Journal of Receptor and Signal Transduction Research (J RECEPT SIG TRANSD )

Publisher: Taylor & Francis

Description

This widely respected journal presents the latest laboratory and clinical studies on biological receptors and associated signal transduction pathways for ligands involved in the regulation of central and peripheral tissues and cells, including the immune system, thus covering the field from neurotransmitters to peptides, steroids, growth factors, cytokines and drugs. The journal repidly communicates important research results to the international scientific community in a variety of stimulating formats, including original and review papers, brief communications, solicited and unsolicited mini reviews, and symposia proceedings. The Journal of Receptors and Signal Transduction maintains a rigorous peer-review process that ensures the originality, timeliness, and significance of topics covered, such as physicochemical and biophysical properties modeling molecular biology and genetics receptor structure and function the pathology of receptors as well as signal transduction pathway components from G proteins and second messengers to enzymes and ionic channels signal transduction pathways activated by receptor-ligand interactions molecular strategies for designing drugs acting on receptors receptors in the diagnosis and therapy of disease and much more! In addition, the Journal fulfills the vital need for a single source of information on all facets of receptor and signal transduction for researchers working in disciplines as diverse as anesthesiology biochemistry biophysics cancer research endocrinology immunology medicinal chemistry microbiology molecular and cell biology molecular physiology neurobiology neuroscience pathology pharmacology physical chemistry radiation oncology toxicology.

  • Impact factor
    1.63
    Show impact factor history
     
    Impact factor
  • 5-year impact
    1.41
  • Cited half-life
    6.20
  • Immediacy index
    0.35
  • Eigenfactor
    0.00
  • Article influence
    0.43
  • Website
    Journal of Receptor and Signal Transduction Research website
  • Other titles
    Journal of receptor and signal transduction research, Journal of receptors and signal transduction
  • ISSN
    1079-9893
  • OCLC
    31634807
  • Material type
    Periodical, Internet resource
  • Document type
    Journal / Magazine / Newspaper, Internet Resource

Publisher details

Taylor & Francis

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Some individual journals may have policies prohibiting pre-print archiving
    • On author's personal website or departmental website immediately
    • On institutional repository or subject-based repository after either 12 months embargo for STM, Behavioural Science and Public Health Journals or 18 months embargo for SSH journals
    • Publisher's version/PDF cannot be used
    • On a non-profit server
    • Published source must be acknowledged
    • Must link to publisher version
    • Set statements to accompany deposits (see policy)
    • The publisher will deposit in on behalf of authors to a designated institutional repository including PubMed Central, where a deposit agreement exists with the repository
    • STM: Science, Technology and Medicine
    • SSH: Social Science and Humanities
    • Publisher last contacted on 25/03/2014
    • 'Taylor & Francis (Psychology Press)' is an imprint of 'Taylor & Francis'
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Hepatic fibrosis is overly exuberant wound healing in which excessive connective tissue builds up in the liver. The treatment of hepatic fibrosis is still difficult and remains a challenge to the clinician. In recent years, the TGF-β signaling pathway regulator tyrosine kinase Abl has been raised as a new and promising target of hepatic fibrosis therapy. Here, considering that there are numerous drugs and drug-like compounds being approved or under clinical development and experimental investigation, it is expected that some of the existing drugs can be re-exploited as new agents to target Abl with the capability of suppressing hepatic fibrosis. To achieve this, a synthetic protocol that integrated molecular docking, affinity scoring dynamics simulation and free energy analysis was described to systematically profile the inhibitory potency of various drugs and drug-like compounds against the kinase domain of Abl. Consequently, 4 out of 13 tested drug candidates were successfully identified to have high-Abl inhibitory activities. By visually examining the dynamics behavior, structural basis and energetic property of few typical Abl-drug complex cases, a significantly different pattern of non-bonded interactions between the binding of active and inactive drug ligands to Abl receptor was revealed; the former is defined by strong, specific chemical forces, while the latter can only form non-specific hydrophobic contacts with slight atomic collisions.
