Characterization of the initial C3 convertase of the alternative pathway of human complement. [PDF]
Zvi Fishelson +2 more
openalex +1 more source
This real‐world study of ROS1+ NSCLC highlights fusion diversity, treatment outcomes with crizotinib and lorlatinib, and in vitro experiments with resistance mechanisms. G2032R drives strong resistance to ROS1‐targeted TKIs, especially lorlatinib. Fusion partner location does not affect overall survival to crizotinib or lorlatinib. Findings support the
Fenneke Zwierenga +8 more
wiley +1 more source
Differential effects of C5 inhibition, C3 inhibition, and alternative pathway inhibition on bacterial killing in vitro. [PDF]
Ter Avest M +6 more
europepmc +1 more source
Correction: A potent complement factor C3-specific nanobody inhibiting multiple functions in the alternative pathway of human and murine complement. [PDF]
Jensen RK +7 more
europepmc +1 more source
Antibody-dependent alternative pathway killing of Haemophilus influenzae type b [PDF]
Norman P. Steele +4 more
openalex +1 more source
Emerging role of ARHGAP29 in melanoma cell phenotype switching
This study gives first insights into the role of ARHGAP29 in malignant melanoma. ARHGAP29 was revealed to be connected to tumor cell plasticity, promoting a mesenchymal‐like, invasive phenotype and driving tumor progression. Further, it modulates cell spreading by influencing RhoA/ROCK signaling and affects SMAD2 activity. Rho GTPase‐activating protein
Beatrice Charlotte Tröster +3 more
wiley +1 more source
Therapeutic targeting of alternative pathway and C5 but not C5a protects from disease development in a preclinical model of autoimmune blistering dermatosis. [PDF]
Laffer B +7 more
europepmc +1 more source
Interferon-β1a-Induced Thrombotic Microangiopathy: Possible Implication of the Alternative Pathway of the Complement. [PDF]
Taghavi M +6 more
europepmc +1 more source
Regulation of the alternative pathway of T cell activation by anti-T3 monoclonal antibody. [PDF]
D A Fox +2 more
openalex +1 more source
Modeling hepatic fibrosis in TP53 knockout iPSC‐derived human liver organoids
This study developed iPSC‐derived human liver organoids with TP53 gene knockout to model human liver fibrosis. These organoids showed elevated myofibroblast activation, early disease markers, and advanced fibrotic hallmarks. The use of profibrotic differentiation medium further amplified the fibrotic signature seen in the organoids.
Mustafa Karabicici +8 more
wiley +1 more source

