The Chlamydia trachomatis Inc Tri1 interacts with TRAF7 to displace native TRAF7 interacting partners.

Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections in the USA and of preventable blindness worldwide. This obligate intracellular pathogen replicates within a membrane-bound inclusion, but how it acquires nutrients from the host while avoiding detection by the innate immune system is incompletely understood. C. trachomatis accomplishes this in part through the translocation of a unique set of effectors into the inclusion membrane, the inclusion membrane proteins (Incs). Incs are ideally positioned at the host-pathogen interface to reprogram host signaling by redirecting proteins or organelles to the inclusion. Using a combination of co-affinity purification, immunofluorescence confocal imaging, and proteomics, we characterize the interaction between an early-expressed Inc of unknown function, Tri1, and tumor necrosis factor receptor-associated factor 7 (TRAF7). TRAF7 is a multi-domain protein with a RING finger ubiquitin ligase domain and a C-terminal WD40 domain. TRAF7 regulates several innate immune signaling pathways associated with C. trachomatis infection and is mutated in a subset of tumors. We demonstrate that Tri1 and TRAF7 specifically interact during infection and that TRAF7 is recruited to the inclusion. We further show that the predicted coiled-coil domain of Tri1 is necessary to interact with the TRAF7 WD40 domain. Finally, we demonstrate that Tri1 displaces the native TRAF7 binding partners, mitogen-activated protein kinase kinase kinase 2 (MEKK2), and MEKK3. Together, our results suggest that by displacing TRAF7 native binding partners, Tri1 has the capacity to alter TRAF7 signaling during C. trachomatis infection.IMPORTANCEChlamydia trachomatis is the leading cause of bacterial sexually transmitted infections in the USA and preventable blindness worldwide. Although easily treated with antibiotics, the vast majority of infections are asymptomatic and therefore go untreated, leading to infertility and blindness. This obligate intracellular pathogen evades the immune response, which contributes to these outcomes. Here, we characterize the interaction between a C. trachomatis-secreted effector, Tri1, and a host protein involved in innate immune signaling, TRAF7. We identified host proteins that bind to TRAF7 and demonstrated that Tri1 can displace these proteins upon binding to TRAF7. Remarkably, the region of TRAF7 to which these host proteins bind is often mutated in a subset of human tumors. Our work suggests a mechanism by which Tri1 may alter TRAF7 signaling and has implications not only in the pathogenesis of C. trachomatis infections but also in understanding the role of TRAF7 in cancer.

The Chlamydia effector IncE employs two short linear motifs to reprogram host vesicle trafficking.

Chlamydia trachomatis, a leading cause of bacteria sexually transmitted infections, creates a specialized intracellular replicative niche by translocation and insertion of a diverse array of effectors (Incs) into the inclusion membrane. Here, we characterize IncE, a multi-functional Inc that encodes two non-overlapping short linear motifs (SLiMs) within its short cytosolic C-terminus. The proximal SLiM mimics an R-SNARE motif to recruit syntaxin (STX) 7 and 12-containing vesicles to the inclusion. The distal SLiM mimics the Sorting Nexin (SNX) 5 and 6 cargo binding site to recruit SNX6-containing vesicles to the inclusion. By simultaneously binding to two distinct vesicle classes, IncE reprograms host cell trafficking to promote the formation of a class of hybrid vesicles at the inclusion that are required for C. trachomatis intracellular development. Our work suggests that Incs may have evolved SLiMs to facilitate rapid evolution in a limited protein space to disrupt host cell processes.

The Chlamydia trachomatis Inc Tri1 interacts with TRAF7 to displace native TRAF7 interacting partners.

Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections in the US and of preventable blindness worldwide. This obligate intracellular pathogen replicates within a membrane-bound inclusion, but how it acquires nutrients from the host while avoiding detection by the innate immune system is incompletely understood. C. trachomatis accomplishes this in part through the translocation of a unique set of effectors into the inclusion membrane, the inc lusion membrane proteins (Incs). Incs are ideally positioned at the host-pathogen interface to reprogram host signaling by redirecting proteins or organelles to the inclusion. Using a combination of co-affinity purification, immunofluorescence confocal imaging, and proteomics, we characterize the interaction between an early-expressed Inc of unknown function, Tri1, and tumor necrosis factor receptor associated factor 7 (TRAF7). TRAF7 is a multi-domain protein with a RING finger ubiquitin ligase domain and a C-terminal WD40 domain. TRAF7 regulates several innate immune signaling pathways associated with C. trachomatis infection and is mutated in a subset of tumors. We demonstrate that Tri1 and TRAF7 specifically interact during infection and that TRAF7 is recruited to the inclusion. We further show that the predicted coiled-coil domain of Tri1 is necessary to interact with the TRAF7 WD40 domain. Finally, we demonstrate that Tri1 displaces the native TRAF7 binding partners, mitogen activated protein kinase kinase kinase 2 (MEKK2) and MEKK3. Together, our results suggest that by displacing TRAF7 native binding partners, Tri1 has the capacity to alter TRAF7 signaling during C. trachomatis infection. Importance: Chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections in the US and preventable blindness worldwide. Although easily treated with antibiotics, the vast majority of infections are asymptomatic and therefore go untreated, leading to infertility and blindness. This obligate intracellular pathogen evades the immune response, which contributes to these outcomes. Here, we characterize the interaction between a C. trachomatis secreted effector, Tri1, and a host protein involved in innate immune signaling, TRAF7. We identified host proteins that bind to TRAF7 and demonstrate that Tri1 can displace these proteins upon binding to TRAF7. Remarkably, the region of TRAF7 to which these host proteins bind is often mutated in a subset of human tumors. Our work suggests a mechanism by which Tri1 may alter TRAF7 signaling and has implications not only in the pathogenesis of C. trachomatis infections, but also in understanding the role of TRAF7 in cancer.

Proliferación miofibroblástica en región mandibular: a propósito de un caso / Myofibroblastic proliferation in the mandibular region: a case report

La proliferación miofibroblastica es una lesión localmente agresiva, benigna, de etiología desconocida, tiene una histopatología distintiva de células fusiformes mi fibroblásticas en proliferación con infiltración de células inflamatorias predominantes células plasmáticas y linfocitos. La incidencia de esta lesión en cabeza y cuello es muy rara. Su diagnóstico definitivo es histológico y el tratamiento de elección es la resección quirúrgica. Reportamos un caso raro en un joven de 13 años de edad. La proliferación miofibroblastica en la cavidad oral es una condición poco común, con poca información, en cuanto a su etiología y patogenia

Glioma difuso pediatrico de tronco encefalico: Reporte de caso / Pediatric Diffuse Brain Stem Glioma: Case Report

El glioma difuso de tronco encefálico es un tumor de mal pronóstico, presentándose principalmente en la población pediátrica entre los 3 a 5 años, sin predisposición de género. Las principales manifestaciones clínicas incluyen la parálisis de los nervios craneales y signos de aumento de la presión intracraneal. Para su diagnóstico se prefieren los estudios de imagen ante el riesgo que conlleva la realización de una biopsia para su estudio anatomopatológico. Presentamos el caso clínico de un niño de 4 años de edad, admitido en el Servicio de Emergencias del Hospital del Niño "Dr. Ovidio Aliaga Uría", donde los estudios complementarios efectuados permitieron alcanzar su diagnóstico correcto, posteriormente confirmado por histopatología. El principal objetivo de tratamiento es la resección total sin embargo no es viable en todos los casos.

Measurement of a Latino cultural value: The Simpatía scale.

OBJECTIVE: Simpatía, a term that captures the tendency to prefer and create social interactions characterized by warmth and emotional positivity while also avoiding conflict and/or overt negativity, is a cultural factor relevant to Latinos. The goal of this article was to develop a scale that measures this cultural value. METHOD: A self-report scale measure of simpatía was developed and administered to a combined sample of Latinos (N = 296) drawn from 3 larger studies. The scale's factor structure was explored, and its internal consistency and validity were tested. RESULTS: Exploratory factor analysis supported an 18-item scale and indicated 2 factors: simpatía-related positivity/warmth and simpatía-related negativity/conflict avoidance. Cronbach's alphas for the overall scale and subscales showed internal consistency. Validity analyses revealed that across subscales, simpatía was positively associated with positive emotion expressivity and dispositional positive emotion. The simpatía-related positivity/warmth subscale was also positively associated with an orientation toward Latino culture. CONCLUSIONS: The Simpatía Scale, which captures dual aspects of simpatía that emphasize the positive and avoid the negative, provides a new tool for advancing the study of Latino culture. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Functional role of PGAM5 multimeric assemblies and their polymerization into filaments.

PGAM5 is a mitochondrial protein phosphatase whose genetic ablation in mice results in mitochondria-related disorders, including neurodegeneration. Functions of PGAM5 include regulation of mitophagy, cell death, metabolism and aging. However, mechanisms regulating PGAM5 activation and signaling are poorly understood. Using electron cryo-microscopy, we show that PGAM5 forms dodecamers in solution. We also present a crystal structure of PGAM5 that reveals the determinants of dodecamer formation. Furthermore, we observe PGAM5 dodecamer assembly into filaments both in vitro and in cells. We find that PGAM5 oligomerization into a dodecamer is not only essential for catalytic activation, but this form also plays a structural role on mitochondrial membranes, which is independent of phosphatase activity. Together, these findings suggest that modulation of the oligomerization of PGAM5 may be a regulatory switch of potential therapeutic interest.

Evaluación de la técnica de contrainmunoelectroforesis para el diagnóstico serológico de la leptospirosis / Assessment of counterimmunoelectrophoresis technic for serological diagnosis of leptospirosis

Se evaluó la técnica de contrainmunoelectroforesis (CIE) para el diagnóstico serológico de la leptospirosis, utilizando un preparado antigénico de la cepa Leptospira bifleza Patoc I. El estudio demostró que la técnica de CIE presentó una sensibilidad del 82

y una especificidad del 100

. El antígeno empleado mostró una reactividad específica de género al detectar anticuerpos en pacientes infectados por distintos serogrupos de leptospira, mediante la prueba de microaglutinación (MA). La estabilidad del antígeno para la técnica de CIE fue de 6 meses sin pérdida de título.

Evaluación de la técnica de contrainmunoelectroforesis para el diagnóstico serológico de la leptospirosis / Assessment of counterimmunoelectrophoresis technic for serological diagnosis of leptospirosis

Se evaluó la técnica de contrainmunoelectroforesis (CIE) para el diagnóstico serológico de la leptospirosis, utilizando un preparado antigénico de la cepa Leptospira bifleza Patoc I. El estudio demostró que la técnica de CIE presentó una sensibilidad del 82 por ciento y una especificidad del 100 por ciento . El antígeno empleado mostró una reactividad específica de género al detectar anticuerpos en pacientes infectados por distintos serogrupos de leptospira, mediante la prueba de microaglutinación (MA). La estabilidad del antígeno para la técnica de CIE fue de 6 meses sin pérdida de título

La técnica de contrainmunoelectroforesis para el diagnóstico serológico de la leptospirosis / Contraimmunoelectrophoresis technique to serologic diagnostic of the leptospirosis

Se evaluó la técnica de contrainmunoelectroforesis (CIE) para el diagnóstico serológico de la leptospirosis, utilizando un preparado antigénico de la cepa leptospira biflexa Patoc I. El estudio demostró que la técnica de CIE, presentó una sensibilidad del 82 por ciento y una especificidad del 100 por ciento. El antígeno empleado mostró una reactividad específica del género al detectar anticuerpos en pacientes infectados por distintos serogrupos de leptospira, mediante la prueba de microaglutinación (MA). La estabilidad del antígeno para la técnica de CIE fue de 6 meses sin pérdida de título