    Journal of Receptor and Signal Transduction Research 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Introduction: Bile acids are recognized as signaling molecules, mediating their effects both through the cell surface receptor TGR5 and the nuclear receptor FXR. After a meal, approximately 95% of the bile acids are transported from terminal ileum and back to the liver via the portal vein, resulting in postprandial elevations of bile acids in blood. During the digestion of fat, components from the microbiota, including LPS, are thought to reach the circulation where it may lead to inflammatory responses after binding TLR4 immune cells. Both LPS and bile acids are present in blood after a high-fat meal; we therefore wanted to study consequences of a possible interplay between TGR5 and TLR4 in human monocytes. Methods: The monocytic cell line U937 stably transfected with the NF-κB reporter plasmid 3x-κB-luc was used as a model system to study the effects of TGR5 and TLR4. Activation of MAP kinases was studied to reveal functional consequences of triggering TGR5 in U937 cells. Effects of TGR5 and TLR4 activation were monitored using NF-κB luciferase assay and by quantification of the pro-inflammatory cytokines IL-6 and IL-8 using ELISA. Results: In this study, results show that triggering TGR5 with the specific agonist betulinic acid (BA), and the bile acids CDCA or DCA, activated both the main MAP kinases ERK1/2, p38 and JNK, and the NF-κB signaling pathway. We further demonstrated that co-triggering of TLR4 and TGR5 enhanced the activation of NF-κB and the release of inflammatory cytokines in a synergistic manner compared to triggering of TLR4 alone. Conclusions: Thus, two different and simultaneous events associated with the digestive process coordinately affect the function of human monocytes and contribute to enhanced inflammation. Because elevated levels of circulatory LPS may contribute to the development of insulin resistance, the results from this study suggest that bile acids through the activation of TGR5 may have a role in the development of insulin resistance as well.
    Journal of Receptor and Signal Transduction Research 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Luffa acutangula (Cucurbitaceae) is widely used as a traditional medicine in India and was reported to possess various pharmacological activities including its anti-proliferative effects. In this study, the bioactive compound of ethanolic extract of L. acutangula (LA) was isolated using bioassay-guided approach. Five major fractions were collected and evaluated for their anti-proliferative activity against non-small cell lung cancer cells (NCI-H460). Among the test fractions, the fraction LA/FII effectively decreased the growth of cancer cells with IC50 values of 10 µg/ml concentration. Furthermore, it significantly increased intracellular reactive oxygen species and decreased the mitochondrial membrane potential. The apoptogenic activity of fraction LA/FII was confirmed by cell shrinkage, membrane blebbing and formation of apoptotic bodies. A single bioactive compound was isolated from the active faction, LA/FII and subsequently identified as 1,8 dihydroxy-4-methylanthracene 9,10-dione (compound 1) by comparing its spectral data [Ultraviolet (UV), Infrared (IR), Nuclear magnetic resonance (NMR) and Electrospray Ionization-Mass Spectroscopy (ESI-MS)] with literature values. This is the first report on the isolation of compound 1 from this plant.
    Journal of Receptor and Signal Transduction Research 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract MicroRNA (miRNA) is a class of small endogenous non-coding RNAs that are ∼ 22 nucleotides in length and can have structural, enzymatic and post-transcriptional regulators of gene expression targeting mRNA for translational repression and/or degradation. miR-497 is high on the list of noncoding, small, regulatory RNAs that plays important roles in the pathogenesis of some diseases and takes part in some signaling pathways in some diseases, but many questions await answers. Vascular endothelial growth factor (VEGF) is a notable chemokine that plays critical roles in angiogenesis and vasculogenesis. There might be an association between miRNA-497 and VEGF. This review was performed to sum up the roles of miR-497 and its potential signaling pathway in diseases and with VEGF.
