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Porcine enterovirus G (EV-G) is a member of the family Picornavirdae, genus Enterovirus. To date, eleven EV-G types (EV-G1 through EV-G11) have been identified in pigs from Asia and Europe however they have never been reported in North America. In this study, we isolated and characterized the complete genome of NP/2013/USA, an EV-G from a porcine diarrhea sample from the United States. The complete genome consists of 7,390 nucleotides excluding the 3′ poly(A) tail, and has an open reading frame that encodes a 2,169 amino acid polyprotein. NP/2013/USA was most similar at the nucleotide (84%) and amino acid (95%) level to the , an EV-G1 type isolated from China in 2012. HM131607相似文献
3.
Telomere integrity in budding yeast depends on the CST (Cdc13-Stn1-Ten1) and shelterin-like (Rap1-Rif1-Rif2) complexes, which are thought to act independently from each other. Here we show that a specific functional interaction indeed exists among components of the two complexes. In particular, unlike RIF2 deletion, the lack of Rif1 is lethal for stn1ΔC cells and causes a dramatic reduction in viability of cdc13-1 and cdc13-5 mutants. This synthetic interaction between Rif1 and the CST complex occurs independently of rif1Δ-induced alterations in telomere length. Both cdc13-1 rif1Δ and cdc13-5 rif1Δ cells display very high amounts of telomeric single-stranded DNA and DNA damage checkpoint activation, indicating that severe defects in telomere integrity cause their loss of viability. In agreement with this hypothesis, both DNA damage checkpoint activation and lethality in cdc13 rif1Δ cells are partially counteracted by the lack of the Exo1 nuclease, which is involved in telomeric single-stranded DNA generation. The functional interaction between Rif1 and the CST complex is specific, because RIF1 deletion does not enhance checkpoint activation in case of CST-independent telomere capping deficiencies, such as those caused by the absence of Yku or telomerase. Thus, these data highlight a novel role for Rif1 in assisting the essential telomere protection function of the CST complex. 相似文献
4.
Balaji V Vanitharani R Karthikeyan AS Anbalagan S Veluthambi K 《Journal of biosciences》2004,29(3):297-308
Mungbean yellow mosaic virus-Vigna (MYMV-Vig), aBegomovirus that causes yellow mosaic disease, was cloned from field-infected blackgram (Vigna mungo). One DNA A clone (KA30) and five different DNA B clones (KA21, KA22, KA27, KA28 and KA34) were obtained. The sequence identity
in the 150-nt common region (CR) between DNA A and DNA B was highest (95%) for KA22 DNA B and lowest (85·6%) for KA27 DNA
B. The Rep-binding domain had three complete 11 -nt (5’-TGTATCGGTGT-3′) iterons in KA22 DNA B (and KA21, KA28 and KA34), while
the first iteron in KA27 DNA B (5’-ATCGGTGT-3’) had a 3-nt deletion. KA27 DNA B, which exhibited 93·9% CR sequence identity
to the mungbean-infecting MYMV, also shared the 3-nt deletion in the first iteron besides having an 18-nt insertion between
the third iteron and the conserved nonanucleotide. MYMV was found to be closely related to KA27 DNA B in amino acid sequence
identity of BV1 (94·1%) and BC1 (97·6%) proteins and in the organization of nuclear localization signal (NLS), nuclear export
signal (NES) and phosphorylation sites. Agroinoculation of blackgram (V. mungo) and mungbean (V. radiata) with partial dimers of KA27 and KA22 DNA Bs along with DNA A caused distinctly different symptoms. KA22 DNA B caused more
intense yellow mosaic symptoms with high viral DNA titre in blackgram. In contrast, KA27 DNA B caused more intense yellow
mosaic symptoms with high viral DNA titre in mungbean. Thus, DNA B of MYMV-Vig is an important determinant of host-range betweenV. mungo andV. radiata. 相似文献
5.
S Ramachandran Y Sridhar S Kishore Gnana Sam M Saravanan J Thomas Leonard N Anbalagan S K Sridhar 《Phytomedicine》2004,11(2-3):165-168
In the present study, the aphrodisiac activity of Butea frondonsa Koen. ex Roxb (Papillionaceae) bark extract was investigated. The extract (400 mg/kg body wt./day) was administered orally by gavage for 28 days. Mount latency (ML), intromission latency (IL), ejaculation latency (EL), mounting frequency (MF), intromission frequency (IF), ejaculation frequency (EF) and post-ejaculatory interval (PEI) were the parameters observed before and during the sexual behavior study at day 0, 7, 10, 14, 21, and 28. The extract reduced significantly ML, IL, EL and PEI (p < 0.05). The extract also increased significantly MF, IF and EF (p < 0.05). These effects were observed in sexually active and inactive male rats. 相似文献
6.
