Search results for: HSPC142 protein -
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Thyroid-Stimulating Hormone-Stimulated Human Adipocytes Express Thymic Stromal Lymphopoietin.When recombinant human (rh) thyroid-stimulating hormone (TSH) is administered to thyroid cancer survivors, an acute extra-thyroidal effect raises pro-inflammatory cytokines and activates platelets. Thymic stromal lymphopoietin (TSLP) is a cytokine recently implicated in platelet activation. Our aim was to measure platelet microparticle levels after rhTSH stimulation in vivo, and to investigate TSLP expression in TSH-stimulated human adipocytes in culture. Blood samples for total and platelet microparticle analysis were obtained from thyroid cancer survivors before (day 1) and after rhTSH administration (day 5). Adipocytes, differentiated from stromal preadipocytes isolated from adipose tissue from surgical patients, were stimulated with TSH. TSLP mRNA expression, protein expression, and protein release into the adipocyte medium were measured. The level of platelet microparticles in thyroid cancer patients rose 5-fold after rhTSH stimulation. TSH upregulated TSLP mRNA expression in adipocytes in culture through a pathway that was inhibited by 66% by H89, a protein kinase A inhibitor. TSLP protein expression rose in response to TSH, and TSH-stimulated TSLP release into the medium was completely blocked by dexamethasone. In conclusion, TSLP is a novel TSH-responsive adipokine. Future studies will be needed to address the potential role of adipocyte-derived TSLP and whether it is linked to TSH-dependent platelet activation.
1710 related Products with: Thyroid-Stimulating Hormone-Stimulated Human Adipocytes Express Thymic Stromal Lymphopoietin.Human Thymic Stromal Lymp Human Thyroid Stimulating Human Ultrasensitive Thyr Mouse Anti-Human Thyroid Mouse Anti-Human Thyroid Macrophage Colony Stimula Rat Thyroid Stimulating H Mouse Anti-Human Thyroid Rat monoclonal anti mouse Mouse Anti-Human Follicle Bone Morphogenetic Protei Epidermal Growth Factor (
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Effects of Curcuminoids Plus Piperine on Glycemic, Hepatic and Inflammatory Biomarkers in Patients with Type 2 Diabetes Mellitus: A Randomized Double-Blind Placebo-Controlled Trial.Curcuminoids have been shown to reduce glycemia and related complications in diabetes. In the present study, we evaluated the impact of curcuminoids plus piperine administration on glycemic, hepatic and inflammatory biomarkers in type 2 diabetes (T2D) patients.
1248 related Products with: Effects of Curcuminoids Plus Piperine on Glycemic, Hepatic and Inflammatory Biomarkers in Patients with Type 2 Diabetes Mellitus: A Randomized Double-Blind Placebo-Controlled Trial.Mouse Macrophage Inflamma High density (188 cases 2 High density (188 cases 2 High density (208 cores), Multiple cancer (12 type) Top 4 types of cancer (co ING1B antisense AKT1 (dn) Inducible Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma Human Macrophage Inflamma
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Alpha-synuclein oligomers impair memory through glial cell activation and via Toll-like receptor 2.Alpha-synuclein oligomers (α-synOs) are emerging as crucial factors in the pathogenesis of synucleinopathies. Although the connection between neuroinflammation and α-syn still remains elusive, increasing evidence suggests that extracellular moieties activate glial cells leading to neuronal damage. Using an acute mouse model, we explored whether α-synOs induce memory impairment in association to neuroinflammation, addressing Toll-like receptors 2 and 4 (TLR2 and TLR4) involvement. We found that α-synOs abolished mouse memory establishment in association to hippocampal glial activation. On brain slices α-synOs inhibited long-term potentiation. Indomethacin and Ibuprofen prevented the α-synOs-mediated detrimental actions. Furthermore, while the TLR2 functional inhibitor antibody prevented the memory deficit, oligomers induced memory deficits in the TLR4 knockout mice. In conclusion, solely α-synOs induce memory impairment likely inhibiting synaptic plasticity. α-synOs lead to hippocampal gliosis that is involved in memory impairment. Moreover, while the oligomer-mediated detrimental actions are TLR2 dependent, the involvement of TLR4 was ruled out.
