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Post-transcriptional Regulation (post-transcriptional + regulation)
Selected AbstractsPost-transcriptional regulation of plasminogen activator inhibitor-1 by intracellular iron in cultured human lung fibroblasts,interaction of an 81-kDa nuclear protein with the 3,-UTRJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2005K. S. RADHA Summary., The proteinase inhibitor, type-1 plasminogen activator inhibitor (PAI-1), is a major regulator of the plasminogen activator system involved in plasmin formation and fibrinolysis. The present study explores the effects of intracellular iron on the expression of PAI-1 and associated cell-surface plasmin activity in human lung fibroblasts; and reports the presence of a novel iron-responsive protein. ELISA revealed a dose-dependent increase in PAI-1 antigen levels expressed in the conditioned medium of cells treated with deferoxamine, in the three cell lines studied. A concomitant increase in mRNA levels was also observed by Northern analyses. Presaturation with ferric citrate quenched the effect of deferoxamine. Experiments with transcription and translation inhibitors on TIG 3-20 cells demonstrated that intracellular iron modulated PAI-1 expression at the post-transcriptional level with the requirement of de-novo protein synthesis. Electrophoretic mobility shift assay and UV crosslinking assays revealed the presence of an ,,81-kDa nuclear protein that interacted with the 3,-UTR of PAI-1 mRNA in an iron-sensitive manner. Finally, we demonstrated that the increased PAI-1 is functional in suppressing cell-surface plasmin activity, a process that can affect wound healing and tissue remodeling. [source] Differential expression of antenna and core genes in Prochlorococcus PCC 9511 (Oxyphotobacteria) grown under a modulated light,dark cycleENVIRONMENTAL MICROBIOLOGY, Issue 3 2001Laurence Garczarek The continuous changes in incident solar light occurring during the day oblige oxyphototrophs, such as the marine prokaryote Prochlorococcus, to modulate the synthesis and degradation rates of their photosynthetic components finely. How this natural phenomenon influences the diel expression of photosynthetic genes has never been studied in this ecologically important oxyphotobacterium. Here, the high light-adapted strain Prochlorococcus sp. PCC 9511 was grown in large-volume continuous culture under a modulated 12 h,12 h light,dark cycle mimicking the conditions found in the upper layer of equatorial oceans. The pcbA gene encoding the major light-harvesting complex showed strong diel variations in transcript levels with two maxima, one before the onset of illumination and the other near the end of the photoperiod. In contrast, the mRNA level of psbA (encoding the reaction centre II subunit D1), the monocistronic transcript of psbD (encoding D2) and the dicistronic transcript of psbDC were all tightly correlated with light irradiance, with a minimum at night and a maximum at noon. The occurrence of a second peak during the dark period for the monocistronic transcript of psbC (encoding one of the PS II core Chl a antenna proteins) suggested the involvement of post-transcriptional regulation. Differential expression of the external antenna and core genes may constitute a mechanism of regulation of the antenna size to cope with the excess photon fluxes that Prochlorococcus cells experience in the upper layer of oceans around midday. The 5, ends of all transcripts were mapped, and a conserved motif, 5,-TTGATGA-3,, was identified within the putative psbA and pcbA promoters. [source] In vivo post-transcriptional regulation of CD154 in mouse CD4+ T cellsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 8 2009Stefano Vavassori Abstract Interactions between CD40 and its ligand CD154 are involved in the progression of both cell mediated and innate immunity. These interactions are brought about by the transient expression of CD154 on activated CD4+ T cells, which is regulated, in part, at the level of mRNA turnover. Here we have focused on analyzing the pattern of post-transcriptional regulation in mouse CD4+ T cells in response to activation. Initial experiments identify a region of the murine CD154 mRNA that binds a polypyrimidine tract-binding protein-containing complex (mComplex I), which is activation-dependent and binds to a single CU-rich site within the 3, uTR Subsequent findings demonstrate that in vivo polyclonal activation of T cells leads to a pattern of differential CD154 mRNA stability that is directly dependent on extent of activation. Furthermore, in vitro activation of antigen-primed T cells shows that the CD154 mRNA half-life increases relative to that of unprimed cells. Importantly, this is the first report demonstrating that the