Polypeptide Modulators of Caspase Recruitment Domain (CARD)-CARD-mediated Protein-Protein Interactions

Palacios, Yadira; García‐Lainez, Guillermo; Sancho, Mónica; Gortat, Anna; Orzáez, Mar; Pérez‐Payá, Enrique

doi:10.1074/jbc.m111.255364

Cited by 16 publications

(13 citation statements)

References 61 publications

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“…The NOD proteins NOD 1 and NOD 2 are important in sensing the presence of bacterial pathogens by identifying peptidoglycan wall peptide ligands gamma-D-glutamylmeso-diaminopimelic acid and muramyl dipeptide components that are associated with bacterial walls, and work with other proteins, specifically the Toll-like receptors (TLRs), in mediating responses to bacterial invasion [ 36 ]. Once NOD proteins detect peptidoglycan group patterns in bacterial cells they are activated through the leucine rich repeat segment, recruit and bind receptor-interacting serine/threonine kinase (RICK) through the caspase-recruitment domain interactions (CARD) [ 30 37 ]. RICK activation then stimulates polyubiquitulanation of Ikk B [ 30 ].…”

Section: Putative Pathogenesismentioning

confidence: 99%

“…The resultant phosphorylation event activates nuclear factor kappa B (NF-κB), mitogen-activated protein kinases (MAPKs) such as JUN-amino terminal kinase (JNLK), JAK, extracellular signal-regulated kinases (Erk) and p38 MAPK while also stimulates pro-inflammatory cytokine expression [ 30 35 37 ]. All of the transcription factors and cytokines involved in this pathway are important mediators of inflammatory disease and immune pathogenesis, and through the CARD system, apoptosis and cysteine-dependent-aspartate directed protease (caspase) protein activation [ 30 35 37 ]. NOD1 is less active in this functional pathway, and has been primarily associated with demonstrating elevated levels in response to bacterial infection such as Helicobacter pylori gastroenteritis [ 30 ].…”

Section: Putative Pathogenesismentioning

confidence: 99%

“…Conversely, individuals with CARD15 mutations show very strong immune reactions to peptidoglycan peptides, elaborate high levels of IL12 and IL23, and can easily support development of Th1 mediated clinical colitis [ 30 ]. Interestingly, the CARD proteins are instrumental in activating caspase proteins that are important mediators of apoptosis, inflammation, necrosis and cell death [ 37 ], and can recognize intracellular double stranded RNA which is commonly found in viral genomes ranging from the Orthomyxoviridae viruses such as Influenza virus, to Rhabdoviridae family viruses such as Rabies virus [ 37 ]. Both NOD and caspase proteins are considered to be part of the inflammasome constituent of nucleotide-binding domain, leucine rich containing (NLR) family proteins [ 37 ].…”

Section: Putative Pathogenesismentioning

confidence: 99%

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Spontaneous and transgenic rodent models of inflammatory bowel disease

Prattis

2015

Lab Anim Res

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Inflammatory Bowel Disease (IBD) is a multifactorial disorder with many different putative influences mediating disease onset, severity, progression and diminution. Spontaneous natural IBD is classically expressed as Crohn's Disease (CD) and Ulcerative Colitis (UC) commonly found in primates; lymphoplasmocytic enteritis, eosinophilic gastritis and colitis, and ulcerative colitis with neuronal hyperplasia in dogs; and colitis in horses. Spontaneous inflammatory bowel disease has been noted in a number of rodent models which differ in genetic strain background, induced mutation, microbiota influences and immunopathogenic pathways. Histological lesions in Crohn's Disease feature noncaseating granulomatous inflammation while UC lesions typically exhibit ulceration, lamina propria inflammatory infiltrates and lack of granuloma development. Intestinal inflammation caused by CD and UC is also associated with increased incidence of intestinal neoplasia. Transgenic murine models have determined underlying etiological influences and appropriate therapeutic targets in IBD. This literature review will discuss current opinion and findings in spontaneous IBD, highlight selected transgenic rodent models of IBD and discuss their respective pathogenic mechanisms. It is very important to provide accommodation of induced putative deficits in activities of daily living and to assess discomfort and pain levels in the face of significant morbidity and/or mortality in these models. Epigenetic, environmental (microbiome, metabolome) and nutritional factors are important in IBD pathogenesis, and evaluating ways in which they influence disease expression represent potential investigative approaches with the greatest potential for new discoveries.

