodin A., Shimko E. and Cohen S. GSK3-β promotes calpain-1-mediated desmin filaments depolymerization, and myofibril loss in atrophy. 2018.  J Cell Biol. 217(10):3698-3714.

Shilo R., Gilad Y., Ber Y., Eisenstein M., Aweida D., Bialik S., Cohen S. and Kimchi A. Non-canonical activation of DAPK2 by AMPK constitutes a new pathway linking metabolic stress to autophagy. 2018. Nature Communications. 9(1):1759.

Bassat E., Mutlak YE., Genzelinakh A., Shadrin IY., Baruch-Umansky K., Yifa, O., Kain D., Rajchman D., Leach J.,‎ Riabov Bassat D., Udi Y., Sarig R., Sagi I., Martin JF., Bursac N., Cohen S. and Tzahor E. The extracellular matrix protein agrin promotes heart regeneration in mice. 2017. Nature. 547(7662):179-184.

Volodin A., Kosti I., Goldberg A.L. and Cohen S. Myofibril breakdown during atrophy is a delayed response requiring the transcription factor PAX4 and Desmin Depolymerization. 2017. PNAS. 114(8):E1375-E1384.

  • Commentary: Losing pieces without disintegrating: Contractile protein loss during muscle atrophy. PNAS. 114(8):1753-1755.

Cohen S., Nathan J. and Goldberg A.L. Muscle wasting in disease: molecular mechanisms and promising therapies. 2015. Nature Reviews Drug Discovery. 14(1):58-74.

Piterman R., Braunstein I., Isakov E., Ziv T., Navon A., Cohen S. and Stanhill A. VWA domain of S5a restricts the ability to bind ubiquitin and UBL to the 26S proteasome. 2014. Mol Biol Cell. 25(25):3988-98.

Cohen S., Zhai B., Lee D., Gygi S.P. and Goldberg A.L. Trim32 reduces PI3K/Akt/FoxO signaling in muscle atrophy by promoting plakoglobin-PI3K dissociation. 2014. J Cell Biol. 204(5):747-58.

Cohen S., Zhai B., Gygi S.P. and Goldberg A.L. Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands and thin filaments in muscle atrophy. 2012. J Cell Biol. 198(4):575-89.

Cohen S., Brault J.J., Gygi S.P., Glass D.J., Valenzuela D.M., Gartner C., Latres E. and Goldberg A.L. During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation. 2009. J Cell Biol. 185:1083-95.

  • Leslie, M. Muscle atrophy through thick but not thin. J Cell Biol 185(6): 931, 2009.
  • Selected as highlighted article on J Cell Biol cover.
  • Selected for the spotlight on research by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS).

Cohen S., Dovrat S., Sarid R., Huberman E. and Salzberg S. JAK-STAT signaling involved in phorbol 12-myristate 13-acetate- and dimethyl sulfoxide-induced 2′-5′ oligoadenylate synthetase expression in human HL-60 leukemia cells. 2005. Leukemia Res. 29:923-31.

Alroy I., Tuvia S., Greener T., Gordon D., Barr H.M., Taglicht D., Mandil-Levin R., Ben-Avraham D., Konforty D., Nir A., Levius O., Bicoviski V., Dori M., Cohen S., Yaar L., Erez O., Propheta-Meiran O., Koskas M., Caspi-Bachar E., Alchanati I., Sela-Brown A., Moskowitz H., Tessmer U., Schubert U., and Reiss Y. The trans-Golgi network-associated human ubiquitin-protein ligase POSH is essential for HIV type 1 production. 2005. PNAS. 102:1478-83.

Salzberg S., Vilchik S., Cohen S., Heller A., and Kronfeld-Kinar Y. Expression of a PKR dominant-negative mutant in myogenic cells interferes with the myogenic process. 2000. Exp Cell Res. 254:45-54.