regulation of CD154 in vivo is connected to an activation-induced program of mRNA decay and thus provides strong evidence for post-transcriptional mechanisms having a physiological role in regulating CD154 expression during an ongoing immune response. [source] Iron regulatory protein-independent regulation of ferritin synthesis by nitrogen monoxideFEBS JOURNAL, Issue 16 2006Marc Mikhael The discovery of iron-responsive elements (IREs), along with the identification of iron regulatory proteins (IRP1, IRP2), has provided a molecular basis for our current understanding of the remarkable post-transcriptional regulation of intracellular iron homeostasis. In iron-depleted conditions, IRPs bind to IREs present in the 5,-UTR of ferritin mRNA and the 3,-UTR of transferrin receptor (TfR) mRNA. Such binding blocks the translation of ferritin, the iron storage protein, and stabilizes TfR mRNA, whereas the opposite scenario develops when iron in the intracellular transit pool is plentiful. Nitrogen monoxide (commonly designated nitric oxide; NO), a gaseous molecule involved in numerous functions, is known to affect cellular iron metabolism via the IRP/IRE system. We previously demonstrated that the oxidized form of NO, NO+, causes IRP2 degradation that is associated with an increase in ferritin synthesis [Kim, S & Ponka, P (2002) Proc Natl Acad Sci USA99, 12214,12219]. Here we report that sodium nitroprusside (SNP), an NO+ donor, causes a dramatic and rapid increase in ferritin synthesis that initially occurs without changes in the RNA-binding activities of IRPs. Moreover, we demonstrate that the translational efficiency of ferritin mRNA is significantly higher in cells treated with SNP compared with those incubated with ferric ammonium citrate, an iron donor. Importantly, we also provide definitive evidence that the iron moiety of SNP is not responsible for such changes. These results indicate that SNP-mediated increase in ferritin synthesis is, in part, due to an IRP-independent and NO+ -dependent post-transcriptional, regulatory mechanism. [source] MicroRNA regulation in Ames dwarf mouse liver may contribute to delayed agingAGING CELL, Issue 1 2010David J. Bates Summary The Ames dwarf mouse is well known for its remarkable propensity to delay the onset of aging. Although significant advances have been made demonstrating that this aging phenotype results primarily from an endocrine imbalance, the post-transcriptional regulation of gene expression and its impact on longevity remains to be explored. Towards this end, we present the first comprehensive study by microRNA (miRNA) microarray screening to identify dwarf-specific lead miRNAs, and investigate their roles as pivotal molecular regulators directing the long-lived phenotype. Mapping the signature miRNAs to the inversely expressed putative target genes, followed by in situ immunohistochemical staining and in vitro correlation assays, reveals that dwarf mice post-transcriptionally regulate key proteins of intermediate metabolism, most importantly the biosynthetic pathway involving ornithine decarboxylase and spermidine synthase. Functional assays using 3,-untranslated region reporter constructs in co-transfection experiments confirm that miRNA-27a indeed suppresses the expression of both of these proteins, marking them as probable targets of this miRNA in vivo. Moreover, the putative repressed action of this miRNA on ornithine decarboxylase is identified in dwarf mouse liver as early as 2 months of age. Taken together, our results show that among the altered aspects of intermediate metabolism detected in the dwarf mouse liver , glutathione metabolism, the urea cycle and polyamine biosynthesis , miRNA-27a is a key post-transcriptional control. Furthermore, compared to its normal siblings, the dwarf mouse exhibits a head start in regulating these pathways to control their normality, which may ultimately contribute to its extended healthspan and longevity. [source] Gene expression of differentiation-specific keratins (K4, K13, K1 and K10) in oral non-dysplastic keratoses and lichen planusJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 8 2000Balvinder K. Bloor Abstract: Gene expression for the differentiation-specific keratins (K4, K13, K1 and K10) was analyzed in oral non-dysplastic keratoses, oral lichen planus (OLP) and lichenoid reactions (LR) by comparative in situ hybridization (ISH) and immunohistochemistry (IHC) to investigate molecular changes in the altered differentiation pattern from non- to para- or orthokeratinization. At the protein level, K4 and K13 were detected homogeneously in the suprabasal compartment of parakeratotic epithelium but showed reduced expression in orthokeratoses, particularly in the presence of lymphocytes. Corresponding transcripts were restricted to