Results 1 to 10 of about 19,284 (185)

A viable kinase-inactive RIPK3 D143N mouse model reveals its scaffold function in driving TNF-induced inflammatory disorder [PDF]

open access: yesCell Death Discovery
RIPK3 is a key regulator of necroptosis, but the specific roles of its kinase-dependent and -independent functions in disease pathogenesis remain poorly understood.
Yayun Du   +13 more
doaj   +2 more sources

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

open access: yesAdvanced 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   +10 more
doaj   +2 more sources

GADD45β inhibits RIPK3-mediated NF-κB activation by interfering with NEMO-RIPK1-RIPK3 interactions [PDF]

open access: yesCell Death Discovery
Necroptosis is a highly inflammatory form of regulated cell death driven by Receptor-Interacting Protein Kinase 3 (RIPK3), which plays a crucial role in immune responses, inflammatory diseases, and tumor microenvironment modulation.
Carmela Casale   +10 more
doaj   +2 more sources

Bilirubin directly activates RIPK3 to induce non-classical necroptosis [PDF]

open access: yesCell Discovery
Bilirubin, a byproduct of heme metabolism, is traditionally recognized for its antioxidant properties. However, its accumulation under pathological conditions can result in severe clinical manifestations, including neurotoxicity.
Qian Xue   +19 more
doaj   +2 more sources

RIPK3 promotes islet amyloid-induced β-cell loss and glucose intolerance in a humanized mouse model of type 2 diabetes

open access: yesMolecular Metabolism
Objective: Aggregation of human islet amyloid polypeptide (hIAPP), a β-cell secretory product, leads to islet amyloid deposition, islet inflammation and β-cell loss in type 2 diabetes (T2D), but the mechanisms that underlie this process are incompletely ...
Noyonika Mukherjee   +8 more
doaj   +2 more sources

Structure-based design of potent and selective inhibitors targeting RIPK3 for eliminating on-target toxicity in vitro

open access: yesNature Communications
The essential role of RIPK3 in necroptosis makes its inhibition a promising therapeutic strategy. However, the development of RIPK3 inhibitors has been hampered by on-target apoptosis and limited kinase selectivity.
Haixia Su   +11 more
doaj   +2 more sources

Evolutionary and functional analyses reveal a role for the RHIM in tuning RIPK3 activity across vertebrates

open access: yeseLife
Receptor interacting protein kinases (RIPK) RIPK1 and RIPK3 play important roles in diverse innate immune pathways. Despite this, some RIPK1/3-associated proteins are absent in specific vertebrate lineages, suggesting that some RIPK1/3 functions are ...
Elizabeth J Fay   +4 more
doaj   +2 more sources

Structure-Based Virtual Screening of Cinnamic Acid Analogs Against RIPK3: Implications for Anti-Inflammatory Drug Discovery [PDF]

open access: yesAvicenna Journal of Medical Biochemistry, 2023
Background: A common oral inflammatory disease known as apical periodontitis (AP) is caused by the intrusion of microorganisms into the dental pulp, resulting in an inflammatory response and bone degradation in periapical tissues.
Elham Khoshbin   +4 more
doaj   +1 more source

Necroptosis: A Novel Pathway in Neuroinflammation

open access: yesFrontiers in Pharmacology, 2021
Neuroinflammation is a complex inflammatory process in the nervous system that is expected to play a significant role in neurological diseases. Necroptosis is a kind of necrosis that triggers innate immune responses by rupturing dead cells and releasing ...
Ziyu Yu   +4 more
doaj   +1 more source

Comparative and evolutionary analysis of RIP kinases in immune responses

open access: yesFrontiers in Genetics, 2022
The group of receptor-interacting protein (RIP) kinases has seven members (RIPK1–7), with one homologous kinase domain but distinct non-kinase regions.
Shangge Lv   +8 more
doaj   +1 more source

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