Results 31 to 40 of about 307,665 (262)
Downregulation of Caspase 8 in a group of Iranian breast cancer patients – A pilot study
Journal of the Egyptian National Cancer Institute, 2017 Purpose: It is now well known that evading apoptosis, as a cancer hallmark, can lead to tumour initiation, progression and metastasis. As a result of genome wide association studies, an initiator protease in this pathway, caspase 8 (CASP8), has been ...
Masoumeh Aghababazadeh +5 more
doaj +1 more source
Caspase‐8 Variant G Regulates Rheumatoid Arthritis Fibroblast‐Like Synoviocyte Aggressive Behavior
ACR Open Rheumatology, 2022 Objective Fibroblast‐like synoviocytes (FLS) play a pivotal role in rheumatoid arthritis (RA) by contributing to synovial inflammation and progressive joint damage. An imprinted epigenetic state is associated with the FLS aggressive phenotype.
Cecilia Ansalone +15 more
doaj +1 more source
Caspase 8: igniting the death machine [PDF]
Structure, 1999 Intense research into the signaling pathways of apoptosis has revealed a dominant role for proteases belonging to the caspase family, which in humans has 11 members at present. Two papers in the September issue of Structure with Folding & Design have for the first time revealed the structure of the key apoptotic initiator, caspase 8.
openaire +2 more sources
Cell Reports, 2017 Formation of the death-inducing signaling complex (DISC) initiates extrinsic apoptosis. Caspase-8 and its regulator cFLIP control death signaling by binding to death-receptor-bound FADD.
Sebastian Horn +9 more
doaj +1 more source
Activation of caspases-8 and -10 by FLIPL [PDF]
Biochemical Journal, 2004 The first step in caspase activation is transition of the latent zymogen to an active form. For the initiator caspases, this occurs through dimerization of monomeric zymogens at an activating complex. Recent studies have suggested that FLIPL [FLICE-like inhibitory protein, long form; FLICE is FADD (Fas-associated death domain protein)-like interleukin ...
Kelly M, Boatright +4 more
openaire +2 more sources
Neurobiology of Disease, 2021 Retinal ganglion cells (RGCs) expanding from the retina to the brain are primary victims of neurodegeneration in glaucoma, a leading cause of blindness; however, the neighboring astroglia survive the glaucoma-related stress and promote neuroinflammation.
Xiangjun Yang, Qun Zeng, Gülgün Tezel
doaj +1 more source
Reciprocal control of viral infection and phosphoinositide dynamics
FEBS Letters, EarlyView.Phosphoinositides, although scarce, regulate key cellular processes, including membrane dynamics and signaling. Viruses exploit these lipids to support their entry, replication, assembly, and egress. The central role of phosphoinositides in infection highlights phosphoinositide metabolism as a promising antiviral target.
Marie Déborah Bancilhon, Bruno Mesmin
wiley +1 more source
Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential
FEBS Letters, EarlyView.Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta +3 more
wiley +1 more source
Journal of Neuroinflammation, 2022 Background Immune activation, neuroinflammation, and cell death are the hallmarks of multiple sclerosis (MS), which is an autoimmune demyelinating disease of the central nervous system (CNS). It is well-documented that the cellular inhibitor of apoptosis
Debolina D. Biswas +10 more
doaj +1 more source
Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment
Molecular Oncology, EarlyView.This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley +1 more source