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#32050589   2020/02/10 To Up

Dynamics and Regulations of BimEL Ser65 and Thr112 Phosphorylation in Porcine Granulosa Cells during Follicular Atresia.

BimEL protein is involved in follicular atresia by regulating granulosa cell apoptosis, but the dynamic changes of BimEL phosphorylation during follicular atresia are poorly understood. The aim of this study was to explore the changes of key BimEL phosphorylation sites and their upstream regulatory pathways. First, the levels of BimEL-Ser65 and BimEL-Thr112 phosphorylation (p-BimEL-S65, p-BimEL-T112) in granulosa cells (GC) from healthy (H), slightly-atretic (SA), and atretic (A) follicles and in cultured GC after different treatments were detected by Western blotting. Next, the effects of the corresponding site mutations of on apoptosis of GC were investigated. Finally, the pathways of two phosphorylation sites were investigated by kinase inhibitors. The results revealed that p-BimEL-S65 levels were higher in GC from H than SA and A, whereas p-BimEL-T112 was reversed. The prosurvival factors like FSH and IGF-1 upregulated the level of p-BimEL-S65, while the proapoptotic factor, heat stress, increased the level of p-BimEL-T112 in cultured GC. Compared with the overexpression of wild BimEL, the apoptotic rate of the GC overexpressed BimEL-S65A (replace Ser65 with Ala) mutant was significantly higher, but the apoptotic rate of the cells overexpressing BimEL-T112A did not differ. In addition, inhibition of the ERK1/2 or JNK pathway by specific inhibitors reduced the levels of p-BimEL-S65 and p-BimEL-T112. In conclusion, the levels of p-BimEL-S65 and p-BimEL-T112 were reversed during follicular atresia. Prosurvival factors promote p-BimEL-S65 levels via ERK1/2 to inhibit GC apoptosis, whereas proapoptotic factor upregulates the level of p-BimEL-T112 via JNK to induce GC apoptosis.
Feng Yang, Yanhong Chen, Qiang Liu, Shizhen Dai, Shenming Zeng

1824 related Products with: Dynamics and Regulations of BimEL Ser65 and Thr112 Phosphorylation in Porcine Granulosa Cells during Follicular Atresia.

100ug50 ug 100ug2 Pieces/Box1000 tests1.00 flask2 Pieces/Box96tests200ul200 25 mg

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#29179437   2017/07/18 To Up

High glucose promotes vascular smooth muscle cell proliferation by upregulating proto-oncogene serine/threonine-protein kinase Pim-1 expression.

Serine/threonine kinase proviral integration site for Moloney murine leukemia virus 1 (Pim-1) plays an essential role in arterial wall cell proliferation and associated vascular diseases, including pulmonary arterial hypertension and aortic wall neointima formation. Here we tested a role of Pim-1 in high-glucose (HG)-mediated vascular smooth muscle cell (VSMC) proliferation. Pim-1 and proliferating cell nuclear antigen (PCNA) expression levels in arterial samples from streptozotocin-induced hyperglycemia rats were increased, compared with their weak expression in normoglycemic groups. In cultured rat VSMCs, HG led to transient Pim-1 expression decline, followed by sustained expression increase at both transcriptional and translational levels. Immunoblot analysis demonstrated that HG increased the expression of the 33-kDa isoform of Pim-1, but at much less extent to its 44-kDa plasma membrane isoform. D-glucose at a concentration of 25 mmol/L showed highest activity in stimulating Pim-1 expression. Both Pim-1 inhibitor quercetagetin and STAT3 inhibitor stattic significantly attenuated HG-induced VSMC proliferation and arrested cell cycle progression at the G1 phase. Quercetagetin showed no effect on Pim-1 expression but decreased the phosphorylated-Bad (T112)/Bad ratio in HG-treated VSMCs. However, stattic decreased phosphorylated-STAT3 (Y705) levels and caused transcriptional and translational down-regulation of Pim-1 in HG-treated VSMCs. Our findings suggest HG-mediated Pim-1 expression contributes to VSMC proliferation, which may be partly due to the activation of STAT3/Pim-1 signaling.
Keke Wang, Xiaojiang Deng, Zhihua Shen, Yanan Jia, Ranran Ding, Rujia Li, Xiaomin Liao, Sisi Wang, Yanping Ha, Yueqiong Kong, Yuyou Wu, Junli Guo, Wei Jie

1246 related Products with: High glucose promotes vascular smooth muscle cell proliferation by upregulating proto-oncogene serine/threonine-protein kinase Pim-1 expression.

100ul96T100 μg100ug Lyophilized100ul100ug Lyophilized100ul100ug100ug Lyophilized100ug 100ul100ul

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#29158405   2017/11/20 To Up

Origin, evolution, and global transmission of community-acquired ST8.

