Results 121 to 130 of about 17,129 (242)

Holding RIPK1 on the Ubiquitin Leash in TNFR1 Signaling [PDF]

, 2016
The kinase RIPK1 is an essential signaling node in various innate immune signaling pathways being most extensively studied in the TNFR1 signaling pathway.
Darding, M, Peltzer, N, Walczak, H
core  

FKBP5 Mediates Alveolar Fibroblast Necroptosis During Acute Respiratory Distress Syndrome

Cell Proliferation, Volume 59, Issue 1, January 2026.
Structure diagram of alveolar fibroblast activation in septic ARDS model. FKBP5‐mediated alveolar fibroblast necroptosis, leading to the activation of NF‐κB signalling and the secretion of cytokines and the recruitment of neutrophils, and further orchestrating the inflammatory environment of the alveolar epithelia in septic ARDS.
Dong Zhang, Wei Liu, Ting Sun, Yangyang Xiao, Qiuwen Chen, Xiao Huang, Xiaozhi Wang, Qian Qi, Hao Wang, Tao Wang   +9 more
wiley   +1 more source

Overexpression and oncogenic role of RIPK3 in acute myeloid leukemia associated with specific subtypes and treatment outcome

BMC Cancer
Background Receptor-interacting protein kinase 3 (RIPK3) has been implicated in the pathogenesis of diverse human cancers. However, the role of RIPK3 in acute myeloid leukemia (AML) is not fully understood, which needs further research and clarification.
Yun Wang, Ting-Juan Zhang, Liu-Chao Zhang, Zi-Jun Xu, Ming-Qiang Chu, Yang-Jing Zhao, Jiang Lin, Jun Qian, Jing-Dong Zhou   +8 more
doaj   +1 more source

Podocyte RIPK3 Deletion Improves Diabetic Kidney Disease by Attenuating NF‐κB p65 Driven Inflammation

Advanced Science
Receptor‐interacting protein kinase 3 (RIPK3) is a key player in necroptosis and an emerging inflammation regulator, whose contribution to podocyte injury in diabetic kidney disease (DKD) remain unclear.
Lu'an Li, Jiaying Li, Ruizhao Li, Xingchen Zhao, Yuanhan Chen, Yating Cai, Yan Yang, Weiteng Wang, Siqi Zheng, Li Zhang, Xinling Liang   +10 more
doaj   +1 more source

Molecular crosstalk between apoptosis, necroptosis, and survival signaling [PDF]

, 2015
Our current knowledge of the molecular mechanisms regulating the signaling pathways leading to cell survival, cell death, and inflammation has shed light on the tight mutual interplays between these processes.
Bertrand, Mathieu, Kaiser, William J, Vanden Berghe, Tom, Vandenabeele, Peter   +3 more
core   +2 more sources

Persistently Elevated Plasma Concentrations of RIPK3, MLKL, HMGB1, and RIPK1 in Patients with COVID-19 in the Intensive Care Unit

, 2022
Katharina Ruskowski, Holger Neb, Steven R. Talbot, Suma Choorapoikayil, Elisabeth Adam, Andreas von Knethen, Kai Zacharowski, Ulrike Heinicke   +7 more
openalex   +1 more source

TET2 amplifies RIPK3/MLKL necroptosis signal by upregulation of PLK3 to promote UVB-induced skin photodamage [PDF]

, 2023
Dan Wang, Shengbo Yang, Yilan Zeng, Ziting Tang, Yuanhong Liu, Xuemei Li, Xiule Zong   +6 more
openalex   +1 more source

Autosis is a Na+,K+-ATPase-regulated form of cell death triggered by autophagy-inducing peptides, starvation, and hypoxia-ischemia. [PDF]

, 2013
A long-standing controversy is whether autophagy is a bona fide cause of mammalian cell death. We used a cell-penetrating autophagy-inducing peptide, Tat-Beclin 1, derived from the autophagy protein Beclin 1, to investigate whether high levels of ...
Clarke, P.G., Ginet, V., Green, D.R., Levine, B., Liu, Y., Posner, B., Puyal, J., Shaw, S.Y., Shoji-Kawata, S., Sumpter, R.M., Tran, K.A., Wei, Y., Xavier, R.J., Zhang, L.   +13 more
core   +1 more source

Caspase-8 functions as a key mediator of inflammation and pro-IL-1β processing via both canonical and non-canonical pathways. [PDF]

, 2015
Caspase-8 is an apical component of cell death pathways. Activated caspase-8 can drive classical caspase-dependent apoptosis and actively inhibits cell death mediated by RIPK3-driven necroptosis.
Bryant, Clare E, Monie, Tom P
core   +2 more sources

Caspase-8 inhibition represses initial human monocyte activation in septic shock model [PDF]

, 2016
In septic patients, the onset of septic shock occurs due to the over-activation of monocytes. We tested the therapeutic potential of directly targeting innate immune cell activation to limit the cytokine storm and downstream phases.
Caballero-Velázquez, Teresa, Carrillo-Jiménez, Alejandro, García-Quintanilla, Alberto, Herrera, Antonio J., Joseph, Bertrand, Oliva-Martín, María J., Pérez-Simón, José A., Rodhe, Johanna, Sánchez-Abarca, Luis Ignacio, Venero, José L., Vlachos, Pinelopi   +10 more
core   +2 more sources