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
    Hide 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 Toll-like receptors (TLRs) play a pivotal role in both innate and adaptive immunity, and TLRs recognize invading pathogens through molecular pattern recognition, and ultimately lead to the activation of transcription factors and inflammatory responses. Myocardial infarction leads to changes in the remodeling of the left ventricle of the heart, and the degree and type of remodeling provides important diagnostic information for the therapeutic management of ischemic heart disease. Innate immune takes a most important role in myocardial infarction. There are some studies reporting that TLRs play an important role in the myocardial infarction. The literatures were searched extensively and this review was performed to review the role of TLRs in myocardial infarction.
    Journal of Receptor and Signal Transduction Research 12/2014;
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    ABSTRACT: Abstract GNE Myopathy (GNEM) is a neuromuscular disorder caused by mutations in the GNE gene. It is a slowly progressive distal and proximal muscle weakness sparing the quadriceps. In this study, we applied our model of mutated M743T GNE enzyme skeletal muscle-cultured myoblasts and paired healthy controls to depict the pattern of signaling proteins controlling survival and/or apoptosis of the PI3K/AKT, BCL2, ARTS/XIAP pathways, examined the effects of metabolic changes/stimuli on their expression and activation, and their potential role in GNEM. Immunoblot analysis of the GNEM myoblasts indicated a notable increased level of activated PTEN and PDK1 and a trend of relative differences in the expression and activation of the examined signaling molecules with variability among the cultures. ANOVA analysis showed a highly significant interaction between the level of PTEN and the patients groups. In parallel, the interaction between the level of BCL2, BAX and PTEN with the specific PI3K/AKT inhibitor-LY294002 was highly significant for BCL2 and nearly significant for PTEN and BAX. The pattern of the ARTS/XIAP signaling proteins of GNEM and the paired controls was variable, with no significant differences between the two cell types. The response of the GNEM cells to the metabolic changes/stimuli: serum depletion and insulin challenge, as indicated by expression of selected signaling proteins, was variable and similar to the control cells. Taken together, our observations provide a clearer insight into specific signaling molecules influencing growth and survival of GNEM muscle cells.
    Journal of Receptor and Signal Transduction Research 12/2014;
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    ABSTRACT: Abstract Tripartite motif 22 (TRIM22) is involved in various cellular processes. It has been reported that TRIM22 can activate nuclear factor-κB (NF-κB) pathway, but the precise mechanism remains unclear. In this study, we explored the exact role of TRIM22 in activating the NF-κB pathway. Different to tumor necrosis factor-α (TNF-α) induction, we found that the overexpression of TRIM22 could induce the processing of p100 to p52 in HEK293T cells. Furthermore, based on the results of co-immunoprecipitation and co-localization experiments, we demonstrated that TRIM22 could interact with IκB kinase (IKK)α but not IKKβ and could increase the level and phosphorylation of IKKα through its really interesting new gene (RING) and spla-ryanodine receptor (SPRY) domains. These results suggest that TRIM22 is able to activate the noncanonical but not the canonical NF-κB pathway by activating IKKα. This finding will aid our understanding of the biological function of TRIM22.
    Journal of Receptor and Signal Transduction Research 12/2014;
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    ABSTRACT: Abstract IL-27 plays an important role in anti-cancer activity. The -964A/G polymorphism in IL-27 gene has been implicated in susceptibility to cancer, but the results were conflicting. The aim of this study was to assess the association between this polymorphism and cancer risk. Pubmed and Wanfang database were searched for all publications concerning IL-27 -964A/G polymorphism and cancer risk. Odds ratio (OR) and 95% confidence interval (CI) were used to assess the strength of association. Statistical analysis was performed using Stata 11.0 software. A total of eight case-control studies including 2044 cancer cases and 2197 controls were identified. Overall, significant association between IL-27 -964A/G polymorphism and cancer risk was observed (GG versus AA: OR = 1.26, 95% CI = 1.03-1.52; GG versus AG + AA: OR = 1.20, 95% CI = 1.00-1.44). In subgroup analysis based on cancer type, significant association was found in colorectal cancer (GG versus AA: OR = 1.55, 95% CI = 1.07-2.27; AG versus AA: OR = 1.31, 95% CI = 1.02-1.67). The current meta-analysis suggests that IL-27 -964A/G polymorphism might enhance cancer risk. However, large-scale and well-designed studies are still needed to confirm the result of our meta-analysis. The association of IL-27 polymorphism with colorectal cancer may provide insight for future therapies.
    Journal of Receptor and Signal Transduction Research 11/2014;
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    ABSTRACT: Abstract Stromal cell-derived factor 1 (CXCL12) and its receptor CXC chemokine receptor 4 (CXCR4) are known to modulate hypoxia-induced pulmonary hypertension (PH) and vascular remodeling by mobilization and recruitment of progenitor cells to the pulmonary vasculature. However, little is known about CXCL12/CXCR4 regulating proliferation and cell cycle progression of pulmonary arterial smooth muscle cells (PASMCs). To determine whether CXCL12/CXCR4 regulates PASMC proliferation and the cell cycle, immunohistochemistry, Western blot, bromodeoxyuridine incorporation and cell cycle analysis were preformed in this study. Our results showed that CXCR4 was induced by hypoxia in pulmonary arteries and PASMCs of rats. Hypoxia-increased cell viability, DNA synthesis and proliferating cell nuclear antigen expression were blocked by administration of CXCR4 antagonist AMD3100, silencing CXCR4 or CXCL12. Furthermore, inhibition of CXCL12/CXCR4 suppressed cell cycle progression, decreased the number of cells in S+G2/M phase and attenuated the expression of proteins that regulate the cell cycle progression at these phases. In addition, PI3K/Akt signaling mediated CXCL12/CXCR4 regulating proliferation and cell cycle progression in PASMCs. Thus, these results indicate that blockade of CXCL12/CXCR4 inhibited PASMC proliferation and cell cycle progression in hypoxia-induced PH via PI3K/Akt signaling pathway.
    Journal of Receptor and Signal Transduction Research 11/2014;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;
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    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;