Signaling in Oncogenesis, Angiogenesis, and Permeability

Cell Death Diff Abstract The cGAS-STING pathway is an evolutionarily conserved DNA-sensing mechanism that triggers innate immune responses. cGAS and STING play dual roles in tumorigenesis, promoting antitumor immunity and cell death while fueling tumor growth and metastasis. However, the mechanisms fine-tuning this pathway remain elusive. Using complementary proteomic approaches, we report that Casein Kinase 1 alpha (CK1α) operates as a bimodal regulator of the cGAS-STING pat

Signal Transduction and Targeted Therapy volume 11, Article number: 264 (2026) Abstract Glycoprotein (GP) VI is a platelet-specific activating receptor for collagen and fibrin(ogen), and a promising target for antithrombotic therapy. Inhibitory Fab fragments against GPVI provide robust protection in mouse models of arterial thrombosis and ischemic stroke without impairing hemostasis in mice or humans. However, their short in vivo half-life limits their suitability for long-te

iScience Summary Activation of the NLRP3 inflammasome by infectious or sterile insults culminates in pyroptosis, a lytic and highly inflammatory form of programmed cell death. A safeguarded two-step process tightly regulates pyroptosis: priming, which drives NF-κB signaling, followed by execution, ultimately leading to plasma membrane rupture. Linear (Met1-linked) ubiquitination, catalyzed by the E3 ligase complex LUBAC, was previously shown to participate in pyroptosis, but

EMBO Rep Abstract Mitochondrial outer membrane permeabilization is a pivotal event in programmed cell death by apoptosis, leading to the activation of the cysteine protease caspase-3 (CASP3) and the release of mitochondrial nucleic acids. This release triggers the activation of the Interferon Regulatory Factor 3 (IRF3) transcription factor and the subsequent IRF3-mediated type I interferon production and cell death. CASP3 ensures apoptosis remains immunologically silent, thou

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Published May 31, 2026 - DOI: 10.1056/NEJMoa26055 Abstract Background Current therapies offer limited benefit for patients with previously treated metastatic pancreatic ductal adenocarcinoma (mPDAC). Aberrant activation of the RAS pathway is the key driver of PDAC, with oncogenic RAS mutations present in more than 90% of cases. Daraxonrasib is an oral RAS(ON) multiselective, tri-complex inhibitor of the active guanosine triphosphate–bound state of mutant and wild-type RAS. Me

EMBO J 2026 May;45(9):3306-3331. doi: 10.1038/s44318-026-00742-y. Epub 2026 Apr 7. Abstract The ubiquitin-specific protease (USP) USP9X is a human deubiquitinase (DUB) with a large number of described targets and cellular roles. In cancer, USP9X is found as an oncogene or as a tumour suppressor depending on context, and its utility as a target for cancer therapy remains unclear. We here describe WEHI-092, a piperazine-based USP9X-specific small-molecule inhibitor, which bind

Nature Communications volume 16, Article number: 9374 (2025) Abstract Yes-associated protein (YAP), a key effector of the Hippo pathway, regulates gene expression and promotes tumorigenesis. YAP is conventionally considered “undruggable”, however, targeted protein degradation offers a promising approach to address the challenges associated with targeting this oncogenic protein. In this study, through naïve nanobody phage library screening, we identify multiple nanobodies agai

Stabilizing MARCH7 as a ferro-guardian against ferroptosis Cell Online nowApril 27, 2026 Highlights • Multi-omics analysis identifies MARCH7 as a master regulator of ferroptosis • MARCH7 degrades NCOA4 by K48 ubiquitination to reduce the labile iron pool • MARCH7 inhibits iron uptake by restricting TFR1 translocation by K63 ubiquitination • Stabilization of MARCH7 by EmodAn inhibits ferroptosis in vitro and in vivo Summary Ferroptosis is an iron-dependent form of regulated ce

Stem cell control in the lung by an autocrine injury-activated Igf complex Science 16 Apr 2026 Vol 392, Issue 67 Structured Abstract INTRODUCTION Adult stem cells are rapidly, but transiently, activated by injury to repair damaged tissue. Repeated or chronic injury predisposes to cancer. Although there has been progress in identifying and characterizing mammalian stem cells and homeostatic mitogens that regulate their proliferation, injury-activated mitogens, the mechanisms t