Sankarappan Anbalagan Sundaram Dinakaran Jeyaraj Pandiarajan Muthukalingan Krishnan 《水生生物学报》2011,35(4):688-692
The effect of tourism on the distribution of larval blackflies during three different seasons of Palni hills was investigated.Six streams were selected(Kumbakkarai,Moolayar,Kurusedi,Silver cascade Pampar and Guntar) for this study,of which,three streams(Silver cascade Pampar and Guntar) were in peak of Palni hills(Kodaikanal town areas) and easy access to the tourists.The remaining three streams(Kumbakkarai,Moolayar and Kurusedi) were in downhill areas.The physico-chemical and stream parameters analyses indicated that the most tourist accessible site of Silver cas-cade stream had poor water quality and the predominant of larval blackfly population when compared to other sampling streams.The highest population of larval blackflies was observed during winter followed by summer and northeast monsoon.Since the effect of tourism causes pollution to streams,which in turn to promote the population of blackfly larvae and affect the other insect community in streams.
相似文献
7.
Maneb (MB) and paraquat (PQ) provoke oxidative stress-mediated cell damage. Role of xanthine oxidase (XO) in oxidative stress and its association with nitric oxide (NO)/NO synthase (NOS) have been widely reported. While inducible NOS (iNOS) is implicated in MB+PQ-induced toxicity in rat polymorphonuclear leukocytes (PMNs), role of XO and its alliance with iNOS have not yet been established. The study investigated the role of XO in MB+PQ-induced oxidative stress in rat PMNs and its regulation by iNOS and inflammatory cytokines. MB+PQ-augmented reactive oxygen species (ROS), superoxide, nitro-tyrosine, lipid peroxidation (LPO), and nitrite levels along with the catalytic activity of iNOS, superoxide dismutase (SOD), and XO. XO inhibitor, allopurinol (AP), alleviated MB+PQ-induced changes except nitrite content and iNOS activity. Conversely, an iNOS inhibitor, aminoguanidine, mitigated MB+PQ-induced LPO, nitrite, iNOS, and nitro-tyrosine levels; however, no change was observed in ROS, SOD, and XO. Nuclear factor-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), tumor necrosis factor-alpha (TNF-α) inhibitor, pentoxyfylline, and an anti-inflammatory agent, dexamethasone, attenuated MB+PQ-induced increase in XO, superoxide, and ROS with parallel reduction in the expression of interferon-gamma (IFN-γ), TNF-α, and interleukin-1β (IL-1β) in rat PMNs. Exogenous IFN-γ, TNF-α, and IL-1β enhanced superoxide, ROS, and XO in the PMNs of control and MB+PQ-treated rats; however, IFN- γ was found to be the most potent inducer. Moreover, AP ameliorated cytokine-induced free radical generation and restored XO activity towards normalcy. The results thus demonstrate that XO mediates oxidative stress in MB+PQ-treated rat PMNs via iNOS-independent but cytokine (predominantly IFN-γ)-dependent mechanism. 相似文献
8.
Girish V. Shah Anbalagan Muralidharan Mitan Gokulgandhi Kamal Soan Shibu Thomas 《The Journal of biological chemistry》2009,284(2):1018-1030
Calcitonin, a neuroendocrine peptide, and its receptor are localized in the
basal epithelium of benign prostate but in the secretory epithelium of
malignant prostates. The abundance of calcitonin and calcitonin receptor mRNA
displays positive correlation with the Gleason grade of primary prostate
cancers. Moreover, calcitonin increases tumorigenicity and invasiveness of
multiple prostate cancer cell lines by cyclic AMP-dependent protein
kinase-mediated actions. These actions include increased secretion of matrix
metalloproteinases and urokinase-type plasminogen activator and an increase in
prostate cancer cell invasion. Activation of calcitonin-calcitonin receptor
autocrine loop in prostate cancer cell lines led to the loss of cell-cell
adhesion, destabilization of tight and adherens junctions, and internalization
of key integral membrane proteins. In addition, the activation of
calcitonin-calcitonin receptor axis induced epithelial-mesenchymal transition
of prostate cancer cells as characterized by cadherin switch and the
expression of the mesenchymal marker, vimentin. The activated calcitonin
receptor phosphorylated glycogen synthase kinase-3, a key regulator of
cytosolic β-catenin degradation within the WNT signaling pathway. This
resulted in the accumulation of intracellular β-catenin, its
translocation in the nucleus, and transactivation of β-catenin-responsive
genes. These results for the first time identify actions of
calcitonin-calcitonin receptor axis on prostate cancer cells that lead to the
destabilization of cell-cell junctions, epithelial-to-mesenchymal transition,
and activation of WNT/β-catenin signaling. The results also suggest that
cyclic AMP-dependent protein kinase plays a key role in calcitonin
receptor-induced destabilization of cell-cell junctions and activation of
WNT-β-catenin signaling.Prostate cancer
(PC)2 is the most
commonly diagnosed cancer and the second leading cause of cancer deaths in men
in the United States (1,
2). Although androgen ablation
therapy is effective in men with advanced disease for some time, the disease
subsequently progresses to the androgen-independent stage. The population of
prostate cells expressing neuroendocrine factors such as calcitonin (CT) also
increases during this progression
(3–5).
