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RISS 인기검색어
- 검색키워드
- 저자 : Gregory B. Martin (검색결과 4 건)
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- 유료
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황인선,Jen Brady,Gregory B. Martin,오창식 한국식물병리학회 2017 Plant Pathology Journal Vol.33 No.2
SlMAPKKKα, a tomato (Solanum lycopersicum)mitogen-activated protein kinase kinase kinase, is apositive regulator of Pto-mediated effector-triggeredimmunity, which elicits programmed cell death (PCD)in plants. In this study, we examined whether putativephosphorylation sites in the conserved activation segmentof the SlMAPKKKα kinase domain are criticalfor eliciting PCD. Three amino acids, threonine353,serine360 (Ser360), or serine364 (Ser364), in the conservedactivation segment of SlMAPKKKα kinase domainwere substituted to alanine (T353A, S360A, or S364A),and these variants were transiently expressed in tomatoand Nicotiana benthamiana plants. Two alaninesubstitutions, S360A and S364A, completely abolishedSlMAPKKKα PCD-eliciting activity in both plants,while T353A substitution did not affect its PCDelicitingactivity. SlMAPKKKα wild type and variantproteins accumulated to similar levels in plant leaves. However, SlMAPKKKα protein with the largest sizewas missed when either S360A or S364A substitutionswere expressed, whereas proteins with the smallermasses were more accumulated than those of fulllengthof SIMAPKKKα and T353A. These results suggestthat phosphorylation of SlMAPKKKα at Ser360and Ser364 is critical for PCD elicitation in plants.
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Molecular Mechanisms Involved in Bacterial Speck Disease Resistance of Tomato
Kim, Young-Jin,Gregory B. Martin The Korean Society of Plant Pathology 2004 Plant Pathology Journal Vol.20 No.1
An important recent advance in the field of plant-microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or insects. Disease resistance (R) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. Plant disease resistance is the result of an innate host defense mechanism, which relies on the ability of plant to recognize pathogen invasion and efficiently mount defense responses. In tomato, resistance to the pathogen Pseudomonas syringae pv. tomato is mediated by the specific recognition between the tomato serine/threonine kinase Pto and bacterial protein AvrPto or AvrPtoB. This recognition event initiates signaling events that lead to defense responses including an oxidative burst, the hypersensitive response (HR), and expression of pathogenesis- related genes.
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Hwang, In Sun,Brady, Jen,Martin, Gregory B.,Oh, Chang-Sik The Korean Society of Plant Pathology 2017 Plant Pathology Journal Vol.33 No.2
$SIMAPKKK{\alpha}$, a tomato (Solanum lycopersicum) mitogen-activated protein kinase kinase kinase, is a positive regulator of Pto-mediated effector-triggered immunity, which elicits programmed cell death (PCD) in plants. In this study, we examined whether putative phosphorylation sites in the conserved activation segment of the $SIMAPKKK{\alpha}$ kinase domain are critical for eliciting PCD. Three amino acids, $threonine^{353}$, $serine^{360}$ ($Ser^{360}$), or $serine^{364}$ ($Ser^{364}$), in the conserved activation segment of $SIMAPKKK{\alpha}$ kinase domain were substituted to alanine (T353A, S360A, or S364A), and these variants were transiently expressed in tomato and Nicotiana benthamiana plants. Two alanine substitutions, S360A and S364A, completely abolished $SIMAPKKK{\alpha}$ PCD-eliciting activity in both plants, while T353A substitution did not affect its PCD-eliciting activity. $SIMAPKKK{\alpha}$ wild type and variant proteins accumulated to similar levels in plant leaves. However, $SIMAPKKK{\alpha}$ protein with the largest size was missed when either S360A or S364A substitutions were expressed, whereas proteins with the smaller masses were more accumulated than those of full-length of $SIMAPKKK{\alpha}$ and T353A. These results suggest that phosphorylation of $SIMAPKKK{\alpha}$ at $Ser^{360}$ and $Ser^{364}$ is critical for PCD elicitation in plants.
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Nicole G. Barra,Isabella Y. Fan,Jenna B. Gillen,Marianne Chew,Katarina Marcinko,Gregory R. Steinberg,Martin J. Gibala,Ali A. Ashkar 대한암예방학회 2017 Journal of cancer prevention Vol.22 No.4
High intensity interval training (HIIT) boosts natural killer (NK) cell number and activity in normal weight breast cancer patients; however, whether this occurs in obese individuals is not well established. The goal of this study was to determine whether HIIT effectively boosts NK cells as a therapeutic strategy against breast cancer in an obese mouse model and in overweight/obese women. Diet induced female C57Bl/6 obese mice were assigned to undergo HIIT for four weeks or remain sedentary. Female participants were subjected to a six weeks HIIT protocol. HIIT mice acclimatized to treadmill running were subsequently injected with 5 × 105 polyoma middle T (MT) breast cancer cells intravenously. NK cell number and activation were monitored using flow cytometry, and tumor burden or lipid content evaluated from histological lung and liver tissues, respectively. In both mice and humans, circulating NK cell number and activation (CD3‒NK1.1+CD27+ and CD3‒CD56+, respectively) markedly increased immediately after HIIT. HIIT obese mice had reduced lung tumor burden compared to controls following MT challenge, and had diminished hepatic lipid deposition despite minimal body weight loss. Our findings demonstrate that HIIT can benefit obese individuals by enhancing NK cell number and activity, reducing tumor burden, and enhancing metabolic health.
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