    Journal of Receptor and Signal Transduction Research 11/2014;
  • Journal of Receptor and Signal Transduction Research 11/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Peroxisome proliferator-activated receptorγ (PPARγ) can regulate the process of cell apoptosis and is related to the progression of renal disorders. Retinoic acid receptor alpha (RARα) is one of the nuclear receptors involved in a variety of kidney diseases. Renal interstitial fibrosis (RIF) is a common denominator of chronic kidney disease (CKD). This study investigated whether a potential signaling pathway existed between PPARγ and RARα in RIF rats with unilateral ureteral obstruction (UUO). The rats were randomly divided into four groups: a model group subjected to UUO (GU), and three other groups treated with rosiglitazone sodium (GRS), GW9662 and dimethyl sulfoxide (DMSO), n = 40, respectively. Renal tissues were collected two and four weeks after post-surgery. The relevant indicators were detected. In comparison with the GU group, the expressions of PPARγ and RARα (protein and mRNA) were increased in the GRS group, and decreased in the GW9662 group (all p < 0.01). The RIF index, mRNA and protein expression of transforming growth factor-β1 (TGF-β1), and the protein expressions of collagen-IV (Col-IV) and fibronectin (FN) in the GRS group were more markedly reduced than those in the GU group; their levels in the GW9662 group were elevated (all p < 0.01). PPARγ or RARα was negatively correlated to the RIF index, TGF-β1, Col-IV and FN. PPARγ was positively correlated with RARα (all p < 0.01). In conclusion, PPARγ agonist can elevate the expression of PPARγ or RARα in RIF rats. There might be a potential signaling pathway between PPARγ and RARα in RIF disease.
    Journal of Receptor and Signal Transduction Research 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Objective: To better understand the risks of rheumatoid arthritis (RA) and certain subsets conferred by mannose-binding lectin (MBL2) polymorphisms in different races. Materials and methods: Eighteen articles (4810 cases and 4585 controls) were identified from the latest literature search carried out in May 2014 using PubMed, Web of Science, Wanfang Database (Chinese) and Chinese National Knowledge Infrastructure. Three single nucleotide polymorphisms of codon 52, 54 and 57, exonic and extended genotypic variance in MBL2 were synthesized. Results: Codon 54 mutation of MBL2 was unlikely to be a risk factor for RA in overall population, but turned out to be deleterious in East Asian (four studies with 523 cases and 647 controls, pooled OR:1.63, 95% CI: 1.23-2.17). Codon 54 mutation increased the risk of seropositive and erosive RA by 44% and 162%, respectively (three studies with 281 cases and 358 controls, 95% CI: 1.01-2.05; 3 studies with 180 cases and 499 controls, 95% CI: 1.77-3.88). Furthermore, those risks were relatively stronger when restricted in East Asian (two studies with 147 cases and 244 controls, pooled OR: 1.85, 95% CI: 1.19-2.87; 2 studies with 170 cases and 291 controls, pooled OR: 2.78, 95% CI: 1.85-4.20). No remarkable associations were detected regarding codon 52, 57, exon 1 and extended genotype of MBL2. Conclusions: Polymorphism of codon 54 in MBL2 may predispose to RA, especially seropositive or erosive RA, which East Asian appears to be more vulnerable.
    Journal of Receptor and Signal Transduction Research 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract In this study, we investigated the anti-tumor activity both in vitro and in vivo of a polysaccharide obtained from Ganoderma lucidum on HL-60 acute myeloid leukemia cells, and focused on its targeting effect on mitogen-activated protein kinase (MAPK) pathways. It was found by the methods such as western blot and flow cytometry (FCM), that G. lucidum polysaccharide (GLP) blocked the extracellular signal-regulated kinase/MAPK signaling pathway, simultaneously activated p38 and JNK MAPK pathways, and therefore regulated their downstream genes and proteins, including p53, c-myc, c-fos, c-jun, Bcl-2, Bax, cleaved caspase-3 and cyclin D1. As a result, cycle arrest and apoptosis of HL-60 cells were induced. Therefore, GLP exerted anti-tumor activity via MAPK pathways in HL-60 acute leukemia cells.
    Journal of Receptor and Signal Transduction Research 10/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract It has been well documented that Momordica charantia polysaccharide (MCP) has multiple biological effects such as immune enhancement, anti-oxidation and anti-cancer. However, the potential protective effects of MCP on stroke damage and its relative mechanisms remain unclear. Our present study demonstrated that MCP could scavenge reactive oxygen species (ROS) in intra-cerebral hemorrhage damage, significantly attenuating the neuronal death induced by thrombin in primary hippocampal neurons. Furthermore, we found that MCP prevented the activation of the c-Jun N-terminal protein kinase (JNK3), c-Jun and caspase-3, which was caused by the intra-cerebral hemorrhage injury. Taken together, our study demonstrated that MCP had a neuroprotective effect in response to intra-cerebral hemorrhage and its mechanisms involved the inhibition of JNK3 signaling pathway.
