Iván G. Gómez
Scientist I

I obtained my degree from UC Berkeley in Molecular Cell Biology many years ago. The scientific area that interests me most is mitochondrial dysfunction, especially in the context of human kidney disease. I have previously worked for various other biotechnology companies, including Exelexis and Dendreon, but I have spent the majority of my career in academia at the University of Washington, as well as at UCSF and FHCRC. I have gained a lot of experience designing angiogenesis assays for small molecule screening, as I did this for 3 years at Exelixis. During my short time at Dendreon, I acquired numerous flow cytometry skills screening clinical samples for markers of immunological responses. At the University of Washington, I was part of the Department of Pathology for nearly 7 years and the focus of my research was on the study of proteins shed from macrophages that play a role in immune response. I recently completed work on the mechanisms by which anti-microRNA-21 compounds can reduce injury and inflammation in the kidney, and I am also planning to study the possible roles of pericytes in tissue repair and regeneration.

In my spare time, I hang out with my wife, my 10-year old son, and my 6-year-old daughter.


Gomez IG, MacKenna DA, Johnson BG, Kaimal V, Roach AM, Ren S, Nakagawa N, Xin C, Newitt R, Pandya S, Xia TH, Liu X, Borza DB, Grafals M, Shankland SJ, Himmelfarb J, Portilla D, Liu S, Chau BN, Duffield JS. Anti-microRNA-21 oligonucleotides prevent Alport nephropathy progression by stimulating metabolic pathways. J Clin Invest. 125(1):141-56 (2015).

• Kawakami T, Gomez IG, Ren S, Hudkins K, Roach A, Alpers CE, Shankland SJ, D'Agati VD, Duffield JS. Deficient Autophagy Results in Mitochondrial Dysfunction and FSGS. J Am Soc Nephrol. 26(5):1040-52 (2015).

Gomez IG, Grafals M, Portilla D, Duffield JS. MicroRNAs as potential therapeutic targets in kidney disease. J Formos Med Assoc. 112(5):237-43 (2013).

Gomez IG, Tang J, Wilson CL, Yan W, Heinecke JW, Harlan JM, Raines EW. Metalloproteinase-mediated shedding of integrin β2 promotes macrophage efflux from inflammatory sites. J Biol Chem. 287(7):4581-9 (2012).

• Tang J, Zarbock A, Gomez I, Wilson CL, Ley K, & Raines EW. Adam17 dependent shedding limits early neutrophil influx, but does not alter early monocyte recruitment to inflammatory sites. Blood 118: 786-794 (2011).

• Vaisar T, Kassim SY, Gomez IG, Green PS, Hargarten S, Gough PJ, Parks WC, Wilson CL, Raines EW , & Heinecke. MMP-9 Sheds the β2 Integrin Subunit (CD18) from Macrophages. Molecular & Cellular Proteomics 8:1044–1060 (2009).

• Gough PJ, Gomez IG, Wille PT, Raines EW. (2006) Macrophage expression of active MMP-9 induces acute plaque disruption in apoE-deficient mice. J. Clin. Invest. 116:59-69 (2006).

• Iritani BM, Delrow J, Grandori C, Gomez I, Klacking M, Carlos LS, Eisenman RN. Modulation of T-lymphocyte development, growth and cell size by the Myc antagonist and transcriptional repressor Mad1. EMBO J., 16;21(18):4820-30 (2002).