2551 related Products with: Alpha-synuclein oligomers impair memory through glial cell activation and via Toll-like receptor 2.anti Transferrin receptor Mouse AntiT cell receptor Human Stromal Cell-Derive Androgen Receptor (Phosph Androgen Receptor (Phosph Mouse Anti-Human Interleu Rabbit Anti-Rat GABA A Re Mouse Anti-Human Thyroid Rabbit Anti-Human Androge Rabbit Anti-Human Androge TNFRSF1B - Goat polyclona RABBIT ANTI HUMAN SDF-1 A
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Adverse childhood experiences and adult inflammation: findings from the 1958 British birth cohort.The relationship between adverse childhood experiences (ACE) and poorer health across the life course is well established. Increased chronic inflammation might be one mechanism through which these associations operate. The aim of this study was to explore the relationship between ACE and adult inflammation using a prospective longitudinal study. We also investigated whether associations were explained by life course socioeconomic, psychological and health behavioural factors, and whether associations differed by gender.
1597 related Products with: Adverse childhood experiences and adult inflammation: findings from the 1958 British birth cohort.BACTERIOLOGY BACTEROIDES Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 TCP-1 theta antibody Sour Recombinant Thermostable Recombinant Thermostable Recombinant Thermostable Recombinant Human PKC the Recombinant Human PKC the
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A direct gateway into the extracellular space: Unconventional secretion of FGF2 through self-sustained plasma membrane pores.As illustrated by a diverse set of examples in this special issue, multiple mechanisms of protein secretion have been identified in eukaryotes that do not involve the endoplasmic reticulum (ER) and the Golgi apparatus. Here we focus on the type I pathway with Fibroblast Growth Factor 2 (FGF2) being the most prominent example. Unconventional secretion of FGF2 from cells is mediated by direct protein translocation across the plasma membrane. A unique feature of this process is the ability of FGF2 to form its own membrane translocation intermediate through oligomerization and membrane insertion. This process depends on the phosphoinositide PI(4,5)Pat the inner leaflet and results in the formation of lipidic membrane pores in the plasma membrane. Various lines of evidence suggest that these pores are characterized by a toroidal architecture with FGF2 oligomers being accommodated in the center of these structures. At the outer leaflet of the plasma membrane, membrane proximal heparan sulfate proteoglycans are required for the final step of FGF2 translocation into the extracellular space. Based upon mutually exclusive interactions of FGF2 with PI(4,5)Pversus heparan sulfates, an assembly/disassembly pathway has been proposed to be the underlying principle of directional transport of FGF2 across the plasma membrane. Thus, the core mechanism of unconventional secretion of FGF2 is based upon three discrete steps with (i) PI(4,5)Pdependent oligomerization of FGF2 at the inner leaflet, (ii) insertion of membrane spanning FGF2 oligomers into the plasma membrane and (iii) disassembly at the outer leaflet mediated by heparan sulfates that subsequently retain FGF2 on cell surfaces. This process has recently been reconstituted with an inside-out membrane model system using giant unilamellar vesicles providing a compelling explanation of how FGF2 reaches the extracellular space in an ER/Golgi independent manner.
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GRP78 Promotes Hepatocellular Carcinoma proliferation by increasing FAT10 expression through the NF-κB pathway.Glucose-regulated protein 78(GRP78) and the ubiquitin-like protein FAT10 each promote proliferation in hepatocellular carcinoma(HCC). However, the relationship of GRP78 and FAT10 in HCC proliferation are still not known. In this study, we found that GRP78 and FAT10 were significantly overexpressed in HCC tissues compare with adjacent non-cancerous tissues, and a positive correlation was found between their expression and associated proliferation characteristics. High expression of GRP78 and FAT10 were positively correlated with tumor proliferation and poor prognosis in HCC. Moreover, GRP78 knockdown reduced FAT10 expression and suppressed HCC proliferation in vitro and in vivo. The effects of GRP78 knockdown were rescued by FAT10 up-regulation, whereas FAT10 knockdown reduced HCC proliferation enhanced by GRP78 up-regulation. Furthermore, GRP78 modulated FAT10 expression by regulating the NF-κB pathway, direct activation of the NF-κB pathway increased the expression of FAT10, a gene counteracting the tumor suppressor p53. Taken together, these results suggest that this newly identified GRP78-NF-κB-FAT10 axis will provide novel insight into the understanding of the regulatory mechanisms of proliferation in human HCC.
