Susan Kandarian, PhD

Susan Kandarian, PhD

Title
Professor, Department of Health Sciences, Boston University Sargent College
Programs in Human Physiology
Research Assistant Professor, Department of Physiology, Boston University School of Medicine
Office
635 Commonwealth Ave
Email
skandar@bu.edu
Phone
(617) 353-5169
Education
1981 B.A., Albion College, Albion, MI, Biology major
1983 M.S., The University of Michigan, Ann Arbor
1988 Ph.D., The University of Michigan, Ann Arbor

Scholarly Interests

Work in my laboratory focuses on understanding the pathways that mediate skeletal muscle atrophy using cellular and molecular approaches. Recent work in collaboration with Professor Jackman is geared toward the identification of ligands, signaling pathways, transcription factors, and genes that are necessary for the induction and progression of muscle wasting due to disuse and due to cancer.

Selection of Recent Publications

  • Seto DN, Kandarian SC, Jackman RW. A Key Role for Leukemia Inhibitory Factor in C26 Cancer Cachexia. J Biol Chem. 2015 Jun 19; 290.
  • Judge SM, Wu CL, Beharry AW, Roberts BM, Ferreira LF, Kandarian SC, Judge AR. Genome-wide identification of FoxO-dependent gene networks in skeletal muscle during C26 cancer cachexia. BMC Cancer. 2014 Dec 24;14:997.
  • Wu CL, Cornwell EW, Jackman RW, Kandarian SC. NF-κB but not FoxO sites in the MuRF1 promoter are required for transcriptional activation in disuse muscle atrophy. Am J Physiol Cell Physiol. 2014 Apr 15;306(8):C762-7.
  • Cornwell EW, Mirbod A, Wu CL, Kandarian SC, Jackman RW. C26 cancer-induced muscle wasting is IKKβ-dependent and NF-kappaB-independent. PLoS One. 2014 Jan 29;9(1):e87776.
  • Snyder CM, Rice AL, Estrella NL, Held A, Kandarian SC, Naya FJ. MEF2A regulates the Gtl2-Dio3 microRNA mega-cluster to modulate WNT signaling in skeletal muscle regeneration. Development. 2013 Jan 1;140(1):31-42.
  • Jackman RW, Cornwell EW, Wu CL, Kandarian SC. Nuclear factor-κBsignalling and transcriptional regulation in skeletal muscle atrophy.Exp Physiol. 2013 Jan;98(1):19-24.
  • Jackman RW, Wu CL, Kandarian SC. The ChIP-seq-defined networks of Bcl-3 gene binding support its required role in skeletal muscle atrophy. PLoS One. 2012;7(12):e51478.
  • Yamaki T, Wu CL, Gustin M, Lim J, Jackman RW, Kandarian SC. Rel A/p65 is required for cytokine-induced myotube atrophy. Am J Physiol Cell Physiol. 2012 Jul 15;303(2):C135-42.
  • Wu CL, Kandarian SC. Protein overexpression in skeletal muscle using plasmid-based gene transfer to elucidate mechanisms controlling fiber size. Methods Mol Biol. 2012;798:231-43.
  • Reed SA, Senf SM, Cornwell EW, Kandarian SC, Judge AR. Inhibition of IkappaB kinase alpha (IKKα) or IKKbeta (IKKβ) plus forkhead box O (Foxo) abolishes skeletal muscle atrophy. Biochem Biophys Res Commun. 2011 Feb 18;405(3):491-6.
  • Wu CL, Kandarian SC, Jackman RW. Identification of genes that elicit disuse muscle atrophy via the transcription factors p50 and Bcl-3. PLoS One. 2011 Jan 13;6(1):e16171.
  • Jackman RW, Rhoads MG, Cornwell E, Kandarian SC. Microtubule-mediated NF-kappaB activation in the TNF-alpha signaling pathway. Exp Cell Res. 2009 Nov 15;315(19):3242-9.
  • Van Gammeren D, Damrauer JS, Jackman RW, Kandarian SC. The IkappaB kinases IKKalpha and IKKbeta are necessary and sufficient for skeletal muscle atrophy. FASEB J. 2009 Feb;23(2):362-70.
  • Koncarevic A, Jackman RW, Kandarian SC. The ubiquitin-protein ligase Nedd4 targets Notch1 in skeletal muscle and distinguishes the subset of atrophies caused by reduced muscle tension. FASEB J. 2007 Feb;21(2):427-37.
  • Judge AR, Koncarevic A, Hunter RB, Liou HC, Jackman RW, Kandarian SC. Role for IkappaBalpha, but not c-Rel, in skeletal muscle atrophy. Am J Physiol Cell Physiol. 2007 Jan;292(1):C372-82.
  • Kandarian SC, Jackman RW. Intracellular signaling during skeletal muscle atrophy. Muscle Nerve. 2006 Feb;33(2):155-65.
  • Giresi PG, Stevenson EJ, Theilhaber J, Koncarevic A, Parkington J,Fielding RA, Kandarian SC. Identification of a molecular signature of sarcopenia. Physiol Genomics. 2005 Apr 14;21(2):253-63.