    Journal of Receptor and Signal Transduction Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Objective: To investigate the function of nephrin in podocytes and its relation to proteinuria in kidney diseases, and to study more clearly theoretical basis for the molecular mechanism of losartan anti-proteinuria and the special beneficial effects of losartan on podocyte injury. Methods: Experiment set up control, Ang II and losartan group. Cell morphology was observed perturbation, and using image processing software to analyze the cell body of cell morphology and size of the difference after 8 h, 24 h and 48 h. Detecting nephrin mRNA and protein expression changes by real time PCR (RT-PCR) and western blotting at different time points. Results: Podocyte cell bodies were significantly reduced after Ang II injury (p < 0.01), losartan directly reduces the rate of apoptotic podocytes induced by Ang. Apoptotic podocytes may related to the decrease of nephrin mRNA and protein expressions, losartan reduced the apoptosis and proteinuria by declining nephrin mRNA and protein expressions. Conclusion: Ang II induced podocyte injury caused abnormal expression and distribution of nephrin in podocytes, losartan maybe maintain the stability of nephrin expression and the integrity of hole diaphragm (SD) structure and function by blocking the signal path, playing a important role in protection mechanisms of anti-proteinuria. Our findings provide some possible clues for further exploring the pharmacological targets to the proteinuria. These novel findings provide new insights into the beneficial effects of losartan on podocytes directly.
    Journal of Receptor and Signal Transduction Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Insulin, when co-applied with GABA, can cause an inhibition of the induced current at GABAA receptors. This study investigated that inhibitory effect of insulin at a variety of receptor isoforms, concentrating on α1, α2 and α4 containing receptors. Various isoforms were expressed in Xenopus oocytes and currents determined using two-electrode voltage clamp. Submaximal GABA currents at all isoforms studied were inhibited by nanomolar concentrations of insulin. At α2 and α4 containing forms, insulin could inhibit maximal GABA currents. The ability to inhibit maximal currents, and the general potency and effects at submaximal currents paralleled the number of potential MAPK sites on the α subunits. The differences in insulin inhibition of GABA currents at different α containing GABAA receptors could be important in autocrine and paracrine control of hormone secretion in the pancreas, and in control of reward and food intake circuits of the brain.
    Journal of Receptor and Signal Transduction Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Macrophage can be alternatively activated by TGF-β1, whether high-ambient glucose can enhance the sensitivity of TGF-β1 and the intracellular mechanisms involved in this process are not fully understood. We examined whether the mitogen-activated protein kinase is involved in the activation of macrophage induced by TGF-β1 and high-ambient glucose. The expression of arginase-1, CD206 and TGF-β1 was accessed by Western blot and immunofluorescence in RAW 264.7 cells stimulated with TGF-β1 and high-ambient glucose. The activation of MAPK pathways in the process was investigated by Western blot. The role of MAPK was assessed using biochemical inhibitors. The protein of arginase-1, CD206 and TGF-β1 was significantly overexpressed in RAW264.7 cells stimulated by TGF-β1 and high-ambient glucose. ERK and JNK phosphorylation occurred in 30 min and p38MAPK phosphorylation occurred in 30 min and 24 h after the stimulation. And the expression of arginase-1 and TGF-β1 was partially blocked by the pretreated ERK biochemical inhibitor (U0126) instead of the JNK inhibitor (SP600125) and p38MAPK inhibitor (SB203580). In conclusion, high-ambient glucose can enhance the sensitivity of TGF-β1 in RAW264.7 cells, which resulted in overexpression of TGF-β1 and arginase-1 in macrophages. ERK plays a role in this process.
    Journal of Receptor and Signal Transduction Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Objective: To explore whether the functional chemokine receptor 5 delta32 (CCR5-Δ32) polymorphism is associated with susceptibility to cancer. Methods: A meta-analysis was conducted on the association between the CCR5-Δ32 polymorphism and cancer using (i) allele contrast and (ii) the dominant model. Results: Thirteen articles, including 16 comparative studies on a total of 3087 patients and 3735 controls, were included in the meta-analysis. These studies encompassed breast cancer (n = 3), bladder cancer (n = 3), cervical cancer (n = 2), pancreatic cancer (n = 2), prostate cancer (n = 2), head and neck cancer (n = 2), lymphoma (n = 1), gallbladder cancer (n = 1), skin cancer (n = 1) and mixed cancer (n = 1). The meta-analysis revealed an association between cancer and the CCR5-Δ32 allele (OR = 1.368, 95% CI = 1.064-1.758, p = 0.014), and stratification by ethnicity showed an association between the CCR5-Δ32 allele and cancer in Indians (OR = 2.480, 95% CI = 1.247-4.932, p = 0.010). The meta-analysis also revealed an association between breast cancer and the CCR5-Δ32 allele (OR = 1.689, 95% CI = 1.012-2.821, p = 0.045). However, allele contrast and the dominant model failed to reveal an association between the CCR5-Δ32 polymorphism and bladder cancer, cervical cancer, pancreatic cancer, prostate cancer, and head and neck cancer. Conclusions: This meta-analysis demonstrates that the CCR5-Δ32 polymorphism is associated with susceptibility to cancer in Indians and is associated with breast cancer.
