1,752,309 research outputs found
IAP-IAP complexes required for apoptosis resistance of C. trachomatis-infected cells
No full textHost cells infected with obligate intracellular bacteria Chlamydia trachomatis are profoundly resistant to diverse apoptotic stimuli. The molecular mechanisms underlying the block in apoptotic signaling of infected cells is not well understood. Here we investigated the molecular mechanism by which apoptosis induced via the tumor necrosis factor (TNF) receptor is prevented in infected epithelial cells. Infection with C. trachomatis leads to the up-regulation of cellular inhibitor of apoptosis (cIAP)-2, and interfering with cIAP-2 up-regulation sensitized infected cells for TNF-induced apoptosis. Interestingly, besides cIAP-2, cIAP-1 and X-linked IAP, although not differentially regulated by infection, are required to maintain apoptosis resistance in infected cells. We detected that IAPs are constitutively organized in heteromeric complexes and small interfering RNA-mediated silencing of one of these IAPs affects the stability of another IAP. In particular, the stability of cIAP-2 is modulated by the presence of X-linked IAP and their interaction is stabilized in infected cells. Our observations suggest that IAPs are functional and stable as heteromers, a thus far undiscovered mechanism of IAP regulation and its role in modulation of apoptosis
Szecernált IAP antagonisták kimutatása makrofág felülúszóból
No full textA diplomamunkám során a T-limfociták, a dendritikus sejtek és az M1, valamint M2 makrofágok felülúszójának citotoxikus hatásait vizsgáltuk. Feltételezéseink szerint ezen sejtek felülúszója apoptózis inhibítor protein (IAP) antagonistákat tartalmaz, amik részt vehetnek a sejthalál indukcióban. Az apoptózis gátló fehérjék felelősek a RIP1 kináz ubiquitinációjáért, amely a RIP függő apoptózis és a programozott nekrózis kulcsfontosságú szabályozó eleme. Jelenlegi ismereteink szerint a RIP1 függő sejthalál utak csak akkor aktiválódnak, ha a RIP1 deubiquitinált állapotban található. A tumor terápia területén számos szintetikus IAP antagonistát tesztelnek, mivel ezek segítségével aktiválhatóak a RIP függő sejthalál szignálok, így áttörést jelenthetnek az apoptózis rezisztens tumorok kezelésében.orvosi laboratóriumi és képalkotó diagnosztikai analitikusnappalimagyarOrvosdiagnosztikai laboratóriumi analitikaBSc/B
Lutte contre les revues et les conférences scientifiques prédatrices
Full text linkVoici le résumé d’un rapport complet préparé par InterAcademy Partnership (IAP) dans le cadre de la lutte contre les revues et les conférences scientifiques prédatrices. L’IAP est un réseau mondial de regroupant plus de 140 académies des sciences, de l’ingénierie et de la médecine qui travaillent ensemble pour soutenir le rôle de la science dans la recherche de solutions aux problèmes les plus difficiles du monde. En 2020, l’IAP a lancé une étude de deux ans intitulée Combatting Predatory Academic Journals and Conferences (Lutter contre les revues et les conférences scientifiques prédatrices), généreusement financée par la Gordon and Betty Moore Foundation (GBMF), et régie par un groupe de travail international appuyé par un secrétariat professionnel. Le principal objectif de l’étude était d’identifier des interventions pratiques et efficaces pouvant freiner et aider à lutter contre la hausse inquiétante des revues et des conférences prédatrices, et de formuler des recommandations à cet effet aux communautés d’intervenants clés. Ainsi, le Groupe de travail a tiré des preuves d’une enquête unique menée auprès d’universitaires et de chercheurs du monde entier ; a recueilli des connaissances et des points de vue dans le cadre de dialogues avec des praticiens mondiaux, régionaux et nationaux issus de communautés d’intervenants clés ; et a effectué une analyse documentaire approfondie
UMCUGenetics/IAP: v2.5.0
No full textNew features:
IAP modules in own namespace
Initial implementation of bcftools roh
Sync IAP with Harwtig Pipeline v1.10 and v1.11
Add VT normalize to freebayes analysis
Update freebayes filter script
Update somatic melt script
Check fastq.gz pattern before submitting jobs
Fingerprint module
Single sample vcf output optional in vcf utils
Bug fixes:
Allow only one mappability track in freec analysis
Add --temporary-directory to vcf-sort in delly analysis
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UMCUGenetics/IAP: v2.2.0
No full text
Added Callable loci module
Move realign bam after flagstat check
Somatic melt script: Check input tumor sample name with name in vcf
Fix pileup error message
Improve prestats checking
Remove pileup if IAP done
Add manta
Replace SOMVAR_REGEX and CNV_REGEX by SOMATIC_REGEX setting, also used in new manta sv analysis.
Add 'tmp' steps to mapping module, move to definitive files if flagstats check succeeds
Ini changes:
Added Callable loci settings
Change gatk filter names
Manta settings
SOMVAR_REGEX
Update VARSCAN to v.2.4.1
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UMCUGenetics/IAP: v2.3.0
No full textNew features:
Sex aware variant calling + new haplotypecaller scala script -> add CALLING_SEXAWARE to ini
Using relative paths for qscripts and IAP scripts
Save submission log automatically
Add flagstat stats to bamMetrics -> needs new version of bamMetrics
Bug fixes:
Delly job submission
Delly chromosome chunks
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Inhibitor of Apoptosis Proteins as Novel Targets in Inflammatory Processes
Full text linkObjective: Inhibitor of apoptosis proteins (IAPs), such as X-linked or cellular IAP 1/2 (XIAP, cIAP1/2), are important regulators of apoptosis. IAP antagonists are currently under clinical investigation as anticancer agents. Interestingly, IAPs participate in the inflammation-associated TNF receptor signaling complex and regulate NFκB signaling. This raises the question about the role of IAPs in inflammation. Here, we investigated the anti-inflammatory potential of IAP inhibitors and the role of IAPs in inflammatory processes of endothelial cells.
Methods and Results: In mice, the small molecule IAP antagonist A-4.10099.1 (ABT) suppressed antigen-induced arthritis, leukocyte infiltration in concanavalin A-evoked liver injury, and leukocyte transmigration in the TNFα-activated cremaster muscle. In vitro, we observed an attenuation of leukocyte– endothelial cell interaction by downregulation of the intercellular adhesion molecule-1. ABT did not impair NFκB signaling but decreased the TNFα-induced activation of the TGF-β–activated kinase 1, p38, and c-Jun N-terminal kinase. These effects are based on the proteasomal degradation of cIAP1/2 accompanied by an altered ratio of the levels of membrane-localized TNF receptor-associated factors 2 and 5.
Conclusion: Our results reveal IAP antagonism as a profound anti-inflammatory principle in vivo and highlight IAPs as important regulators of inflammatory processes in endothelial cells
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