At this stage, the disease is metastatic and chemoresistant. Present evidence
suggests that cancer metastasis is usually preceded by the disruption of
normal cell-cell adhesion and the loss of integrity of the primary tumor site
(6,
7). This process may include
several genetic, molecular, and morphological changes characterized by
epithelial-to-mesenchymal transition (EMT)
(8–10).
The EMT is characterized by the loss of cell polarity, altered cell-cell and
cell-matrix adhesion, and acquisition of migratory, mesenchymal phenotype.
Other reported changes include down-regulation of E-cadherin, induction of
N-cadherin, release of β-catenin from junctional complexes, and its
translocation to the nucleus
(11–13).
However, the precise molecular mechanisms associated with this process are
obscure.Several growth factors, including hepatocyte growth factor, transforming
growth factor-β, vascular endothelial growth factor, and epidermal growth
factor, have been reported to induce EMT in tumor cell lines
(14–16).
We have shown that the expression of CT and its G protein-coupled receptor
(CTR) is remarkably higher in advanced PCs, and the CT-CTR autocrine axis is a
potent stimulator of PC cell tumorigenicity, invasion, and metastasis
(4,
17–19).
Although CT-stimulated increase in the motility and invasion of PC cells may
be mediated by CT-stimulated secretion of matrix metalloproteinases and
urokinase-type plasminogen activator, the precise molecular mechanisms
preceding these CTR actions remain to be elucidated
(18,
20). We tested the hypothesis
that CT induces biochemical and morphological changes associated with EMT to
increase the invasiveness of PC cells.Our results indicate that activation of the CT-CTR autocrine axis in
prostate cancer cells induced several changes associated with EMT such as
remodeling of tight and adherens junctions, cadherin switching, and activation
of WNT/β-catenin signaling. In contrast, the silencing of the CT-CTR axis
reversed this process. Moreover, cyclic AMP-dependent protein kinase (PKA)
plays a key role in this CT-CTR-mediated process. This is the first study
demonstrating the action of prostate CTR on junctional complexes and
WNT/β-catenin signaling of PC cell lines. 相似文献
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10.
Mansoureh Sameni Arulselvi Anbalagan Mary B. Olive Kamiar Moin Raymond R. Mattingly Bonnie F. Sloane 《Journal of visualized experiments : JoVE》2012,(60)
We have developed 3D coculture models, which we term MAME (mammary architecture and microenvironment engineering), and used them for live-cell imaging in real-time of cell:cell interactions. Our overall goal was to develop models that recapitulate the architecture of preinvasive breast lesions to study their progression to an invasive phenotype. Specifically, we developed models to analyze interactions among pre-malignant breast epithelial cell variants and other cell types of the tumor microenvironment that have been implicated in enhancing or reducing the progression of preinvasive breast epithelial cells to invasive ductal carcinomas. Other cell types studied to date are myoepithelial cells, fibroblasts, macrophages and blood and lymphatic microvascular endothelial cells. In addition to the MAME models, which are designed to recapitulate the cellular interactions within the breast during cancer progression, we have developed comparable models for the progression of prostate cancers. Here we illustrate the procedures for establishing the 3D cocultures along with the use of live-cell imaging and a functional proteolysis assay to follow the transition of cocultures of breast ductal carcinoma in situ (DCIS) cells and fibroblasts to an invasive phenotype over time, in this case over twenty-three days in culture. The MAME cocultures consist of multiple layers. Fibroblasts are embedded in the bottom layer of type I collagen. On that is placed a layer of reconstituted basement membrane (rBM) on which DCIS cells are seeded. A final top layer of 2% rBM is included and replenished with every change of media. To image proteolysis associated with the progression to an invasive phenotype, we use dye-quenched (DQ) fluorescent matrix proteins (DQ-collagen I mixed with the layer of collagen I and DQ-collagen IV mixed with the middle layer of rBM) and observe live cultures using confocal microscopy. Optical sections are captured, processed and reconstructed in 3D with Volocity visualization software. Over the course of 23 days in MAME cocultures, the DCIS cells proliferate and coalesce into large invasive structures. Fibroblasts migrate and become incorporated into these invasive structures. Fluorescent proteolytic fragments of the collagens are found in association with the surface of DCIS structures, intracellularly, and also dispersed throughout the surrounding matrix. Drugs that target proteolytic, chemokine/cytokine and kinase pathways or modifications in the cellular composition of the cocultures can reduce the invasiveness, suggesting that MAME models can be used as preclinical screens for novel therapeutic approaches. 相似文献