USA300 is a pandemic clonal lineage of hypervirulent, community-acquired, methicillin-resistant (CA-MRSA) with specific molecular characteristics. Despite its high clinical relevance, the evolutionary origin of USA300 remained unclear. We used comparative genomics of 224 temporal and spatial diverse isolates of multilocus sequence type (ST) 8 to reconstruct the molecular evolution and global dissemination of ST8, including USA300. Analyses of core SNP diversity and accessory genome variations showed that the ancestor of all ST8 most likely emerged in Central Europe in the mid-19th century. From here, ST8 was exported to North America in the early 20th century and progressively acquired the USA300 characteristics Panton-Valentine leukocidin (PVL), SCC IVa, the arginine catabolic mobile element (ACME), and a specific mutation in capsular polysaccharide gene Although the PVL-encoding phage ϕSa2USA was introduced into the ST8 background only once, various SCC types were introduced to ST8 at different times and places. Starting from North America, USA300 spread globally, including Africa. African USA300 isolates have aberrant -types (t112, t121) and form a monophyletic group within the clade of North American USA300. Large parts of ST8 methicillin-susceptible (MSSA) isolated in Africa represent a symplesiomorphic group of ST8 (i.e., a group representing the characteristics of the ancestor), which are rarely found in other world regions. Isolates previously discussed as USA300 ancestors, including USA500 and a "historic" CA-MRSA from Western Australia, were shown to be only distantly related to recent USA300 clones.
Lena Strauß, Marc Stegger, Patrick Eberechi Akpaka, Abraham Alabi, Sebastien Breurec, Geoffrey Coombs, Beverly Egyir, Anders Rhod Larsen, Frederic Laurent, Stefan Monecke, Georg Peters, Robert Skov, Birgit Strommenger, François Vandenesch, Frieder Schaumburg, Alexander Mellmann

2153 related Products with: Origin, evolution, and global transmission of community-acquired ST8.

2.5 mg200ug10 mg1000 tests100ug

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#28071058   2017/01/27 To Up

H-Abstraction by OH from Large Branched Alkanes: Overall Rate Measurements and Site-Specific Tertiary Rate Calculations.

Reaction rate coefficients for the reaction of hydroxyl (OH) radicals with nine large branched alkanes (i.e., 2-methyl-3-ethyl-pentane, 2,3-dimethyl-pentane, 2,2,3-trimethylbutane, 2,2,3-trimethyl-pentane, 2,3,4-trimethyl-pentane, 3-ethyl-pentane, 2,2,3,4-tetramethyl-pentane, 2,2-dimethyl-3-ethyl-pentane, and 2,4-dimethyl-3-ethyl-pentane) are measured at high temperatures (900-1300 K) using a shock tube and narrow-line-width OH absorption diagnostic in the UV region. In addition, room-temperature measurements of six out of these nine rate coefficients are performed in a photolysis cell using high repetition laser-induced fluorescence of OH radicals. Our experimental results are combined with previous literature measurements to obtain three-parameter Arrhenius expressions valid over a wide temperature range (300-1300 K). The rate coefficients are analyzed using the next-nearest-neighbor (N-N-N) methodology to derive nine tertiary (T, T, T, T, T, T, T, T, and T) site-specific rate coefficients for the abstraction of H atoms by OH radicals from branched alkanes. Derived Arrhenius expressions, valid over 950-1300 K, are given as (the subscripts denote the number of carbon atoms connected to the next-nearest-neighbor carbon): T = 1.80 × 10 exp(-2971 K/T) cm molecule s; T = 9.36 × 10 exp(-3024 K/T) cm molecule s; T = 4.40 × 10 exp(-4162 K/T) cm molecule s; T = 1.47 × 10 exp(-3587 K/T) cm molecule s; T = 6.06 × 10 exp(-3010 K/T) cm molecule s; T = 3.98 × 10 exp(-1617 K/T) cm molecule s; T = 9.08 × 10 exp(-3661 K/T) cm molecule s; T = 6.74 × 10 exp(-7547 K/T) cm molecule s; T = 3.47 × 10 exp(-1802 K/T) cm molecule s.
Dapeng Liu, Fethi Khaled, Binod R Giri, Emmanuel Assaf, Christa Fittschen, Aamir Farooq

2344 related Products with: H-Abstraction by OH from Large Branched Alkanes: Overall Rate Measurements and Site-Specific Tertiary Rate Calculations.

100 UG200ug2 Pieces/Box0.05 mg 6 ml Ready-to-use 100 1000 tests4 Membranes/Box2 Pieces/Box100ug96T

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#25948581   2015/05/06 To Up

CDK-mediated RNF4 phosphorylation regulates homologous recombination in S-phase.

There are the two major pathways responsible for the repair of DNA double-strand breaks (DSBs): non-homologous end-joining (NHEJ) and homologous recombination (HR). NHEJ operates throughout the cell-cycle, while HR is primarily active in the S/G2 phases suggesting that there are cell cycle-specific mechanisms that regulate the balance between NHEJ and HR. Here we reported that CDK2 could phosphorylate RNF4 on T26 and T112 and enhance RNF4 E3 ligase activity, which is important for MDC1 degradation and proper HR repair during S phase. Mutation of the RNF4 phosphorylation sites results in MDC1 stabilization, which in turn compromised HR during S-phase. These results suggest that in addition to drive cell cycle progression, CDK also targets RNF4, which is involved in the regulatory network of DSBs repair.
Kuntian Luo, Min Deng, Yunhui Li, Chenming Wu, Ziwen Xu, Jian Yuan, Zhenkun Lou

2272 related Products with: CDK-mediated RNF4 phosphorylation regulates homologous recombination in S-phase.

