Eirı́kur Steingrı́msson

This study shows that MITF regulates autophagy in RPE cells, with reduced MITF causing autophagy defects and lysosomal dysfunction linked to retinal degeneration.

The paper shows that loss of MITF activity in zebrafish melanocyte stem cells leads to premature expansion and novel transcriptional states during embryogenesis, with stage-specific effects on regeneration.

This study shows MITF maintains genome stability in non-melanocytic cells by suppressing Hippo pathway signaling through LATS2 and ATR.

This study identifies TFE3 and the non-canonical mTORC1 pathway as regulators of melanoma cell state plasticity, showing MITF suppresses the mesenchymal phenotype by modulating TFE3 expression.

The paper identifies MITF target genes in olfactory bulb projection neurons, revealing their role in regulating neuronal activity and middle tufted cell function.

The paper identifies a novel regulatory mechanism of MITF through SUMOylation and phosphorylation interactions, revealing how mutations affect melanoma predisposition in a mouse model.

This study shows that aged Mitf mutant mice have reduced olfactory ability without neurodegeneration, but increased potassium channel gene expression suggests compensatory mechanisms.

The paper shows TFAP2 paralogs enhance MITF's ability to activate pigmentation genes but independently repress cell adhesion genes, affecting melanocyte and melanoma cell behavior.

The paper identifies cell-type-specific meQTLs in melanocytes and melanomas, enhancing GWAS annotation and revealing regulatory mechanisms involving IRF4.

The paper identifies genetic causes of inherited hearing loss in the Israeli Jewish population, finding a novel deafness gene ATOH1 and demonstrating the effectiveness of targeted genomic sequencing.

The paper shows Mitf regulates intrinsic plasticity in olfactory bulb neurons by controlling Kcnd3 expression, linking neuronal activity to long-term homeostatic changes in neuronal function.

The paper identifies ATG7 as a genetic risk factor for cholangiocarcinoma through germline mutations and population studies, linking autophagy dysfunction to cancer development.