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Robert Krauss

  • PROFESSOR Developmental and Regenerative Biology
  • PROFESSOR Oncological Sciences
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  • Ph.D., University of North Carolina

  • Postdoc, Columbia University



  • 2010 - present
    Editorial Board
    Skeletal Muscle

  • 2006 - 2009
    Society for Muscle Biology

  • 2006 - present
    Editorial Board
    Molecular and Cellular Biology

  • 2004 - present
    Editorial Board
    Journal of Cell Science

  • 1999 - 2001
    Established Investigator Award
    American Heart Association

  • 1996 - 2000
    Career Scientist Award
    Irma T. Hirschl Trust


The Krauss lab is interested in regulation of cell adhesion and signal transduction pathways during embryonic development and tissue regeneration, and how such processes may go awry in disease. The lab has two major areas of focus.


First, we are interested in development and regeneration of skeletal muscle. We have identified multiprotein cell surface complexes that promote differentiation of skeletal muscle precursor cells in response to cell-cell contact and adhesion. We use a combination of approaches, including mouse genetics, cell biology and biochemistry to probe the biological functions and molecular mechanisms of such complexes in skeletal myogenesis. We have recently turned our attention to how specific cell adhesion molecules regulate the niche and activity of muscle stem cells during homeostasis and regeneration following injury.


We are also interested mechanisms whereby the Hedgehog signaling pathway regulates development of the midline of the forebrain and midface. Mutations in Hedgehog pathway genes are associated with the common and often devastating developmental defect holoprosencephaly (HPE). However, the clinical outcome of mutation carriers is extremely variable, and additional genetic or environmental factors are required for strong defects. Using mouse models of such interactions and functional analyses of human HPE-associated mutations, we aim to provide information on mechanisms of HPE that will be valuable for genetic counseling and preventive action.


For more information, please visit the Krauss Laboratory website.


Lee HJ, Jo SB, Romer AI, Lim HJ, Kim MJ, Koo SH, Krauss RS, Kang JS. Overweight in mice and enhanced adipogenesis in vitro are associated with lack of the Hedgehog coreceptor Boc. Diabetes 2015; 64: 2092-2103.

Hong M, Krauss RS. Rescue of holoprosencephaly in fetal alcohol-exposed Cdon mutant mice by reduced gene dosage of Ptch1. PLOS ONE 2013; 8(11): e79269.

Romer AI, Singh J, Rattan S, Krauss RS. Smooth muscle fascicular reorientation is required for esophageal morphogenesis and dependent on Cdo. J. Cell Biol. 2013; 201: 309-323.

Hong M, Krauss RS. Cdon mutation and fetal ethanol exposure synergize to produce midline signaling defects and holoprosencephaly spectrum disorders in mice. PLoS Genet. 2012; 8(10): e1002999.

Bae GU, Domené S, Roessler E, Schachter K, Kang JS, Muenke M, Krauss RS. Mutations in CDON, encoding a hedgehog receptor, result in holoprosencephaly and defective interactions with other hedgehog receptors. Amer. J. Hum. Genet. 2011; 89: 231-240.

Allen BL, Song JY, Izzi L, Althaus IW, Kang JS, Charron F, Krauss RS, McMahon AP. Overlapping roles and collective requirement for the co-receptors Gas1, Cdo and Boc in Shh pathway function. Dev Cell 2011; 20: 775-787.

Zhang W, Hong M, Bae GU, Kang JS, Krauss RS. Boc modifies the holoprosencephaly spectrum of Cdo mutant mice. Dis Model Mech 2011; 4: 368-380.

Lu M, Krauss RS. N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts. Proc. Natl. Acad. Sci. (USA) 2010; 107: 4212-4217.

Bae GU, Yang YJ, Jiang G, Hong M, Lee HJ, Tessier-Lavigne M, Kang JS, Krauss RS. The Ig superfamily member neogenin regulates myofiber size and focal adhesion kinase and extracellular signal-regulated kinase activities in vivo and in vitro. Mol. Biol. Cell 2009; 20: 4920-4931.

Kang JS, Bae GU, Yi MJ, Yang YJ, Oh JE, Takaesu G, Zhou YT, Low BC, Krauss RS. A Cdo/Bnip-2/Cdc42 signaling pathway regulates p38α/β MAPK activity and myogenic differentiation. J. Cell Biol. 2008; 182: 497-507.

Industry Relationships

Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.

Dr. Krauss did not report having any of the following types of financial relationships with industry during 2015 and/or 2016: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.

Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website. Patients may wish to ask their physician about the activities they perform for companies.

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