    Journal of Receptor and Signal Transduction Research 09/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Γ-aminobutyric acid (GABA) is a multifunctional molecule found in the nervous system and non-neuronal tissues. GABA receptors combine with GABA molecules and transmit signal stimuli into cells. In addition to traditional neurotransmission and regulation of secretion, GABA and GABA receptors are involved in cell differentiation and proliferation throughout peripheral organs, as well as in tumorigenesis. The exact mechanism of the GABAergic system in regulating tumor development is unclear, but many studies have revealed that GABA receptors exert critical regulative effects on tumor cell proliferation and migration. In this review, the molecular structure, distribution and biological function of GABA receptors associated with tumorigenesis are described. Recent advances in the elucidation of mechanisms underlying GABAergic signaling control over tumor growth are also discussed.
    Journal of Receptor and Signal Transduction Research 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: The estrogen-related receptor alpha (ERRα) governs multitude of biological functions by working as specific transcriptional regulator in animals. Over the past few years, one aspect of ERRα which has seen optimal progress is its control over the mitochondrial physiology. The ERRα not only regulates an array of nuclear genes devoted to mitochondrial functions but also numerous mitochondrial DNA genes that ultimately culminates into this organelle’s homeostasis. In fact, ERRα expression is correlated with genes whose functional products are part of the mitochondrial physiology. Studies have indicated that nearly half of the proteins encoded by the mitochondrial genome are regulated by ERRα. Moreover, ERRα controls vital mitochondrial processes such as oxidative metabolism through a network of protein kinases and by regulating the expression of sirtuins like Sirt3. Furthermore, new findings also show that ERRα regulate mitochondrial biogenesis in association with PGC family co-activators such as PRC and PGC-1β and also via cross-talk with MAPKKs and PI3K/(AKT) signaling. The current understanding of the pathways and networks shows strong influence of ERRα in coordinating mitochondrial physiology. This review focuses on the new advances made in understanding the complex and important interface between ERRα and mitochondrial physiology.
    Journal of Receptor and Signal Transduction Research 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract The conclusions of the published reports on the relationship between glutathione S-transferase P1 (GSTP1) gene polymorphism and the risk of small-cell carcinoma of lung cancer are still debated. GSTP1 is one of the important mutant sites reported at present. This meta-analysis was performed to evaluate the association between GSTP1 and the risk of small-cell carcinoma of lung cancer. The association investigations were identified from PubMed and Cochrane Library, and eligible studies were included and synthesized using meta-analysis method. Ten reports were included into this meta-analysis for the association of GSTP1 A/G gene polymorphism and small-cell carcinoma of lung cancer. The G allele and GG genotype were not associated with the susceptibility of risk of small-cell carcinoma in overall populations, East-Asians and Turkish population. However, there was an association between GG genotype with the risk of small-cell carcinoma in Caucasians. In conclusion, GG genotype was associated with the risk of small-cell carcinoma in Caucasian patients with lung cancer. However, GSTP1 A/G gene polymorphism is not associated with the susceptibility of small-cell carcinoma in overall populations, East-Asians and Turkish population.
