J. Fernando Bazán

SVEP1 enables efficient binding of Angiopoietin-2 to the TIE1 receptor, allowing receptor phosphorylation and downstream signaling

This study identifies SVEP1 as a mediator of ANG2-TIE1 binding, leading to TIE1 phosphorylation and downstream signaling in lymphatic endothelial cells.

TCF25 emerges as a cytoplasmic regulator of GPRASP2 stability

TCF25 is mostly cytoplasmic with a perinuclear membrane-proximal pool, stabilises GPRASP2 against proteasomal degradation, and its C-terminal residues 604-664 are required for their association.

Rapidly evolving aphid gall effector proteins exhibit saposin-like folds

The paper predicts structures of rapidly evolving aphid effector proteins using Alphafold2 with custom multiple sequence alignments, revealing saposin-like folds and structural diversity.

Design principles of a membrane-spanning ubiquitin ligase

The paper describes the structure and function of a membrane-spanning E3 ubiquitin ligase complex, revealing its role in developmental processes and linking mutations to human birth defects.

Proteomic Ligandability Maps of Phosphorus(V) Stereoprobes Iden-tify Covalent TLCD1 Inhibitors

The paper uses stereoprobes to identify covalent ligands for proteins, revealing TLCD1 as a lipid acyltransferase inhibited by OTP stereoprobes.

Overcoming cryo-EM map anisotropy reveals ALK-cytokine assemblies with distinct stoichiometries

The paper reanalyzes cryo-EM data to reveal a 2:1 stoichiometry of ALK-ALKAL2 complexes, resolving discrepancies with previous structural studies.

A brown fat-enriched adipokine, ASRA, is a leptin receptor antagonist that stimulates appetite

This study identifies ASRA as a leptin receptor antagonist that stimulates appetite and contributes to obesity by counteracting leptin signaling.

Mechanism of receptor assembly via the pleiotropic adipokine Leptin

This study reveals the structure and mechanism of Leptin-mediated LEP-R assembly, showing a 3:3 stoichiometry and highlighting the role of Leptin restructuring in activating signaling.

Gene-teratogen interactions influence the penetrance of birth defects by altering Hedgehog signaling strength

The paper shows that gene-teratogen interactions affect birth defect penetrance by altering Hedgehog signaling through the MMM complex and SMO degradation.