TGF-β signaling in diseases

This paper develops a bifunctional antibody-fusion protein that targets CD24 and TGF-β1 to disrupt immunosuppression and enhance anti-tumor therapy.

The paper identifies interactions between the DBL-1 signaling pathway and BLMP-1/PRDM1 in C. elegans, showing how they regulate organismal traits through chromatin remodeling and gene expression.

This study shows that chemotherapy activates fibroblasts in TNBC, promoting pro-invasive ECM production, and that nintedanib can suppress this effect.

This study identifies HDAC6 as a regulator of endothelial-to-mesenchymal transition (EndMT) in venous thrombosis, showing that inhibiting HDAC6 reduces thrombus size and EndMT markers.

This study identifies DLX5 as a key driver of myofibroblastic carcinoma-associated fibroblasts (myCAFs) in breast cancer, showing its role in promoting tumor invasion through TGF-β signaling.

The paper reproduces and validates a previously reported model of TGF-β2-induced EndMT through Smad-dependent and independent pathways across multiple studies and laboratories.

This study shows that Th2-polarized CD4+ T-cells drive TNBC recurrence through TGFβ-induced pro-invasive signaling in irradiated mammary tissue.

The paper develops a bispecific antibody targeting TGFBR2 on human fibroblasts, showing cell selectivity and enhanced potency while avoiding systemic toxicity.

The paper investigates how different LTBP isoforms regulate TGF-β spatial localization and activation through structural and functional analyses.

This study shows that TGF-β2 induces endothelial plasticity and EndoMT in 3D vascular networks, revealing distinct responses compared to 2D cultures.

The paper shows that blocking integrin αvβ8 suppresses TGFβ in tumor-draining lymph nodes and enhances DC-T cell activation, offering a new immunotherapy strategy distinct from TGFβ ligand blockade.

This paper develops a co-culture assay to measure integrin αvβ8-mediated activation of latent TGF-β1, showing it is sensitive and effective for screening antibodies.

This study shows that SMAD4 MH2 mutations in colorectal cancer impair CREBBP/EP300 recruitment and TGF-β-induced transcription, explaining their loss-of-function effects.

This study identifies GDF6 as a driver of melanoma progression and shows a monoclonal antibody targeting GDF6 inhibits tumor growth in vivo.

The paper investigates how BMP and TGFβ pathways interact asymmetrically, showing that TGFβ inhibits BMP and BMP enhances TGFβ responses, reducing signaling ambiguity.

This paper improves the folding and targeting of an engineered TGF-β monomer for gene-based delivery by modifying its pro-domain and adding a CD44 binding domain.

The paper shows coreceptors inhibit TGFβ signaling more often than they promote it, altering ligand perception through competition in multi-ligand systems.

This study shows BMP9 regulates ET-1 through coordinated SMAD1/5 and SMAD2/3 signaling in endothelial cells, revealing a non-canonical mechanism relevant to pulmonary arterial hypertension.

This study shows that N-cadherin in osteolineage cells inhibits breast cancer growth by blocking a Tgf-β1-driven feed-forward loop involving PI3K-Akt-β-catenin signaling.

This study identifies a rapid NEU3-TGF-β1 positive feedback loop that amplifies TGF-β1 signaling through DDX3-mediated translation of NEU3 mRNA.

This study investigates SMAD2's role in integrating TGF-β and antigen signaling in mast cells, showing its necessity for both anti-inflammatory and pro-inflammatory responses.

This study identifies LOX as a key mediator of TGF-β-induced myCAF state in breast cancer, showing its role in promoting tumor growth through a LOX/FAK/GSK3β/β-catenin pathway.

This paper identifies Latrophilin-2 as a mediator of flow-induced Smad1/5 activation in endothelial cells through interactions with Endoglin and Shank3, independent of G-proteins.

The paper develops Pathway Sculptor to systematically modulate TGF-β receptor subsets, revealing functional interactions between BMP and TGF-β pathways and their collaborative signaling mechanisms.

This study shows anti-activin treatment reduces desmoplastic barriers and increases T cell infiltration in tumors, improving survival in SMAD4-null pancreatic cancer models.

The paper investigates how MIG-6/papilin and TGF-β signaling interact to regulate extracellular matrix remodeling and neuronal architecture maintenance.

This paper develops a computational model of TGF-β-induced ERK and SMAD pathways, showing how ERK can modulate SMAD dynamics and how these changes may contribute to cancer progression.

This study shows MKP-5 promotes TGF-β signaling via JNK-dependent pathway by affecting SMAD2 phosphorylation and fibrogenic gene activation.