    Journal of Receptor and Signal Transduction Research 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract The NR4A subfamily is orphan nuclear receptors that belong to the larger nuclear receptors (NRs) superfamily of eukaryotic transcription factors. The NR4A subfamily includes three members, namely Nur77 (NR4A1), Nurr1 (NR4A2) and Nor1 (NR4A3) which are gene regulators and participate in diverse biological functions. Though the ligands for these receptors are presently unidentified, they are thought to be constitutively active. NR4A acts as molecular switches in gene regulation and their action is increasingly seen to be modulated by complex network of cellular signaling pathways. Members of the NR4A are expressed in tissue-specific fashion which indicates their selective control of various biological processes. Data reveal a host of functions governed by the NR4A subfamily members including general metabolism, immunity, cellular stress, memory, insulin sensitivity and cardiac homeostasis by regulating specific target genes whose products participates in such processes. Moreover, these receptors have a role in the onset and progression of various diseases such as various types of cancer, inflammation, atherosclerosis and obesity. In this review, a concise overview of the current understanding of the important metabolic roles governed by NR4A members including their participation in a number of diseases shall be provided.
    Journal of Receptor and Signal Transduction Research 08/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Respiratory complex I, the biggest enzyme of respiratory chain, plays a key role in energy production by the mitochondrial respiratory chain and has been implicated in many human neurodegenerative diseases. Recently, the crystal structure of respiratory complex I is reported. We perform 50 ns molecular dynamics simulations on the membrane domain of respiratory complex I under two hypothetical states (oxidized state and reduced state). We find that the density of water molecules in the trans-membrane domain under reduced state is bigger than that under oxidized state. The connecting elements (helix HL and β-hairpins-helix element) fluctuate stronger under reduced state than that under oxidized state, causing more internal water molecules and facilitating the proton conduction. The conformational changes of helix HL and the crucial charged residue Glu in TM5 play key roles in the mechanism of proton translocation. Our results illustrate the dynamic behavior and the potential mechanism of respiratory complex I, which provides the structural basis for drug design of respiratory complex I.
    Journal of Receptor and Signal Transduction Research 07/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Staphylococcus aureus has been recognized as an important human pathogen for more than 100 years. It is among the most important causative agent of human infections in the twenty-first century. DNA ligase is the main protein responsible for the replication of S. aureus. In order to control the replication mechanism, DNA ligase is a successive drug target, hence we have chosen this protein for this study. We performed virtual screening using ZINC database for identification of potent inhibitor against DNA ligase. Based on the scoring methods, we have selected best five compounds from the ZINC database. In order to improve the accuracy, selected compounds were subjected into Quantum Polarized Ligand Docking (QPLD) docking, for which the results showed high docking score, compared to glide docking score. QPLD is more accurate as it includes charges in the scoring function, which was not available in the glide docking. Binding energy calculation results also indicated that selected compounds have good binding capacity with the target protein. In addition, these compounds on screening have good absorption, distribution, metabolism, excretion and toxicity property. In this study, we identified few compounds that particularly work against DNA ligase protein, having better interaction phenomenon and it would help further the experimental analysis.
    Journal of Receptor and Signal Transduction Research 07/2014;
  • [Show abstract] [Hide abstract]
    ABSTRACT: Abstract Atherosclerosis is a life-threatening disease and a major cause of mortalities worldwide. While many of the atherosclerotic sequelae are reflected as microvascular effects in the eye, the molecular mechanisms of their development is not yet known. In this study, we employed a systems biology approach to unveil the most significant events and key molecular mediators of ophthalmic sequelae caused by atherosclerosis. Literature mining was used to identify the proteins involved in both atherosclerosis and ophthalmic diseases. A protein-protein interaction (PPI) network was prepared using the literature-mined seed nodes. Network topological analysis was carried out using Cytoscape, while network nodes were annotated using database for annotation, visualization and integrated discovery in order to identify the most enriched pathways and processes. Network analysis revealed that mitogen-activated protein kinase 1 (MAPK1) and protein kinase C occur with highest betweenness centrality, degree and closeness centrality, thus reflecting their functional importance to the network. Our analysis shows that atherosclerosis-associated ophthalmic complications are caused by the convergence of neurotrophin signaling pathways, multiple immune response pathways and focal adhesion pathway on the MAPK signaling pathway. The PPI network shares features with vasoregression, a process underlying multiple vascular eye diseases. Our study presents a first clear and composite picture of the components and crosstalk of the main pathways of atherosclerosis-induced ocular diseases. The hub bottleneck nodes highlight the presence of molecules important for mediating the ophthalmic complications of atherosclerosis and contain five established drug targets for future therapeutic modulation efforts.
    Journal of Receptor and Signal Transduction Research 07/2014;