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#25338187   // To Up

Treating prolonged grief disorder: a randomized clinical trial.

Prolonged grief disorder (PGD) is a potentially disabling condition that affects approximately 10% of bereaved people. Grief-focused cognitive behavior therapy (CBT) has been shown to be effective in treating PGD. Although treatments for PGD have focused on exposure therapy, much debate remains about whether exposure therapy is optimal for PGD.
Richard A Bryant, Lucy Kenny, Amy Joscelyne, Natasha Rawson, Fiona Maccallum, Catherine Cahill, Sally Hopwood, Idan Aderka, Angela Nickerson

1536 related Products with: Treating prolonged grief disorder: a randomized clinical trial.



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#24744147   2014/04/17 To Up

O-GlcNAcylation stabilizes β-catenin through direct competition with phosphorylation at threonine 41.

Dysfunctions in Wnt signaling increase β-catenin stability and are associated with cancers, including colorectal cancer. In addition, β-catenin degradation is decreased by nutrient-dependent O-GlcNAcylation. Human colon tumors and colons from mice fed high-carbohydrate diets exhibited higher amounts of β-catenin and O-GlcNAc relative to healthy tissues and mice fed a standard diet, respectively. Administration of the O-GlcNAcase inhibitor thiamet G to mice also increased colonic expression of β-catenin. By ETD-MS/MS, we identified 4 O-GlcNAcylation sites at the N terminus of β-catenin (S23/T40/T41/T112). Furthermore, mutation of serine and threonine residues within the D box of β-catenin reduced O-GlcNAcylation by 75%. Interestingly, elevating O-GlcNAcylation in human colon cell lines drastically reduced phosphorylation at T41, a key residue of the D box responsible for β-catenin stability. Analyses of β-catenin O-GlcNAcylation mutants reinforced T41 as the most crucial residue that controls the β-catenin degradation rate. Finally, inhibiting O-GlcNAcylation decreased the β-catenin/α-catenin interaction necessary for mucosa integrity, whereas O-GlcNAcase silencing improved this interaction. These results suggest that O-GlcNAcylation regulates not only the stability of β-catenin, but also affects its localization at the level of adherens junctions. Accordingly, we propose that O-GlcNAcylation of β-catenin is a missing link between the glucose metabolism deregulation observed in metabolic disorders and the development of cancer.
Stéphanie Olivier-Van Stichelen, Vanessa Dehennaut, Armelle Buzy, Jean-Luc Zachayus, Céline Guinez, Anne-Marie Mir, Ikram El Yazidi-Belkoura, Marie-Christine Copin, Didier Boureme, Denis Loyaux, Pascual Ferrara, Tony Lefebvre

2389 related Products with: O-GlcNAcylation stabilizes β-catenin through direct competition with phosphorylation at threonine 41.

1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set1 Set100.00 ul200ul

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#23832115   2013/07/05 To Up

Apoptosis induced by the fungal pathogen gliotoxin requires a triple phosphorylation of Bim by JNK.

We previously reported that gliotoxin (GT), the major virulence factor of the mold Aspergillus fumigatus causing invasive aspergillosis (IA) in immunocompromised patients, induces apoptosis in a Bak-dependent manner. The signaling pathway leading to Bak activation and subsequent mitochondrial outer membrane permeabilization (MOMP) is elusive. Here, we show that GT and the supernatant of A. fumigatus (but not its GT-defective mutant) activate the JNK pathway and require a co-operative JNK-mediated BimEL phosphorylation at three sites (S100, T112 and S114) to induce apoptosis in mouse fibroblasts, human bronchial and mouse alveolar epithelial cells. Cells (i) treated with the JNK inhibitor SP600125, (ii) deleted or knocked down for JNK1/2 or Bim or (iii) carrying the BimEL triple phosphomutant S100A/T112A/S114A instead of wild-type BimEL are similarly resistant to GT-induced apoptosis. Triple-phosphorylated BimEL is more stable, redistributes from a cytoskeletal to a membrane fraction, better interacts with Bcl-2 and Bcl-xL and more effectively activates Bak than the unphosphorylated mutant. These data indicate that JNK-mediated BimEL phosphorylation at S100, T112 and S114 constitutes a novel regulatory mechanism to activate Bim in response to apoptotic stimuli.
A Geissler, F Haun, D O Frank, K Wieland, M M Simon, M Idzko, R J Davis, U Maurer, C Borner

2931 related Products with: Apoptosis induced by the fungal pathogen gliotoxin requires a triple phosphorylation of Bim by JNK.

2 Pieces/Box2 Pieces/Box1 Set100 assays1 kit1 Set1 Set50 ul1 Set1 Set2 Sample Kit1 Set

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