Search results for "SIGNALLING"

showing 10 items of 249 documents

ZNF518B as a transcriptional factor involved in colorectal cancer progression through the epithelial to mesenchymal transition

2019

Abstract Background Colorectal cancer (CRC) represents a relevant public health problem. The identification of new markers involved in the mechanisms of invasiveness represents a priority in order to better understand cancer development and generate new therapeutic targets. Recently, our group demonstrated overexpression of ZNF518B gene, which encodes an unknown zinc finger transcription factor, in CRC. A transcriptome-wide gene expression profile revealed its implication in different biological processes related to the progression of CRC, especially in the epithelial to mesenchymal transition (EMT). Methods To study the biological processes regulated by ZNF518B, we performed a ClariomS Arr…

HCT116 CellOncologymedicine.medical_specialtyTranscriptional factorColorectal cancerbusiness.industryeducationTranslational researchHematologymedicine.diseaseIn vitro analysisOncologyInternal medicinemedicineCancer developmentEpithelial–mesenchymal transitionbusinessSignalling pathwayshealth care economics and organizationsAnnals of Oncology
researchProduct

P1086 : Complex effects of adenosine receptor antagonists in models of liver fibrosis

2015

HepatologyChemistryLiver fibrosisPharmacologyPurinergic signallingAdenosine A3 receptorAdenosine receptorJournal of Hepatology
researchProduct

The "honest signalling theory" in gynecological endocrinology: teaching and research implications.

2004

Honest signalling theory gynecology endocrinology teaching researchSettore MED/40 - Ginecologia E Ostetricia
researchProduct

Different regulation of T helper 1- and T helper 2-promoting cytokine signalling factors in human dendritic cells after exposure to protein versus co…

2008

Cytokine-dependent T helper 1 (Th1) differentiation versus T helper 2 (Th2) differentiation is controlled by distinct transcription factors. Previously, we have demonstrated that immature human dendritic cells (DC) from blood donors with allergies show rapid phosphorylation of the Th2-associated signal transducer and activator of transcription 6 (STAT6) upon contact with protein allergens. In the present study we investigated whether this process is regulated by the downstream molecules suppressor of cytokine signalling (SOCS) and/or by the factors T-bet and GATA3. Therefore, immature DC of grass or birch pollen-allergic donors were treated with the respective Th2-promoting protein allergen…

ImmunologyBiologySuppressor of cytokine signallingImmune systemTh2 CellsAntigenHypersensitivityTetanus ToxoidImmunology and AllergyHumansCells CulturedSTAT6Suppressor of cytokine signaling 1Gene Expression ProfilingGATA3ProteinsOriginal ArticlesDendritic CellsAllergensTh1 CellsThiazolesImmunologyInterleukin 13STAT proteinCytokinesDisinfectantsSignal Transduction
researchProduct

Nitric Oxide Promotes Resistance to Tumor Suppression by CTLs

2006

Abstract Many human tumors express inducible NO synthetase (NOS2), but the roles of NO in tumor development are not fully elucidated. An important step during tumor development is the acquisition of apoptosis resistance. We investigated the dose-dependent effects of endogenously produced NO on apoptosis using ecdysone-inducible NOS2 cell lines. Our results show that short-term NOS2 expression enhances CD95-mediated apoptosis and T cell cytotoxicity dose dependently. Furthermore, we could show that during chronic exposure to NO, besides the primary cytotoxic NO effect, there is selection of cell clones resistant to NO that show cross-resistance to CD95-induced apoptosis and the killing by CT…

ImmunologyCellNitric Oxide Synthase Type IIApoptosisBiologyEndoplasmic ReticulumNitric OxideCell LineMalignant transformationParacrine signallingImmune systemNeoplasmsmedicineHumansImmunology and AllergyCytotoxic T cellfas ReceptorAutocrine signallingMitochondriamedicine.anatomical_structureGene Expression RegulationApoptosisCell cultureMitochondrial MembranesImmunologyCancer researchSignal TransductionT-Lymphocytes CytotoxicThe Journal of Immunology
researchProduct

Increased expression of leptin and the leptin receptor as a marker of breast cancer progression: possible role of obesity-related stimuli.

