Results 121 to 130 of about 15,294 (209)
Oligodendrocyte progenitor cells (OPCs) death is a key contributor to cerebral white matter injury (WMI) in the developing brain. A previous study by our group indicated that receptor-interacting proteins (RIPs) are crucial in mediating necroptosis in ...
Dezhi Mu +7 more
core +1 more source
Bilirubin directly activates RIPK3 to induce non-classical necroptosis
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 +1 more source
BRAF and AXL oncogenes drive RIPK3 expression loss in cancer
Necroptosis is a lytic programmed cell death mediated by the RIPK1-RIPK3-MLKL pathway. The loss of Receptor-interacting serine/threonine-protein kinase 3 (RIPK3) expression and necroptotic potential have been previously reported in several cancer cell ...
Ursula A Matulonis +21 more
core +1 more source
RIPK3 Orchestrates Scar‐Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis
Idiopathic pulmonary fibrosis (IPF) is characterized by aberrant tissue remodeling and immune dysregulation. While receptor‐interacting protein kinase 3 (RIPK3) is canonically recognized as a central executioner of necroptosis, its non‐necroptotic ...
Tao Yang +12 more
doaj +1 more source
RIPK3 is required for cisplatin-induced necrosis.
(A) Effects of RIPK3 knockdown were determined using western blot analysis, β-Actin as a loading control. (B) RIPK3-KD-F2 clones and the parental cells were treated with 10 µM cisplatin for 24 h. Cell viability was assessed by MTT assay.
Zbigniew Cichacz (315940) +8 more
core +1 more source
Two distinct mechanisms are involved in PmPOD-induced necroptosis, including the autocrine production of TNF-α and the restoration of RIPK3 expression in RIPK3-silenced cells.
Ru Wang, Zhuanhua Wang, Xiaodong Cui
core +1 more source
The kinase domain of RIPK3 tunes its scaffolding functions
Abstract The pro-inflammatory programmed cell death pathway, necroptosis, relies on phosphorylation of the terminal effector, MLKL, by RIPK3. RIPK3-deficient mice or those harboring the kinase-inactivating mutation, RIPK3 K51A , are ostensibly normal in the absence of ...
Shene Chiou +16 more
openaire +2 more sources
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 +1 more source
Elevated RIPK3 correlates with disease burden in myelofibrosis
Veronika Dill +19 more
openaire +3 more sources

