Ramon Serrano Email & Phone Number

San Diego, California, United States

San Diego, California, United States

San Diego, California, United States

La Jolla, Ca

I researched pathways to reduce and remedy damage from atherosclerosis.► I studied an XBP1 and TG2 (Transglutaminase 2) deficiency in the vascular smooth muscle cells of mice. I uncovered a relationship between XBP1 and TG2. XBP1 deficiency causes a ubiquitylation SUMOylation mechanism, affecting TG2 stability. Generated XBP1 and TG2 conditional knockout mice to study the effects of the deficiency; the result was a progression of plaque formation post -surgery for days 14 and 21 in the carotid artery. Additionally, I discovered that XBP1 deficiency plays an important role in driving autophagy and cellular apoptosis in vitro in smooth muscle cells isolated from mice aorta.► I researched the biochemical interaction between AMPK and TG2. TG2 is able to transamidase AMPK. I did in silico analysis showing the potential consensus sequences used by TG2 as targets. Designed and conducted a two-hybrid system assay to verify the predicted interaction and effects TG2 mutants would have on AMPK.

La Jolla, Ca

Under the direction of Dr. Robert Terkeltaub, I research pathways with the potential to positively impact care and outcomes for patients with or at risk for developing osteoarthritis (OA).► I have discovered an increase of K48-ubiquitinated protein/aggregates in chondrocytes extracted from patients with OA. I have also determined that there was a lower amount proteasome activity in OA. I proposed and discovered that PSMD11, a proteasome non-ATPase subunit, was responsible for lower proteasome activity in samples taken from patients with OA. Likewise, I discovered that overexpression of PSMD11 in OA chondrocytes increased proteasome activity; additionally, PSMD11 overexpression reduced catabolic response and increased aggrecan and SOX9 stabilization. This mechanism is critical to understand chondrocyte homeostasis and holds potential for a translational target for OA.► I have also studied XBP1 (X-box binding protein), a transcription factor, and the effects of its deficiency in chondrocytes, as well as its homeostasis and stress response in vitro and in vivo. To verifiably study deficiency effects, I generated a conditional knockout of XBP1 in the C57BL/6 black mice strain. I determined the effects of destabilization in surgery of the medial meniscus (DMM) in male mice knees during onset and development of OA. I also discovered XBP1 does not exhibit chondroprotective qualities during the progression or development of OA when compared to control animals, despite positive data showing a reduced catabolic response in vitro upon XBP1 deletion.

Utrecht Area, Netherlands

I had the privilege of working under the direction of Dr. Bernd Helms. I performed structural studies of the Golgi-associated plant pathogenesis-related-1 protein with phospholipids and fatty acids.► I discovered a lipid-protein interaction of unusual binding characteristics of a novel plant pathogenesis-related protein (GAPR-1) to phosphatidylinositol in the mammalian Golgi apparatus.

Pittsburgh

I worked under the direction of Dr. Guillermo Calero and characterized transcription factors in yeast to study the structures of major protein complexes.

Palo Alto, Ca

Working under the direction of Dr. Suzanne Pfeffer, I characterized hypervariable domains for Rab proteins responsible for localization and vesicular trafficking. I investigated a novel TBC protein GTPase activity and identified its Rab protein substrates and their potential function in membrane trafficking. I worked on the preliminary role of Rab25 GTPase in breast epithelial cell proliferation. I also Supervised Ph.D. students and research technicians in protein purification and binding assays.• Developed radiobiochemical assay to determine protein interaction in vitro.• Contributed to the study TBC1D20 GAP activity in HCV replication.

Vesicular Trafficking

Phd, Biochemistry, Magna Cum Laude

Biochemistry