basal and lower prickle cells. Synthesis of K1 and K10 was upregulated and more pronounced in orthokeratotic epithelia. The study showed an alteration in the pattern of differentiation-specific keratins, although involvement of the lymphocytic infiltrate in OLP and LR resulted in further gene modulation. In both diseases, K1 and K10 showed transcriptional control, proteins having the same distribution as their transcripts. This represented a change from post-transcriptional regulation in normal buccal epithelium, in which mRNAs for K1 and K10 are more widely expressed than their proteins. Thus, the pattern of keratin gene expression may be altered in response to frictional/smoking stimuli or immune-mediated mechanisms. [source] Hippocampal N -Methyl- d -Aspartate Receptor Subunit Expression Profiles in a Mouse Model of Prenatal Alcohol ExposureALCOHOLISM, Issue 2 2010Sabrina L. Samudio-Ruiz Background:, Although several reports have been published showing prenatal ethanol exposure is associated with alterations in N -methyl- d- aspartate (NMDA) receptor subunit levels and, in a few cases, subcellular distribution, results of these studies are conflicting. Methods:, We used semi-quantitative immunoblotting techniques to analyze NMDA receptor NR1, NR2A, and NR2B subunit levels in the adult mouse hippocampal formation isolated from offspring of dams who consumed moderate amounts of ethanol throughout pregnancy. We employed subcellular fractionation and immunoprecipitation techniques to isolate synaptosomal membrane- and postsynaptic density protein-95 (PSD-95)-associated pools of receptor subunits. Results:, We found that, compared to control animals, fetal alcohol-exposed (FAE) adult mice had: (i) increased synaptosomal membrane NR1 levels with no change in association of this subunit with PSD-95 and no difference in total NR1 expression in tissue homogenates; (ii) decreased NR2A subunit levels in hippocampal homogenates, but no alterations in synaptosomal membrane NR2A levels and no change in NR2A-PSD-95 association; and (iii) no change in tissue homogenate or synaptosomal membrane NR2B levels but a reduction in PSD-95-associated NR2B subunits. No alterations were found in mRNA levels of NMDA receptor subunits suggesting that prenatal alcohol-associated differences in subunit protein levels are the result of differences in post-transcriptional regulation of subunit localization. Conclusions:, Our results demonstrate that prenatal alcohol exposure induces selective changes in NMDA receptor subunit levels in specific subcellular locations in the adult mouse hippocampal formation. Of particular interest is the finding of decreased PSD-95-associated NR2B levels, suggesting that synaptic NR2B-containing NMDA receptor concentrations are reduced in FAE animals. This result is consistent with various biochemical, physiological, and behavioral findings that have been linked with prenatal alcohol exposure. [source] Specific and pleiotropic patterns of mRNA regulation by ArcZ, a conserved, Hfq-dependent small RNAMOLECULAR MICROBIOLOGY, Issue 1 2009Kai Papenfort Summary The small RNA, ArcZ (previously RyhA/SraH), was discovered in several genome-wide screens in Escherichia coli and Salmonella. Its high degree of genomic conservation, its frequent recovery by shotgun sequencing, and its association with the RNA chaperone, Hfq, identified ArcZ as an abundant enterobacterial ,core' small RNA, yet its function remained unknown. Here, we report that ArcZ acts as a post-transcriptional regulator in Salmonella, repressing the mRNAs of the widely distributed sdaCB (serine uptake) and tpx (oxidative stress) genes, and of STM3216, a horizontally acquired methyl-accepting chemotaxis protein (MCP). Both sdaCB and STM3216 are regulated by sequestration of the ribosome binding site. In contrast, the tpx mRNA is targeted in the coding sequence (CDS), arguing that CDS targeting is more common than appreciated. Transcriptomic analysis of an arcZ deletion strain further argued for the existence of a distinct set of Salmonella loci specifically regulated by ArcZ. In contrast, increased expression of the sRNA altered the steady-state levels of > 16% (> 750) of all Salmonella mRNAs, and rendered the bacteria non-motile. Deep sequencing detected a dramatically changed profile of Hfq-bound sRNAs and mRNAs, suggesting that the unprecedented pleiotropic effects by a single sRNA might in part be caused by altered post-transcriptional regulation. [source] The RNA chaperone Hfq is essential for the virulence of Salmonella typhimuriumMOLECULAR MICROBIOLOGY, Issue 1 2007Alexandra Sittka Summary The RNA chaperone, Hfq, plays a diverse role in bacterial physiology beyond its original role as a host factor required for replication of Q, RNA bacteriophage. In this