Dr. Math Cuajungco, Biology


Dr. Cuajungco is a Neuroscientist who earned his Ph.D. at the University of Auckland, New Zealand, where he worked on zinc neurotoxicity 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. His current research interests involve lysosomal storage disease called Mucolipidosis type IV, and characterizing the function of several transmembrane proteins (TMEM163, TMEM176A, and TMEM176B).


  • Bachelor of Science (Psychology and Mathematics)
  • Master of Science in Medical Science (First Class Honours)
  • Doctor of Philosophy (Neuroscience)

Research Areas

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 ion channel and transporter (zinc transporters such as ZNTs, TMEM163, ZIPs) 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 both prokaryotic and eukaryotic cell culture models, as well as molecular and cellular biology methods to accomplish our research goals. One of our projects use membrane-based yeast two-hybrid genetic screens to identify protein-protein interactors for TRP channels found in lysosomes. Subsequently, we aim to characterize the functional significance of identified transmembrane protein interactors for the TRP channels using biochemical and microscopy techniques. Another aspect of our research is to study the relationships between lysosomes and metal transport or storage using fluorescence imaging and spectroscopy. Finally, we use CRISPR/Cas9 and RNA interference to target lysosomal membrane proteins, and analyze functional defects, as well as uncover any unknown signaling pathways involved in cellular endocytosis and exocytosis events.


Chacon, J.* , Rosas, L. #, and Cuajungco, M.P. (2019) ZnT3 expression levels are down-regulated in the brain of Mcoln1 knockout mouse brain . Molecular Brain, 26, 24. * Undergraduate student; # Post-bac  student

Cuajungco, M.P. and Kiselyov, K.I. (2017) The mucolipin-1 (TRPML1) ion channel, transmembrane-163 (TMEM163) protein and lysosomal zinc handling. Frontiers in Bioscience (Landmark), 22, 1330-1343

Cuajungco, M.P., Silva, J.*, Habibi, A. # , and Valadez, J.A. #  (2016) The Mucolipin-2 (TRPML2) ion channel: a tissue-specific protein crucial to normal cell function. Pflügers Archiv – European Journal of Physiology, 468, 177-192 . *Undergraduate student; # Graduate students

Valadez, J.A. # and Cuajungco, M.P. (2015) PAX5 is the transcriptional activator of the Mucolipin-2 (MCOLN2) gene. Gene, 555, 194-202. # Graduate student

Cuajungco, M.P., Basilio, L.C.*, Silva, J.*, Hart, T., Tringali, J., Chen, C.C., Biel, M. and Grimm, C. (2014) Cellular zinc levels are modulated by TRPML1-TMEM163 interaction. Traffic, 15, 1247-1265. *Undergraduate students .

Cuajungco, M.P., Podevin, W.#, Valluri, V.K.*, Bui, Q.*, Nguyen, V.H.*, and Taylor, K.* (2012) Abnormal accumulation of human transmembrane (TMEM)-176A and 176B is associated with cancer pathology. Acta Histochemica, 114, 705-712. *Undergraduate students; # Graduate student

Eichelsdoerfer, J.L.*, Evans, J.A.*, Slaugenhaupt, S.A. and Cuajungco, M.P. (2010) Zinc dyshomeostasis is linked with the loss of Mucolipidosis IV-associated TRPML1 ion channel. Journal of Biological Chemistry, 285, 34304-34308. *Undergraduate students