2006

Abstract Purpose: Recent in vitro studies suggested that the autocrine leptin loop might contribute to breast cancer development by enhancing cell growth and survival. To evaluate whether the leptin system could become a target in breast cancer therapy, we examined the expression of leptin and its receptor (ObR) in primary and metastatic breast cancer and noncancer mammary epithelium. We also studied whether the expression of leptin/ObR in breast cancer can be induced by obesity-related stimuli, such as elevated levels of insulin, insulin-like growth factor-I (IGF-I), estradiol, or hypoxic conditions. Experimental Design: The expression of leptin and ObR was examined by immunohistochemistry…

LeptinCancer ResearchER-BETAmedicine.medical_treatmentHYPOXIA-INDUCIBLE FACTOR-1NeoplasmsTumor Cells CulturedBreastInsulin-Like Growth Factor Iskin and connective tissue diseasesReceptorAged 80 and overEstradiolIGF-I RECEPTORCELL-LINEReverse Transcriptase Polymerase Chain ReactionLeptindigestive oral and skin physiologyCarcinoma Ductal BreastMiddle AgedMetastatic breast cancerINSULINCell HypoxiaESTROGENOncologyDisease ProgressionIGF-I RECEPTOR; HYPOXIA-INDUCIBLE FACTOR-1; OB GENE; GROWTH-FACTOR; CELL-LINE; ER-BETA; ESTROGEN; ALPHA; INSULIN; MCF-7Receptors LeptinFemaleOB GENEhormones hormone substitutes and hormone antagonistsAdultmedicine.medical_specialtyGROWTH-FACTORBreast NeoplasmsReceptors Cell SurfaceBreast cancerInternal medicinemedicineBiomarkers TumorHumansObesityAutocrine signallingAgedLeptin receptorbusiness.industryInsulinmedicine.diseaseALPHAEndocrinologyTumor progressionCase-Control StudiesMCF-7business
researchProduct

Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
researchProduct

Paracrine dialogue in implantation

2002

We know that the implantation process requires a functionally normal embryo at the blastocyst stage and a receptive endometrium, but also a communication link between them is needed. This paracrine dialogue between the embryo, endometrium and the corpus luteum are known to occur in ruminants and primates, more specifically endometrial-embryonic interactions have been reported in rodents and primates but not in humans. This process is a highly regulated mechanism and many molecules take part in this cross-talk. Here, we present updated information in humans on the embryonic regulation of endometrial epithelial molecules such as chemokines, adhesion and anti-adhesion molecules, and leptin dur…

Leptinmedicine.medical_specialtyReceptors Cell SurfaceBiologyEndometriumBiochemistryEndometriumParacrine signallingEndocrinologyPregnancyInternal medicineParacrine CommunicationCell AdhesionmedicineHumansEmbryo ImplantationEndotheliumBlastocystGonadal Steroid HormonesMolecular Biologyurogenital systemMechanism (biology)Mucin-1Epithelial CellsEmbryoEmbryo TransferEmbryonic stem cellCell biologyAppositionBlastocystmedicine.anatomical_structureEndocrinologyCytokinesReceptors LeptinFemaleChemokinesCarrier ProteinsCorpus luteumMolecular and Cellular Endocrinology
researchProduct

Theories and Mechanisms of Aging

2013

The more one learns about single processes and genes known to be involved in aging, the more it becomes evident that these are connected and there is no unifying theory of aging. The individual theories put individual factors and processes in focus and for each theory there are direct links to life span or to age-related disorders. In the following chapter, the key theories of aging focusing on telomeres, DNA damage, oxidative stress as well as possible roles of nutrition, the interplay between genes and environment (epigenetics) and cellular protein homeostasis are presented. In animal models the life span can be altered by targeting specific genes, proteins and signalling pathways. After …

Life spanDNA repairDNA damageProcess (engineering)EpigeneticsBiologyNeuroscienceSignalling pathwaysCellular proteinTelomere
researchProduct

Release of IL-12 by dendritic cells activated by TLR ligation is dependent on MyD88 signaling, whereas TRIF signaling is indispensable for TLR synerg…

2010

Abstract Synergistic activation of dendritic cells by combinations of TLR ligands requires both MyD88- and TRIF-dependent signaling. Recently, it has been shown that certain combinations of TLR ligands act in synergy to induce the release of IL-12 by DCs. In this study, we sought to define the critical parameters underlying TLR synergy. Our data show that TLR ligands act synergistically if MyD88- and TRIF-dependent ligands are combined. TLR4 uses both of these adaptor molecules, thus activation via TLR4 proved to be a synergistic event on its own. TLR synergy did not affect all aspects of DC activation but enhanced primarily the release of certain cytokines, particularly IL-12, whereas the …

LipopolysaccharidesT cellImmunologyBiologyLymphocyte ActivationInterferon-gammaMicemedicineImmunology and AllergyAnimalsCD40 AntigensAutocrine signallingMice Inbred BALB CToll-Like ReceptorsSignal transducing adaptor proteinCell PolarityCell BiologyDendritic CellsInterleukin-12Cell biologyMice Inbred C57BLAdaptor Proteins Vesicular Transportmedicine.anatomical_structurePoly I-CTRIFImmunologyMyeloid Differentiation Factor 88TLR4Interleukin 12Myeloid Differentiation Factor 88Signal transductionSignal TransductionJournal of leukocyte biology
researchProduct