study, we show that Hfq is involved in the expression and secretion of virulence factors in the facultative intracellular pathogen, Salmonella typhimurium. A Salmonella hfq deletion strain is highly attenuated in mice after both oral and intraperitoneal infection, and shows a severe defect in invasion of epithelial cells and a growth defect in both epithelial cells and macrophages in vitro. Surprisingly, we find that these phenotypes are largely independent of the previously reported requirement of Hfq for expression of the stationary phase sigma factor, RpoS. Our results implicate Hfq as a key regulator of multiple aspects of virulence including regulation of motility and outer membrane protein (OmpD) expression in addition to invasion and intracellular growth. These pleiotropic effects are suggested to involve a network of regulatory small non-coding RNAs, placing Hfq at the centre of post-transcriptional regulation of virulence gene expression in Salmonella. In addition, the hfq mutation appears to cause a chronic activation of the RpoE-mediated envelope stress response which is likely due to a misregulation of membrane protein expression. [source] Proteasome- and SCF-dependent degradation of yeast adenine deaminase upon transition from proliferation to quiescence requires a new F-box protein named Saf1pMOLECULAR MICROBIOLOGY, Issue 4 2006Stéphanie Escusa Summary In response to nutrient limitation, Saccharomyces cerevisiae cells enter into a non-proliferating state termed quiescence. This transition is associated with profound changes in gene expression patterns. The adenine deaminase encoding gene AAH1 is among the most precociously and tightly downregulated gene upon entry into quiescence. We show that AAH1 downregulation is not specifically due to glucose exhaustion but is a more general response to nutrient limitation. We also found that Aah1p level is tightly correlated to RAS activity indicating thus an important role for the protein kinase A pathway in this regulation process. We have isolated three deletion mutants, srb10, srb11 and saf1 (ybr280c) affecting AAH1 expression during post-diauxic growth and in early stationary phase. We show that the Srb10p cyclin-dependent kinase and its cyclin, Srb11p, regulate AAH1 expression at the transcriptional level. By contrast, Saf1p, a previously uncharacterized F-box protein, acts at a post-transcriptional level by promoting degradation of Aah1p. This post-transcriptional regulation is abolished by mutations affecting the proteasome or constant subunits of the SCF (Skp1,Cullin,F -box) complex. We propose that Saf1p targets Aah1p for proteasome-dependent degradation upon entry into quiescence. This work provides the first direct evidence for active degradation of proteins in quiescent yeast cells. [source] RNase R affects gene expression in stationary phase: regulation of ompAMOLECULAR MICROBIOLOGY, Issue 1 2006José Marques Andrade Summary In nature, bacteria remain mostly in the stationary phase of the life cycle. Although mRNA is a major determinant of gene expression, little is known about mRNA decay in the stationary phase. The results presented herein demonstrate that RNase R is induced in stationary phase and is involved in the post-transcriptional regulation of ompA mRNA. This work is the first report of RNase R activity on a full length mRNA. In the absence of RNase R in a single rnr mutant, higher levels of ompA mRNA are found as a consequence of the stabilization of ompA full transcript. This effect is growth-phase-specific and not a growth-rate-dependent event. These higher levels of ompA mRNA were correlated with increases in the amounts of OmpA protein. We have also analysed the role of other factors that could affect ompA mRNA stability in stationary phase. RNase E was found to have the most important role, followed by polyadenylation. PNPase also affected the decay of the ompA transcript but RNase II did not seem to contribute much to this degradation process. The participation of RNase R in poly(A)-dependent pathways of decay in stationary phase of growth is discussed. The results show that RNase R can be a modulator of gene expression in stationary phase cells. [source] Involvement of a novel transcriptional activator and small RNA in post-transcriptional regulation of the glucose phosphoenolpyruvate phosphotransferase systemMOLECULAR MICROBIOLOGY, Issue 4 2004Carin K. Vanderpool Summary RyaA is a small non-coding RNA in Escherichia coli that was identified by its ability to bind tightly to the RNA chaperone Hfq. This study reports the role of RyaA in mediating the cellular response to glucose-specific phosphoenolypyruvate phosphotransferase system (PTS)-dependent phosphosugar stress. Aiba and co-workers have shown that a block in the metabolism of glucose 