Search Within


Applied Filters:
Showing 1-21 of 21 results for "C1354" within Papers
Xing Liu et al.
Nature, 535(7610), 153-158 (2016-07-08)
Inflammatory caspases (caspases 1, 4, 5 and 11) are activated in response to microbial infection and danger signals. When activated, they cleave mouse and human gasdermin D (GSDMD) after Asp276 and Asp275, respectively, to generate an N-terminal cleavage product (GSDMD-NT)
Alexander M Skeldon et al.
Journal of immunology (Baltimore, Md. : 1950), 196(1), 437-447 (2015-11-20)
Inflammation is well established to significantly impact metabolic diseases. The inflammatory protease caspase-1 has been implicated in metabolic dysfunction; however, a potential role for the related inflammatory caspases is currently unknown. In this study, we investigated a role for caspase-11
S Wang et al.
The Journal of biological chemistry, 271(34), 20580-20587 (1996-08-23)
We report here the isolation and characterization of a new member of the ice/ced-3 family of cell death genes, named ich-3. The predicted amino acid sequence of Ich-3 protein shares 54% identity with murine interleukin-1beta converting enzyme (ICE). Overexpression of
Brooke A Napier et al.
The Journal of experimental medicine, 213(11), 2365-2382 (2016-11-05)
Cell death and release of proinflammatory mediators contribute to mortality during sepsis. Specifically, caspase-11-dependent cell death contributes to pathology and decreases in survival time in sepsis models. Priming of the host cell, through TLR4 and interferon receptors, induces caspase-11 expression
Ewelina Flis et al.
Cancers, 13(9) (2021-05-01)
Chronic inflammation plays an important role in the pathogenesis of oesophageal adenocarcinoma (EAC) and its only known precursor, Barrett's oesophagus (BE). Recent studies have shown that oesophageal TLR2 levels increase from normal epithelium towards EAC. TLR2 signalling is therefore likely
Caspase functions in cell death and disease
McIlwain DR, et al.
Cold Spring Harbor Perspectives in Biology, 5(4), a008656-a008656 (2013)
Julien Moretti et al.
Cell, 171(4), 809-823 (2017-10-24)
Constitutive cell-autonomous immunity in metazoans predates interferon-inducible immunity and comprises primordial innate defense. Phagocytes mobilize interferon-inducible responses upon engagement of well-characterized signaling pathways by pathogen-associated molecular patterns (PAMPs). The signals controlling deployment of constitutive cell-autonomous responses during infection have remained
Arwa Abu Khweek et al.
Cellular immunology, 370, 104425-104425 (2021-11-21)
Asthma is an inflammatory lung disorder characterized by mucus hypersecretion, cellular infiltration, and bronchial hyper-responsiveness. House dust mites (HDM) are the most prevalent cause of allergic sensitization. Canonical and noncanonical inflammasomes are multiprotein complexes that assemble in response to pathogen
Caspase-11: the driving factor for noncanonical inflammasomes
Vigano E and Mortellaro A
European Journal of Immunology, 43(9), 2240-2245 (2013)
Qi Zhou et al.
Frontiers in bioengineering and biotechnology, 10, 823933-823933 (2022-03-31)
The communication between macrophages and tendon cells plays a critical role in regulating the tendon-healing process. However, the potential mechanisms through which macrophages can control peritendinous fibrosis are unknown. Our data showed a strong pro-inflammatory phenotype of macrophages after a
Sang-Uk Seo et al.
Nature communications, 6, 8010-8010 (2015-08-14)
Monocytes play a crucial role in antimicrobial host defence, but the mechanisms by which they protect the host during intestinal infection remains poorly understood. Here we show that depletion of CCR2(+) monocytes results in impaired clearance of the intestinal pathogen
Naoya Sakaguchi et al.
Frontiers in immunology, 11, 561948-561948 (2020-10-13)
Sepsis is a life-threating multi-organ disease induced by host innate immunity to pathogen-derived endotoxins including lipopolysaccharide (LPS). Direct sensing of LPS by caspase-11 activates inflammasomes and causes lethal sepsis in mice. Inhibition of caspase-11 inflammasomes is important for the prevention
S Wang et al.
Cell, 92(4), 501-509 (1998-03-10)
We report here the inactivation of a member of the Ice/Ced-3 (caspase) family of cell death genes, casp-11, by gene targeting. Like Ice-deficient mice, casp-11 mutant mice are resistant to endotoxic shock induced by lipopolysaccharide. Production of both IL-1alpha and
Yikun Yao et al.
Nature communications, 8, 15402-15402 (2017-05-26)
The connection between innate and adaptive immunity is best exemplified by antigen presentation. Although antigen-presenting cells (APCs) are required for antigen receptor-mediated T-cell activation, how T-cells feedback to APCs to sustain an antigen-specific immune response is not completely clear. Here
Kathrin Krause et al.
Autophagy, 14(11), 1928-1942 (2018-09-01)
CASP4/caspase-11-dependent inflammasome activation is important for the clearance of various Gram-negative bacteria entering the host cytosol. Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila but not those enclosing nonpathogenic
Chuang Yuan et al.
Cell death & disease, 13(8), 722-722 (2022-08-19)
Sepsis is a life-threatening syndrome with disturbed host responses to severe infections, accounting for the majority of death in hospitalized patients. However, effective medicines are currently scant in clinics due to the poor understanding of the exact underlying mechanism. We
M Dagenais et al.
Mucosal immunology, 9(1), 146-158 (2015-06-04)
Cellular inhibitors of apoptosis proteins (cIAPs) are critical arbiters of cell death and key mediators of inflammation and innate immunity. cIAP2 is frequently overexpressed in colorectal cancer and in regenerating crypts of ulcerative colitis patients. However, its corresponding functions in
Xinyu Yang et al.
Immunity, 51(6), 983-996 (2019-12-15)
Excessive activation of the coagulation system leads to life-threatening disseminated intravascular coagulation (DIC). Here, we examined the mechanisms underlying the activation of coagulation by lipopolysaccharide (LPS), the major cell-wall component of Gram-negative bacteria. We found that caspase-11, a cytosolic LPS receptor, activated the
Tzvi Y Pollock et al.
PLoS pathogens, 19(6), e1010767-e1010767 (2023-06-06)
The inflammatory cytokine tumor necrosis factor (TNF) is necessary for host defense against many intracellular pathogens, including Legionella pneumophila. Legionella causes the severe pneumonia Legionnaires' disease and predominantly affects individuals with a suppressed immune system, including those receiving therapeutic TNF
Michael Carty et al.
Immunity, 50(6), 1412-1424 (2019-05-12)
Assembly of inflammasomes after infection or injury leads to the release of interleukin-1β (IL-1β) and to pyroptosis. After inflammasome activation, cells either pyroptose or enter a hyperactivated state defined by IL-1β secretion without cell death, but what controls these different
Chengliang Yuan et al.
Journal of biochemical and molecular toxicology, 36(1), e22943-e22943 (2021-11-02)
Eriocitrin, a lemons flavanone, exhibits several biological properties, antiproliferative, and proapoptotic effects. However, its molecular mechanical action is not entirely clarified. Oxidative stress causes abnormal stimulation of signal transducer and activator of transcription 3 (STAT3) and c-Jun NH2-terminal kinase (JNK), p38
Page 1 of 1