A. P. Wiita

SLAPSHOT labels extracellular proteins rapidly and specifically, revealing dynamic changes in the proteome during calcium-induced membrane scrambling.

The paper identifies an AML-specific conformation of Integrin-β2 using structural surfaceomics and demonstrates its targeting by CAR-T cells.

This study defines the myeloma cell surface proteome, identifies therapeutic targets and resistance biomarkers, and presents a miniaturized surface proteomics protocol.

This study identifies a secretory autophagy pathway that releases autophagy cargo receptors via extracellular vesicles when endolysosomal function is inhibited or autophagosome maturation is disrupted.

The paper shows that ECM dimensionality affects actin tension, which in turn modulates endoplasmic reticulum function and spheroid resilience in mammary epithelial cells.

This paper describes engineered ACE2 receptor traps that potently neutralize SARS-CoV-2 by blocking viral entry through enhanced binding affinity.

This study identifies allosteric HSP70 inhibitors that overcome proteasome inhibitor resistance in multiple myeloma by targeting mitochondrial HSPA9 and disrupting mitoribosome stability.

This study uses CRISPR screens to identify mechanisms increasing BCMA expression and enhancing anti-myeloma efficacy of BCMA-targeted therapies in multiple myeloma.

This study shows that malignant B-cell transformation requires convergence on a single oncogenic pathway, while divergent pathways can subvert transformation and are targets for new therapeutic strategies.

This study evaluates how well multiple myeloma cell lines represent patient tumors using transcriptomic correlation analysis, finding significant variation in their similarity to patient tumors.

The paper identifies OMA1, DELE1, and HRI as a pathway that relays mitochondrial dysfunction to the integrated stress response, showing its role in activating eIF2 kinase activity and potential therapeutic relevance.

The paper uses phosphoproteomics and transcriptomics to analyze RAS signaling in multiple myeloma, identifying distinct signaling patterns and clinical outcomes associated with NRAS and KRAS mutations.

The paper shows proteasome inhibitors modulate splicing in multiple myeloma, revealing spliceosome inhibition as a therapeutic target.

This paper validates tofacitinib as an effective anti-myeloma therapy by reversing bone marrow microenvironment-driven growth signals in vitro and in vivo.

The paper compares time-resolved proteomics and ribosome profiling to study translation dynamics under stress in multiple myeloma cells treated with bortezomib.