6-phosphate causes transient growth inhibition and post-transcriptional regulation of ptsG, encoding the glucose-specific PTS transporter. We found that RyaA synthesis was induced by a non-metabolizable glucose phosphate analogue and was necessary for relief of the toxicity of glucose phosphate stress. Expression of RyaA was sufficient to cause a rapid loss of ptsG mRNA, probably reflecting degradation of the message mediated by RyaA:ptsG pairing. The ryaA gene was renamed sgrS, for sugar transport-related sRNA. Expression of sgrS is regulated by a novel transcriptional activator, SgrR (formerly YabN), which has a putative DNA-binding domain and a solute-binding domain similar to those found in certain transport proteins. Our results suggest that under conditions of glucose phosphate accumulation, SgrR activates SgrS synthesis, causing degradation of ptsG mRNA. Decreased ptsG mRNA results in decreased production of glucose transport machinery, thus limiting further accumulation of glucose phosphate. [source] Combining subproteome enrichment and Rubisco depletion enables identification of low abundance proteins differentially regulated during plant defensePROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 1 2009Ivy Widjaja Abstract Transgenic Arabidopsis conditionally expressing the bacterial avrRpm1 type III effector under the control of a dexamethasone-responsive promoter were used for proteomics studies. This model system permits study of an individual effector without interference from additional bacterial components. Coupling of different prefractionation approaches to high resolution 2-DE facilitated the discovery of low abundance proteins , enabling the identification of proteins that have escaped detection in similar experiments. A total of 34 differentially regulated protein spots were identified. Four of these (a remorin, a protein phosphatase 2C (PP2C), an RNA-binding protein, and a C2-domain-containing protein) are potentially early signaling components in the interaction between AvrRpm1 and the cognate disease resistance gene product, resistance to Pseudomonas syringae pv. maculicola 1 (RPM1). For the remorin and RNA-binding protein, involvement of PTM and post-transcriptional regulation are implicated, respectively. [source] Cold-inducible zinc finger-containing glycine-rich RNA-binding protein contributes to the enhancement of freezing tolerance in Arabidopsis thalianaTHE PLANT JOURNAL, Issue 6 2005Yeon-Ok Kim Summary Glycine-rich RNA-binding proteins (GR-RBPs) have been implicated to play roles in post-transcriptional regulation of gene expression in plants under various stress conditions, but the functional roles of GR-RBPs under stress conditions remain to be verified. Here, we examine the biological roles of a GR-RBP, designated atRZ-1a, in Arabidopsis thaliana under stress conditions. atRZ-1a was expressed ubiquitously in various Arabidopsis organs including stems, roots, leaves, flowers, and siliques. The transcript level of atRZ-1a increased markedly by cold stress, whereas its expression was marginally downregulated by drought stress or abscisic acid treatment. Germination and seedling growth of the loss-of-function mutants were retarded remarkably compared with those of the wild type under cold stress. In contrast, the transgenic Arabidopsis plants that overexpress atRZ-1a displayed earlier germination and better seedling growth than the wild type under cold stress. Moreover, the atRZ-1a-overexpressing transgenic Arabidopsis plants were more freezing tolerant than the wild-type plants. Heterologous expression of atRZ-1a in Escherichia coli demonstrated that the E. coli cells expressing atRZ-1a displayed much higher growth rate than the non-transformed cells after cold shock. These results provide evidence that atRZ-1a affects seed germination and seedling growth under low temperature and plays a role in the enhancement of freezing tolerance in Arabidopsis plants. [source] Life-span phenotypes of elav and Rbp9 in Drosophila suggest functional cooperation of the two elav-family protein genesARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 4 2010Gakuta Toba Abstract The ELAV family of RNA-binding proteins is involved in various aspects of the post-transcriptional regulation of gene expression, from alternative splicing to translation. The members of this family have been shown to interact with each other and have been suggested to function as homo- and/or hetero-multimers. However, the functional interactions among them have not been demonstrated in vivo. In this study, we examined the genetic interaction between elav and Rbp9, two of the three genes encoding ELAV-family proteins in Drosophila. Mutants of both elav and Rbp9 showed shorter life spans than the control, with elav showing a shorter