Results 81 to 90 of about 3,236 (190)
RIPK1 is a master regulator of inflammatory signaling and cell death and increased RIPK1 activity is observed in human diseases, including Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS).
Maurits F. J. M. Vissers +24 more
doaj +1 more source
Introduction RIPK1 is a key regulator for mediating inflammatory signaling and cell death. This includes apoptosis, necroptosis, and innate immune signaling. Given these important functions of RIPK1, abnormalities in its pathway can lead to immune deficiency and/or autoinflammatory disease, with autosomal dominant ...
Andrea Janis, Joao Pedro Lopes
openaire +1 more source
ABSTRACT Autoinflammatory disorders (AIDs) are a clinically heterogeneous group of inborn errors of immunity primarily caused by dysregulation in the innate immune system. Clinical diagnosis is often challenging due to clinical heterogeneity and the overlapping phenotypes with other inborn errors of immunity and monogenic conditions that mimic AIDs ...
Vaishnavi Ashok Badiger +28 more
wiley +1 more source
Receptor-interacting protein kinase 1 (RIPK1) plays an essential role in regulating the necroptosis and apoptosis in cerebral ischemia-reperfusion (I/R) injury.
Tengfei Liu +15 more
doaj +1 more source
PLEKHO2 inhibits TNFα-induced cell death by suppressing RIPK1 activation
Receptor interaction protein kinase 1 (RIPK1) plays a diverse role in tumor necrosis factor α (TNFα) signalings. The ubiquitination of RIPK1 is essential for NF-κB activation, whereas its kinase activity promotes apoptosis and necroptosis.
Chenchen Zhou +4 more
doaj +1 more source
Objective Still disease represents a prototypical polygenic systemic autoinflammatory disease, characterized by recurrent systemic inflammation and dysregulation of innate immunity. Despite extensive clinical characterization, familial clustering Still disease remains unreported.
Longfang Chen +23 more
wiley +1 more source
Human Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome
Objectives VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.
Kana Higashitani +10 more
wiley +1 more source
Targeting the RAGE–RIPK1 binding site attenuates diabetes-associated cognitive deficits
Microglial activation can cause neuroinflammation and the consequent neurological impairments play prominent roles in diabetes-associated cognitive deficits.
Lin Gao +13 more
doaj +1 more source
The effects of NETs on regeneration of various diabetic tissues, and strategies targeting NETs for diabetes tissue regeneration. In the diabetic environment, NETs undergo complex metabolic and immune reprogramming, leading to dynamic changes in antibacterial and proinflammatory functions, and affecting regeneration of multiple systemic tissues.
Xinyi Jiang +6 more
wiley +1 more source
Serum RIPK1, Acute Lung Injury, and Outcomes in Severe Traumatic Brain Injury: A Multicenter Prospective Study [PDF]
Liang Cai,1,* Xianghong Dou,2,* Wensheng Dong,1 Kangqin Zou,1 Lixin Zhang,3 Huayong Hong,3 Xiaole Zhang,3 Jin Liu,4 Da Tian,4 Xiaoyu Wu,4 Jianhua Zhang1 1Department of Neurosurgery, The second People’s Hospital of Lianyungang Affiliated to Kangda
Dou X +10 more
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