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HMGB1

PLP2-Derived Peptide Rb4 Triggers PARP-1-Mediated Necrotic Death in Murine Melanoma Cells

[Scientific Reports] Researchers studied the antitumor activity of peptide Rb4 derived from Proteolipid protein 2 (PLP2). In vitro, Rb4 induced F-actin polymerization, prevented F-actin depolymerization and increased the ER-derived cytosolic calcium.

Endothelial Cell Ferroptosis Mediates Monocrotaline-Induced Pulmonary Hypertension in Rats by Modulating NLRP3 Inflammasome Activation

[Scientific Reports] The effects of the ferroptosis inhibitor ferrostatin-1 on endothelial cell ferroptosis and pulmonary vascular remodelling in monocrotaline-induced rats were studied in vitro and in vivo.

Autophagy-Based Unconventional Secretion of HMGB1 in Glioblastoma Promotes Chemosensitivity to Temozolomide through Macrophage M1-Like Polarization

[Journal of Experimental & Clinical Cancer Research] The authors demonstrated that enhanced secretory autophagy in glioblastoma (GB) facilitated M1-like polarization of tumor associated macrophages to enhance temozolomide sensitivity of GB cells.

TIRAP Drives Myelosuppression through an Ifnγ–Hmgb1 Axis That Disrupts the Endothelial Niche in Mice

[Journal of Experimental Medicine] The authors showed that toll/interleukin-1 receptor domain containing adaptor protein (TIRAP) was overexpressed in various types of myelodysplastic syndromes and suppressed all three major hematopoietic lineages.

Deubiquitylase USP12 Induces Pro-Survival Autophagy and Bortezomib Resistance in Multiple Myeloma by Stabilizing HMGB1

[Oncogene] Researchers identified an important role of the deubiquitylase ubiquitin-specific protease-12 (USP12) in pro-survival autophagy and resultant bortezomib resistance in multiple myeloma by stabilizing high mobility group box-1 (HMGB1).

Air Pollution-Regulated E-Cadherin Mediates Contact Inhibition of Proliferation via the Hippo Signaling Pathways in Emphysema

[Chemico-Biological interactions] Researchers investigated the role of components of the Hippo signaling pathway for E-cadherin-mediated contact inhibition of proliferation in the lungs after air pollution exposure.

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