2806 related Products with: GRP78 Promotes Hepatocellular Carcinoma proliferation by increasing FAT10 expression through the NF-κB pathway.NF-kB Phospho-Specific Ar NF-kB II Phospho-Specific Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Liver hepatocellular carc Liver cancer (hepatocellu Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma
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Maintenance of hematopoietic stem and progenitor cells in fetal intra-aortic hematopoietic clusters by the Sox17-Notch1-Hes1 axis.The aorta-gonad-mesonephros region, from which definitive hematopoiesis first arises in midgestation mouse embryos, has intra-aortic hematopoietic clusters (IAHCs) containing hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs). We previously reported expression of the transcription factor Sox17 in IAHCs, and overexpression of Sox17 in CD45c-KITcells comprising IAHCs maintains the formation of cell clusters and their multipotency in vitro over multiple passages. Here, we demonstrate the importance of NOTCH1 in IAHC formation and maintenance of the HSC/HPC phenotype. We further show that Notch1 expression is positively regulated by SOX17 via direct binding to its gene promoter. SOX17 and NOTCH1 were both found to be expressed in vivo in cells of IAHCs by whole mount immunostaining. We found that cells transduced with the active form of NOTCH1 or its downstream target, Hes1, maintained their multipotent colony-forming capacity in semisolid medium. Moreover, cells stimulated by NOTCH1 ligand, Jagged1, or Delta-like protein 1, had the capacity to form multilineage colonies. Conversely, knockdown of Notch1 and Hes1 led to a reduction of their multipotent colony-forming capacity. These results suggest that the Sox17-Notch1-Hes1 pathway is critical for maintaining the undifferentiated state of IAHCs.
2545 related Products with: Maintenance of hematopoietic stem and progenitor cells in fetal intra-aortic hematopoietic clusters by the Sox17-Notch1-Hes1 axis.Macrophage Colony Stimula Macrophage Colony Stimula anti CD34 Hematopoietic p anti CD38 Hematopoietic p anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi
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Networks that link cytoskeletal regulators and diaphragm proteins underpin filtration function in Drosophila nephrocytes.Insect nephrocytes provide a valuable model for kidney disease, as they are structurally and functionally homologous to mammalian kidney podocytes. They possess an exceptional macromolecular assembly, the nephrocyte diaphragm (ND), which serves as a filtration barrier and helps maintain tissue homeostasis by filtering out wastes and toxic products. However, the elements that maintain nephrocyte architecture and the ND are not understood. We show that Drosophila nephrocytes have a unique cytoplasmic cluster of F-actin, which is maintained by the microtubule cytoskeleton and Rho-GTPases. A balance of Rac1 and Cdc42 activity as well as proper microtubule organization and endoplasmic reticulum structure, are required to position the actin cluster. Further, ND proteins Sns and Duf also localize to this cluster and regulate organization of the actin and microtubule cytoskeleton. Perturbation of any of these inter-dependent components impairs nephrocyte ultrafiltration. Thus cytoskeletal components, Rho-GTPases and ND proteins work in concert to maintain the specialized nephrocyte architecture and function.
