RONAI LAB

Sanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA

Research Publications in Graphic Abstracts

ATF2

Control of p53 on translationally active polysomes. JNK phosphorylation of p53 occurring on polysomes causes the dissociation of Ubc13 from p53, enabling p53 multimerization and transcriptional activation.

RNF5 ubiquitin ligase controls stability of glutamine carrier proteins, defining glutamine uptake and sensitivity of breast cancer to ER stress inducing therapies (paclitaxel)

ATF2

ERK

Siah2 ubiquitin ligase controls the formation of neuroendocrine prostate tumors by regulation of HIF1a availability to form transcriptional complex with FOXA2, resulting in the activation of SOX9, HES6, JMJD1a, PLOD2.

Siah2 ubiquitin ligase controls the stability of prolyl hydroxylase 1 and 3, defining the stability of HIF1a and hypoxia, under physiological hypoxia (4-6% O2).

RNF5 ubiquitin ligase controls UPR signaling in intestinal epithelial cells, with concomitant effect on gut microbiota composition and activation of anti-tumor immunity

RNF5 limits levels of S100A8 in intestinal epithelial cells, and thus controls intestinal inflammation (IBD like phenotypes).

$Siah2 ubiquitin ligase controls stability of AKAP121 regulating mitochondrial fission, with implications on heart infract$

Transcriptionally inactive ATF2 (spliced form) functions as super oncogene, drives melanoma development only in the presence of BRAF mutant.

Translational Reprogramming Marks Adaptation to Asparagine Restriction in Cancer; Nature Cell Biology In press;
In this study we unveil a previously unknown axis of adaptation to asparagine deprivation, which provides the basis for clinical evaluation of MAPK inhibitors in combination with asparagine restriction approaches.