Faculty Information

Rodrigo S. Lacruz, MSc, PhD

Professor
Molecular Pathobiology
Room 916 Dental Center, 421 First Avenue
Phone: 212-998-9433
E-mail: rodrigo.lacruz@nyu.edu


Visit the Lacruz Lab website >>>

 

Education

PhD, University of the Witwatersrand, Johannesburg, South Africa 2007
MSc, University of the Witwatersrand, Johannesburg, South Africa 2002

Research Interests / Professional Overview

The main research focus of my lab is to understand how deficiencies in calcium signaling affect human diseases. Calcium is a key regulator of several cell functions through changes in its intracellular concentration that is decoded by several proteins leading to the initiation of important cell functions including metabolism. We focus on several diseases including amelogenesis imperfecta (deficient enamel), Sjogren’s syndrome -an autoimmune disease affecting the salivary glands-, and Down syndrome, caused by trisomy of all or part of human chromosome 21 (HSA21), the most common genetic cause of intellectual disability. My research combines molecular biology, physiology, confocal and electron microscopy, genetics and morphology to identify key growth processes and pathways.

My lab originally discovered several proteins involved in Ca2+ uptake in the enamel forming ameloblast cells. The main pathway for Ca2+ influx is the store operated Ca2+ entry (SOCE) formed by the ER-membrane bound STIM1 protein, and the plasma membrane protein forming the pore of the channel known as ORAI1. Activation of the ORAI1 channel results in a sustained influx of calcium into the cell. SOCE is also an important regulator of saliva production. Mutations in STIM1 or ORAI1 genes result in severe combined immune deficiency, ectodermal dysplasia and amelogenesis imperfecta, and has been implicated in Sjogren’s syndrome. Our lab also reported that ORAI1 is an important mediator of nociceptive pain associated with oral cancer.

Current Funding

  • R01. Role: PI. NIDCR (2023-2028). Title: Redox and Ca2+ signaling regulation of enamel mineralization.  
  • R01. Role: PI. NIDCR (2023-2028). Title: Molecular mechanisms of oral deficiencies in Down syndrome.
  • R01. Role: multi-PI (2019-2024). Title: Ca2+ signaling via SOCE in the pathogenesis of Sjogren’s syndrome

Representative Publications

Complete listing available on the NYU Health Sciences Library site.

2023: Ga-Yeon Son, Huu Tu N, Santi MD, Loya Lopez S, Souza Bomfim GH, Vinu M, Zhou F, Chaloemtoem A, Alhariri R, Idaghdour Y, Khanna R, Ye Y, Lacruz RS. (2023) The Ca2+ channel ORAI1 is a regulator of oral cancer growth and nociceptive pain. Science Signaling. Sept 05, vol 16, issue 801. DOI: 10.1126/scisignal.adf9535.

2023: Souza Bomfim GH, Schnetkamp P, Lacruz, RS.  (2024) Na+/Ca2+ exchange in enamel cells is dominated by the K+-dependent NCKX exchanger. J. General Physiology. vol 156 (1) https://doi.org/10.1085/jgp.202313372.

2023 : Bomfim, G.H.S, Giacomello M, Lacruz RS. (2023) PMCA Ca2+ clearance in dental enamel cells depends on the magnitude of cytosolic Ca2+ elevation. FASEB Journal. Jan;37(1):e22679, PMID: 36515675.

2022 : Li X, Costiniti V, Bomfim, G.H.S., Neginskaya M, Son G-Y, Rothermel B, Pavlov E, Lacruz R.S. (2022). Overexpression of RCAN1, a gene on human chromosome 21, alters mitochondrial function and redox in enamel cells. Cells, 11, 3576.

2020: Aulestia FJ, Groeling J, Costiniti V, Bomfim GH, Concepcion-Gonzalez A, Wagner L, Yule DI, Lacruz RS. (2020) Fluoride alters Ca2+ signaling and mitochondrial function in enamel cells. Science Signaling. eaay0086. doi: 10.1126/scisignal.aay0086.

2019: Eckstein M, Vaeth M, Aulestia FJ, Costiniti V, Kassam SN, Bromage TG, Pedersen P, Issekutz T, Moursi AM, Feske S, Lacruz RS (2019) Differential regulation of Ca2+ influx by ORAI channels mediate enamel mineralization. Science Signaling, 12, eaav4663. DOI:10.1126/scisignal.aav4663

2017: Lacruz RS, Habelitz S, Wright TJ, Paine ML. Dental Enamel Formation and Implications for Oral Health and Disease. Physiol Rev. 97(3): 939-993.

2017: Lacruz RS. Enamel: Molecular identity of its transepithelial ion transport system. Cell Calcium. PMID: 28389033, DOI: 10.1016/j.ceca.2017.03.006

2017: Eckstein M, Vaeth M, Fornai C, Bromage TG, Vinu M, Nurbaeva MK, Sorge J, Idaghdour Y; Feske S, Lacruz RS. Store-operated Ca2+ entry (SOCE) controls ameloblast cell function and enamel development. JCI Insight. 2(6):e91166.­­­

2017: Vaeth M, Yang J, Yamashita M, Zee I, Eckstein M, Kaufmann U, Knosp C, Lacruz RS, Prakriya M, Feske S. ORAI2 modulates store-operated calcium entry (SOCE) and T cell-mediated immune responses. Nature Communications. doi: 10.1038/ncomms14714. PMID: 28294127.

2016: Concepcion AR, Vaeth M, Wagner II LE, Eckstein M, Hecht, Yang J, Crottes D, Seidl M, Shin HP, Weidinger C, Cameron S, Turvey SE, Issekutz T, Meyts I, Lacruz RS, Cuk M, Yule DI, Feske S. Store-operated Ca2+ entry regulates Ca2+-activated chloride channels and eccrine sweat gland function. Journal of Clinical Investigation 26:4303-4318. PMID: 27721237.

2016: Nurbaeva MK, Eckstein M, Feske S, Lacruz RS. Calcium signaling and transport in dental enamel cells. Review. J. Physiology. PMID: 27510811.

2015: Lacruz RS, Feske S. Diseases caused by mutations in ORAI1 and STIM1 genes. Annals New York Acad. Sci. doi: 10.1111/nyas.12938

2015: Nurbaeva MK, Eckstein M, Smith CE, Srikanth S, Paine ML, Gwack Y, Feske S, Hubbard MJ, Lacruz RS. Dental Enamel cells express SOCE channels. Scientific Reports. 5:15803 DOI: