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- 저자 : Ribot, Wilson J. (검색결과 3 건)
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Type VI secretion is a major virulence determinant in <i>Burkholderia mallei</i>
Schell, Mark A.,Ulrich, Ricky L.,Ribot, Wilson J.,Brueggemann, Ernst E.,Hines, Harry B.,Chen, Dan,Lipscomb, Lyla,Kim, H. Stanley,Mrá,zek, Jan,Nierman, William C.,DeShazer, David Blackwell Publishing Ltd 2007 Molecular microbiology Vol.64 No.6
<P><B>Summary</B></P><P> <I>Burkholderia mallei</I> is a host‐adapted pathogen and a category B biothreat agent. Although the <I>B. mallei</I> VirAG two‐component regulatory system is required for virulence in hamsters, the virulence genes it regulates are unknown. Here we show with expression profiling that overexpression of <I>virAG</I> resulted in transcriptional activation of ∼60 genes, including some involved in capsule production, actin‐based intracellular motility, and type VI secretion (T6S). The 15 genes encoding the major sugar component of the homopolymeric capsule were up‐expressed > 2.5‐fold, but capsule was still produced in the absence of <I>virAG</I>. Actin tail formation required <I>virAG</I> as well as <I>bimB</I>, <I>bimC</I> and <I>bimE</I>, three previously uncharacterized genes that were activated four‐ to 15‐fold when VirAG was overproduced. Surprisingly, actin polymerization was found to be dispensable for virulence in hamsters. In contrast, genes encoding a T6S system were up‐expressed as much as 30‐fold and mutations in this T6S gene cluster resulted in strains that were avirulent in hamsters. SDS‐PAGE and mass spectrometry demonstrated that BMAA0742 was secreted by the T6S system when <I>virAG</I> was overexpressed. Purified His‐tagged BMAA0742 was recognized by glanders antiserum from a horse, a human and mice, indicating that this Hcp‐family protein is produced <I>in vivo</I> during infection.</P>
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Bernard, Clé,mence,Vincent, Clé,mentine,Testa, Damien,Bertini, Eva,Ribot, Jé,rô,me,Di Nardo, Ariel A.,Volovitch, Michel,Prochiantz, Alain Public Library of Science 2016 PLoS genetics Vol.12 No.5
<▼1><P>During postnatal life the cerebral cortex passes through critical periods of plasticity allowing its physiological adaptation to the environment. In the visual cortex, critical period onset and closure are influenced by the non-cell autonomous activity of the Otx2 homeoprotein transcription factor, which regulates the maturation of parvalbumin-expressing inhibitory interneurons (PV cells). In adult mice, the maintenance of a non-plastic adult state requires continuous Otx2 import by PV cells. An important source of extra-cortical Otx2 is the choroid plexus, which secretes Otx2 into the cerebrospinal fluid. Otx2 secretion and internalization requires two small peptidic domains that are part of the DNA-binding domain. Thus, mutating these “transfer” sequences also modifies cell autonomous transcription, precluding this approach to obtain a cell autonomous-only mouse. Here, we develop a mouse model with inducible secretion of an anti-Otx2 single-chain antibody to trap Otx2 in the extracellular milieu. Postnatal secretion of this single-chain antibody by PV cells delays PV maturation and reduces plasticity gene expression. Induced adult expression of this single-chain antibody in cerebrospinal fluid decreases Otx2 internalization by PV cells, strongly induces plasticity gene expression and reopens physiological plasticity. We provide the first mammalian genetic evidence for a signaling mechanism involving intercellular transfer of a homeoprotein transcription factor. Our single-chain antibody mouse model is a valid strategy for extracellular neutralization that could be applied to other homeoproteins and signaling molecules within and beyond the nervous system.</P></▼1><▼2><P><B>Author Summary</B></P><P>Classically, cell signaling is based on the secretion of molecules that bind cell surface receptors. Lipophilic agents can do without cell-surface receptors due to their ability to diffuse through the plasma membrane, but this is normally not the case for proteins, which cannot pass the membrane barrier. However, homeoprotein transcription factors represent an exception as they are secreted and internalized by live cells owing to two peptidic domains. An important illustration of this novel signaling mechanism is provided by Otx2, a homeoprotein that travels from the choroid plexus to specific inhibitory neurons in the cerebral cortex, where it regulates physiological plasticity throughout life. Because the two transfer peptides are in the DNA-binding domain of Otx2, it is impossible to mutate them without altering both cell signaling and cell-autonomous functions. We have therefore developed a mouse in which a secreted anti-Otx2 single-chain antibody can be induced to trap extracellular Otx2 while leaving its cell autonomous function untouched. We show that neutralizing extracellular Otx2 modifies the expression of plasticity genes in the visual cortex, thus providing the first genetic demonstration for homeoprotein signaling in a mammal.</P></▼2>
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Patel Madhav Rajesh,Jacob Kevin Chacko,Amin Kanhai S.,Ribot Max A.,Pawlowski Hanna,Prabhu Michael C.,Vanjani Nisheka Navin,Singh Kern 대한척추외과학회 2023 Asian Spine Journal Vol.17 No.1
Study Design: This was a retrospective cohort study.Purpose: This study investigated the influence of preoperative mental health on patient-reported outcome measures (PROMs) and minimal clinically important difference (MCID) among workers’ compensation (WC) recipients undergoing minimally invasive transforaminal lumbar interbody fusion (MIS TLIF).Overview of Literature: No studies have evaluated the impact of preoperative mental functioning on outcomes following MIS TLIF among WC claimants.Methods: WC recipients undergoing single-level MIS TLIF were identified. PROMs of Visual Analog Scale (VAS) for back and leg pain, Oswestry Disability Index (ODI), 12-item Short Form Physical and Mental Composite Scale (SF-12 PCS/MCS), and Patient-Reported Outcomes Measurement Information System Physical Function evaluated subjects preoperatively/postoperatively. Subjects were grouped according to preoperative SF-12 MCS: <41 vs. ≥41. Demographic/perioperative variables, PROMs, and MCID were compared using inferential statistics. Multiple regression was used to account for differences in spinal pathology.Results: The SF-12 MCS <41 and SF-12 MCS ≥41 groups included 48 and 45 patients, respectively. Significant differences in ΔPROMs were observed at SF-12 MCS at all timepoints, except at 6 months (p≤0.041, all). The SF-12 MCS <41 group had worse preoperative to 6-months SF-12 MCS, 12-weeks/6-months VAS back, 12-week VAS leg, and preoperative to 6-months ODI (p≤0.029, all). The SF-12 MCS <41 group had greater MCID achievement for overall ODI and 6-weeks/1-year/overall SF-12 MCS (p≤0.043, all); the SF-12 MCS ≥41 group had greater attainment for 6-month VAS back (p=0.004).Conclusions: Poorer mental functioning adversely affected the baseline and intermediate postoperative quality-of-life outcomes pertaining to mental health, back pain, and disability among WC recipients undergoing lumbar fusion. However, outcomes did not differ 1–2 years after surgery. While MCID achievement for pain and physical function was largely unaffected by preoperative mental health score, WC recipients with poorer baseline mental health demonstrated higher rates of overall clinically meaningful improvements for disability and mental health
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