life span than Rbp9. The survival curve of elav-Rbp9 double-mutant flies was indistinguishable from that of elav single-mutant flies, suggesting that both mutations affect longevity through the same pathway. Considering the fact that both genes are co-expressed in adult neurons, we hypothesize that ELAV and Rbp9 cooperate to maintain the functional integrity of the adult nervous system. © 2010 Wiley Periodicals, Inc. [source] The H19 locus: Role of an imprinted non-coding RNA in growth and developmentBIOESSAYS, Issue 6 2010Anne Gabory Abstract The H19 gene produces a non-coding RNA, which is abundantly expressed during embryonic development and down-regulated after birth. Although this gene was discovered over 20 years ago, its function has remained unclear. Only recently a role was identified for the non-coding RNA and/or its microRNA partner, first as a tumour suppressor gene in mice, then as a trans-regulator of a group of co-expressed genes belonging to the imprinted gene network that is likely to control foetal and early postnatal growth in mice. The mechanisms underlying this transcriptional or post-transcriptional regulation remain to be discovered, perhaps by identifying the protein partners of the full-length H19 RNA or the targets of the microRNA. This first in vivo evidence of a functional role for the H19 locus provides new insights into how genomic imprinting helps to control embryonic growth. [source] Hypertonic upregulation of betaine transport in renal cells is blocked by a proteasome inhibitorCELL BIOCHEMISTRY AND FUNCTION, Issue 5 2005Philip E. Lammers Abstract The renal betaine transporter (BGT1) protects cells in the hypertonic medulla by mediating uptake and accumulation of the osmolyte betaine. Transcription plays an essential role in upregulating BGT1 transport in MDCK cells subjected to hypertonic stress. During hypertonic stress, the abundance of the transcription factor TonEBP increases and it shifts from the cytoplasm to the nucleus where it activates transcription of the BGT1 gene. Little is known about post-transcriptional regulation of BGT1 protein. In the presence of the proteasome inhibitor MG-132, which blocked nuclear translocation of TonEBP, the hypertonic upregulation of BGT1 protein and transport was prevented and cell viability in hypertonic medium was impaired over 24,h. Urea also prevented the hypertonic upregulation of BGT1 protein and transport, but did not interfere with TonEBP translocation and cell viability. Shorter treatments of hypertonic cells with MG-132 avoided viability problems and produced dose-dependent inhibition of translocation and transport. When stably transfected MDCK cells that over-expressed BGT1 were treated for 6,h with hypertonic medium containing 3,µM MG-132, there was 43% inhibition of nuclear translocation, 83% inhibition of BGT1 transport, and no change in viability. While other proteasome functions may be involved, these data are consistent with a critical role for nuclear translocation of TonEBP in upregulation and membrane insertion of BGT1 protein. Copyright © 2005 John Wiley & Sons, Ltd. [source] Sam68 is tyrosine phosphorylated and recruited to signalling in peripheral blood mononuclear cells from HIV infected patientsCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2005S. Najib Summary Human immunodeficiency virus (HIV) codes for a protein, Rev, that mediates the viral RNA export from the nucleus to the cytoplasm. Recently, it has been found that Sam68, the substrate of Src associated in mitosis, is a functional homologue of Rev, and a synergistic activator of Rev activity. Thus, it has been suggested that Sam68 may play an important role in the post-transcriptional regulation of HIV. Sam68 contains an RNA binding motif named KH [homology to the nuclear ribonucleoprotein (hnRNP) K]. Tyrosine phosphorylation of Sam68 and binding to SH3 domains have been found to negatively regulate its RNA binding capacity. Besides, tyrosine phosphorylation of Sam68 allows the formation of signalling complexes with other proteins containing SH2 and SH3 domains, suggesting a role in signal transduction of different systems in human lymphocytes, such as the T cell receptor, and leptin receptor, or the insulin receptor in other cell types. In the present work, we have found that Sam68 is tyrosine phosphorylated in peripheral blood mononuclear cells (PBMC) from HIV infected subjects, leading to the formation of signalling complexes with p85 the regulatory subunit of PI3K, GAP and STAT-3, and decreasing its RNA binding capacity. In contrast, PBMC from HIV infected subjects have lower expression levels of Sam68 compared with controls. These results suggest that Sam68 may play some role in the immune function of lymphocytes in HIV infection. [source] | ||||||||||||||||