1538 related Products with: Networks that link cytoskeletal regulators and diaphragm proteins underpin filtration function in Drosophila nephrocytes.Native Influenza HA (A Br Native Influenza HA (A Br Native Influenza HA (A Br Native Influenza HA (A Ca Native Influenza HA (A Ca Native Influenza HA (A Ca Recombinant Influenza HA Recombinant Influenza HA Recombinant Influenza HA Native Influenza HA (B Fl Native Influenza HA (B Fl Native Influenza HA (B Fl
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Deregulation of Nrf2/ARE signaling pathway causes susceptibility of dystrophin-deficient myotubes to menadione-induced oxidative stress.Duchenne muscular dystrophy (DMD) is an X chromosome-linked disorder caused by a mutation in the dystrophin gene. Many previous studies reported that the skeletal muscles of DMD patients were more susceptible to oxidative stress than those of healthy people. However, not much has been known about the responsible mechanism of the differential susceptibility. In this study, we established dystrophin knock-down (DysKD) cell lines by transfection of dystrophin shRNA lentiviral particles into C2 cells and found that DysKD myotubes are more vulnerable to menadione-induced oxidative stress than control myotubes. We focused on the nuclear erythroid 2-related factor 2 (Nrf2) which is a transcription factor that regulates the expression of phase II antioxidant enzymes by binding to the antioxidant response element (ARE). Under menadione-induced oxidative stress, the translocation of Nrf2 to the nucleus is significantly decreased in the DysKD myotubes. In addition, the binding of Nrf2 to ARE site of Bcl-2 gene as well as protein expression of Bcl-2 is decreased compared to the control cells. Interestingly, sulforaphane increased Akt activation and Nrf2 translocation to the nucleus in the DysKD myotubes. These results suggest that the Nrf2 pathway might be the responsible pathway to the oxidative stress-induced muscle damage in DMD.
1926 related Products with: Deregulation of Nrf2/ARE signaling pathway causes susceptibility of dystrophin-deficient myotubes to menadione-induced oxidative stress.OXI TEK (Oxidative Stress Hh Signaling Pathway Anta AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF 8 Isoprostane oxidative s AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp ErbB Her Signaling Phosph ERK Signaling Phospho-Spe GPCR Signaling to MAPK ER IGF-1R Signaling Phospho- NF-kB II Phospho-Specific
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Downregulation of metabotropic glutamate receptor 5 inhibits hepatoma development in a neurotoxin rotenone-induced Parkinson's disease model.Clinical epidemiological studies have shown that there is a link between Parkinson's disease (PD) and cancer, but how PD regulates cancer development remains unknown. In our study, the effect of metabotropic glutamate receptor 5 (mGlu) on hepatoma was explored in a rotenone-induced PD model both in vitro and in vivo. We found that conditioned media derived from MN9D dopaminergic neuronal cells by rotenone-induced toxicity inhibited the growth, migration, invasion and promoted apoptosis of Hepa1-6 cells, which corresponded with decreased expression of mGlu. Furthermore, treatment with 2-methyl-6-(phenylethynyl)pyridine (MPEP), a mGluantagonist and knockdown of mGlu, further reduced ATP levels and migration distance, and increased cleavage of caspase-3 in Hepa1-6 cells. Additionally, we found that conditioned media derived from rotenone-treated MN9D dopaminergic neuronal cells enhanced reactive oxygen species (ROS) generation and JNK phosphorylation, which could be further increased by MPEP treatment, and attenuated by mGluagonist, (RS)-2-Chloro-5-hydroxyphenylglycine (CHPG) and ROS scavenger, N-acetyl-L-cysteine (NAC). The results indicated that down-regulation of mGlupromoted cell apoptosis through the intracellular ROS/JNK signaling pathway in a rotenone-induced cellular PD model. These findings were confirmed in vivo in a rotenone-induced rat model of PD combined with diethylnitrosamine (DEN)-induced hepatoma. Expression of Ki67 was decreased, and the levels of caspase-3 and p-JNK were increased in this model, which was accompanied by a decrease in protein expression of mGlu. The study suggest that negative regulation of mGlumay inhibit hepatoma development in a rotenone-induced PD model, and as such may help with our further understanding of the correlation between PD and cancer.
2834 related Products with: Downregulation of metabotropic glutamate receptor 5 inhibits hepatoma development in a neurotoxin rotenone-induced Parkinson's disease model.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Glutamate receptor 2 (Pre Interferon-a Receptor Typ Anti-HBeAg (HBeAb) test s Anti-HBcAg (HBcAb) test s HCV antibody test strip, H. Pylori antibody test s Glutamate receptor 2 (Pre Anti 3 DG imidazolone Mon Antibody to Parkinson Dis Nuclear Membrane Receptor
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