Dr. Math Cuajungco, Biology

Education and Professional Positions

BSc in Psychology and Mathematics, University of Auckland, New Zealand, 1992-1995
MSc in Medical Science, University of Auckland, New Zealand, 1995-1997
PhD in Neuroscience, University of Auckland, New Zealand, 1997-1999
Postdoc Fellow, Human Genetics, Massachusetts General Hospital/Harvard Med School, 2000-2003
Postdoc Fellow, Auditory Neuroscience, Massachusetts Eye & Ear Infirmary/Harvard Med School, 2003-2005
Postdoc Fellow, Neuroscience, Stanford University School of Medicine, 2005-2007

Dr. Cuajungco is Professor of Biological Science at CSUF. He is a Neuroscientist from New Zealand. He earned his Ph.D. in Neuroscience at the University of Auckland, where he worked very productively on zinc metabolism and toxicity in the brain. As a pre-doctoral researcher at Harvard Medical School, he pursued a link between metal toxicity and Alzheimer ’s disease.  He then undertook post-doctoral work at Harvard, and acquired molecular biology expertise in studying a rare sensory neuropathy known as familial dysautonomia. His work evolved to problems in the sensory system and joined another Harvard laboratory to study molecules and nerve cells involved in hearing. His laboratory subsequently moved to Stanford School of Medicine, and his project led to his current interest in a family of membrane channels known as the Transient Receptor Potential (TRP) ion channels.  The TRP ion channels mediate cell response to sensory stimuli such as taste, sight, sound, pain, or temperature. Their dysfunction results in many human diseases, including the current lab research focus – Mucolipidosis type IV.In addition to the research projects supported in his laboratory, Dr. Cuajungco also serves as the MARC Program Coordinator.

Current Research Interests

Transient Receptor Potential (TRP) ion channels and lysosomes in human health and neurodegenerative diseases.

Lysosomes are important cell organelles involved in the breakdown of membrane proteins and other molecules. These intracellular vesicles have been implicated in many neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Mucolipidosis type IV. The lysosomal membrane contains a diverse number of receptor and ion channel proteins that mediate its normal function. Some of these proteins are also involved in protein trafficking through processes known as endocytosis and exocytosis. It is thus not surprising that dysfunction of these proteins result in human pathological conditions.

The Cuajungco lab is interested in the roles that specific lysosomal membrane proteins and ion channels play during normal and pathological states. Our investigations involve collaborations from various disciplines within CSUF and other renowned institutions. We use mammalian cell culture model, as well as molecular and cellular biology methods to accomplish our research goals. One of our projects aims to characterize the function of transmembrane proteins, TMEM163, TMEM176A, and TMEM176B, using molecular, biochemical, and microscopy techniques. We are also interested in Mucolipidosis type IV, and currently investigating the possibility of using TRPML2 (MCOLN2) or TRPML3 (MCOLN3) gene complementation for the missing TRPML1 (MCOLN1) gene as a therapeutic approach for the disease.

Selected Publications

  1. Cuajungco MP, Silva J, Habibi A, Valadez JA. The mucolipin-2 (TRPML2) ion channel: a tissue-specific protein crucial to normal cell function. Pflugers Arch. 2016 Feb;468(2):177-92. doi: 10.1007/s00424-015-1732-2. Epub 2015 Sep 4. PubMed PMID: 26336837; PubMed Central PMCID: PMC4715775.
  2. Stott KV, Wood SM, Blair JA, Nguyen BT, Herrera A, Mora YG, Cuajungco MP, Murray SR. (p)ppGpp modulates cell size and the initiation of DNA replication in Caulobacter crescentus in response to a block in lipid biosynthesis. Microbiology. 2015 Mar;161(Pt 3):553-64. doi: 10.1099/mic.0.000032. Epub 2015 Jan 8. PubMed PMID: 25573769; PubMed Central PMCID: PMC4339654.
  3. Valadez JA, Cuajungco MP. PAX5 is the transcriptional activator of mucolipin-2 (MCOLN2) gene. Gene. 2015 Jan 25;555(2):194-202. doi: 10.1016/j.gene.2014.11.003. Epub 2014 Nov 6. PubMed PMID: 25445271; PubMed Central PMCID: PMC4276718.
  4. McEligot AJ, Behseta S, Cuajungco MP, Van Horn JD, Toga AW. Wrangling Big Data Through Diversity, Research Education and Partnerships. Calif J Health Promot. 2015;13(3):vi-ix. PubMed PMID: 27257409; PubMed Central PMCID: PMC4886736.
  5. Cuajungco MP, Basilio LC, Silva J, Hart T, Tringali J, Chen CC, Biel M, Grimm C. Cellular zinc levels are modulated by TRPML1-TMEM163 interaction. Traffic. 2014 Nov;15(11):1247-65. doi: 10.1111/tra.12205. Epub 2014 Sep 2. PubMed PMID: 25130899; PubMed Central PMCID: PMC4205267.
  6. Cuajungco MP, Podevin W, Valluri VK, Bui Q, Nguyen VH, Taylor K. Abnormal accumulation of human transmembrane (TMEM)-176A and 176B proteins is associated with cancer pathology. Acta Histochem. 2012 Nov;114(7):705-12. doi: 10.1016/j.acthis.2011.12.006. Epub 2012 Jan 12. PubMed PMID: 22244448.
  7. Schredl AT, Perez Mora YG, Herrera A, Cuajungco MP, Murray SR. The Caulobacter crescentus ctrA P1 promoter is essential for the coordination of cell cycle events that prevent the overinitiation of DNA replication. Microbiology. 2012 Oct;158(Pt 10):2492-503. Epub 2012 Jul 12. PubMed PMID: 22790399; PubMed Central PMCID: PMC3541797.
  8. Eichelsdoerfer JL, Evans JA, Slaugenhaupt SA, Cuajungco MP. Zinc dyshomeostasis is linked with the loss of mucolipidosis IV-associated TRPML1 ion channel. J Biol Chem. 2010 Nov 5;285(45):34304-8. doi: 10.1074/jbc.C110.165480. Epub 2010 Sep 23. PubMed PMID: 20864526; PubMed Central PMCID: PMC2966043.

Honors and Awards