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Section: Putative Pathogenesismentioning

confidence: 99%

Section: Putative Pathogenesismentioning

confidence: 99%

Section: Putative Pathogenesismentioning

confidence: 99%

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Spontaneous and transgenic rodent models of inflammatory bowel disease

Prattis

2015

Lab Anim Res

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“…Determination of K d for Procaspase-9 Binding to Apaf-1-The K d value for binding of procaspase-9 to Apaf-1 was determined from an IC 50 value reported by Palacios-Rodriguez et al (26). The approach is described in brief in the following.…”

Section: Methodsmentioning

confidence: 99%

“…For the parameterization of the CARD-CARD interaction, we took into account that procaspase-9 binds to the Apaf-1 CARD with a K d of ϳ0.7 M, as calculated from Palacios-Rodriguez et al (26) (see "Experimental Procedures") and that procaspase-9 binds ϳ10-fold more efficient to the apoptosome than processed caspase-9 (17). To obtain the related k on and k off rate constants, we conducted sensitivity analyses with both APO-PTO-ALL and APOPTO-DIM, aiming to reproduce experimental data on caspase-3-dependent substrate cleavage in HeLa cervical cancer cells.…”

Section: Model Extensions To Investigate Allosteric or Homo-dimerizatmentioning

confidence: 99%

A Systems Biology Analysis of Apoptosome Formation and Apoptosis Execution Supports Allosteric Procaspase-9 Activation

Würstle

Rehm

2014

Journal of Biological Chemistry

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Background: Mathematical simulations of apoptosome formation and mechanisms of caspase-9 activation were conducted and validated against experimental data. Results: Only simulations that assume allosteric caspase-9 activation can accurately reproduce all experimental data. Conclusion: A mechanism of allosteric caspase-9 activation is favored over homodimerization-based activation. Significance: Our findings challenge the dogma that all initiator caspases are activated by homodimerization.

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Phage survival: The biodegradability of M13 phage display library in vitro

Tóthová

Bábíčková

Celec

2012

Biotech and App Biochem

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Administration of bacteriophages is used for phage therapy modulation of gut microbiome or for in vivo phage display. The aim of the study was to analyze the survival of M13 phage in different body fluids and tissues in vitro. The survival of M13 phage was measured in vitro in human blood, saliva, urine, artificial gastric juice (AGJ), and mouse homogenates of stomach, jejunum, and colon after defined time points (5, 15, or 45 Min). The plates were inspected after overnight incubation and the plaques were counted. No phage was recovered after 5 Min of incubation with AGJ. In urine, the phage survival was decreased by 44% after 5 Min of incubation (P = 0.004). In saliva, the recovered titer was decreased by 33% and 88% (P < 0.05) after 15 and 45 Min, respectively. Phage coincubation with jejunum homogenate led to significant decrease of phage titer by 72% (P < 0.01) after 15 Min and by 99% (P < 0.001) after 45 Min. Decreased survival of M13 phage depending on time of incubation was proved under several in vitro conditions, with low pH in the AGJ having the most detrimental effect on phage survival. Phage pharmacokinetics described in vitro might have applications for the use of bacteriophages in vivo.

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Polypeptide Modulators of Caspase Recruitment Domain (CARD)-CARD-mediated Protein-Protein Interactions

Cited by 16 publications

References 61 publications

Spontaneous and transgenic rodent models of inflammatory bowel disease

Spontaneous and transgenic rodent models of inflammatory bowel disease

A Systems Biology Analysis of Apoptosome Formation and Apoptosis Execution Supports Allosteric Procaspase-9 Activation

Phage survival: The biodegradability of M13 phage display library in vitro

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