Search results for: Recombinant Human TNF-alpha [+His] Proteins
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Clusterin Reduces Cold Ischemia-Reperfusion Injury in Heart Transplantation Through Regulation of NF-kB Signaling and Bax/Bcl-xL Expression.Ischemia-reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation and is a key factor in graft failure and the long-term survival rate of recipients. Therefore, there is an urgent need for the development of new therapies to prevent I/R injury. Clusterin is a hetero-dimeric glycoprotein with an antiapoptotic function. In this study, we investigated whether clusterin was cardioprotective in heart transplantation against I/R injury using an in vivo rat model and an in vitro cell culture system, and examined the underlying mechanisms of I/R injury.
2828 related Products with: Clusterin Reduces Cold Ischemia-Reperfusion Injury in Heart Transplantation Through Regulation of NF-kB Signaling and Bax/Bcl-xL Expression.NF-kB II Phospho-Specific DNA (cytosine 5) methyltr NF-kB Phospho-Specific Ar GLP 2 ELISA Kit, Rat Prog Anti beta3 AR Human, Poly ABT-263 Mechanisms: Bcl-2 ABT-737 Mechanisms: Bcl-2 XL-147 Mechanisms: PI3K i XL-765 (SAR-245409) Mecha XL-184 (Cabozantinib) Mec GDC-0973 (XL-518) Mechani ABT-199 Mechanisms: Bcl-2
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A Novel Choroidal Endothelial Cell Line Has a Decreased Affinity for the Age-Related Macular Degeneration-Associated Complement Factor H Variant 402H.Choroidal endothelial cells play a central role in the pathogenesis of age-related macular degeneration (AMD). Protocols for isolating primary choroidal endothelial cells have been described but require access to human donor eyes, which is a limiting factor. Therefore, a conditionally immortalized choroidal endothelial cell (ciChEnC) line has been established.
2669 related Products with: A Novel Choroidal Endothelial Cell Line Has a Decreased Affinity for the Age-Related Macular Degeneration-Associated Complement Factor H Variant 402H.Epidermal Growth Factor ( Epidermal Growth Factor ( anti SLAM anti CDw150 IgG Growth Differentiation Fa Human Stromal Cell-Derive Sheep Anti-Human Compleme RABBIT ANTI HUMAN SDF-1 A RANK Ligand Soluble, Huma Complement factor H antib platelet factor 4 variant thymic dendritic cell-der AP-1 Reporter – HEK293
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Contrasting Function of Structured N-Terminal and Unstructured C-Terminal Segments ofPPE37 Protein.Pathogens frequently employ eukaryotic linear motif (ELM)-rich intrinsically disordered proteins (IDPs) to perturb and hijack host cell networks for a productive infection.has a relatively high percentage of IDPs in its proteome, the significance of which is not known. The-specific PE-PPE protein family has several members with unusually high levels of structural disorder and disorder-promoting Ala/Gly residues. PPE37 protein, a member of this family, carries an N-terminal PPE domain capable of iron binding, two transmembrane domains, and a disordered C-terminal segment harboring ELMs and a eukaryotic nuclear localization signal (NLS). PPE37, expressed as a function of low iron stress, was cleaved byprotease into N- and C-terminal segments. A recombinant N-terminal segment (P37N) caused proliferation and differentiation of monocytic THP-1 cells, into CD11c, DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin)-positive semimature dendritic cells exhibiting high interleukin-10 (IL-10) but negligible IL-12 and also low tumor necrosis factor alpha (TNF-α) secretion-an environment suitable for maintaining tolerogenic immune cells. The C-terminal segment entered the macrophage nucleus and induced caspase-3-dependent apoptosis of host cells. Mice immunized with recombinant PPE37FL and PPE37N evoked strong anti-inflammatory response, validating theimmunostimulatory effect. Analysis of the IgG response of PPE37FL and PPE37N revealed significant immunoreactivities in different categories of TB patients,pulmonary TB (PTB) and extrapulmonary TB (EPTB), vis-a-vis healthy controls. These results support the role of IDPs in performing contrasting activities to modulate the host processes, possibly through molecular mimicry and cross talk in two spatially distinct host environments which may likely aidsurvival and pathogenesis.To hijack the human host cell machinery to enable survival inside macrophages, the pathogenrequires a repertoire of proteins that can mimic host protein function and modulate host cell machinery. Here, we have shown how a single protein can play multiple functions and hijack the host cell for the benefit of the pathogen. Full-length membrane-anchored PPE37 protein is cleaved into N- and C-terminal domains under iron-depleted conditions. The N-terminal domain facilitates the propathogen semimature tolerogenic state of dendritic cells, whereas the C-terminal segment is localized into host cell nucleus and induces apoptosis. The immune implications of theseobservations were assessed and validated in mice and also human TB patients. This study presents novel mechanistic insight adopted byto survive inside host cells.
2635 related Products with: Contrasting Function of Structured N-Terminal and Unstructured C-Terminal Segments ofPPE37 Protein.Anti-PCOLE-1 (Procollagen Anti PCOLE 1 (Procollagen Anti-Amyloid Precursor Pr Anti Amyloid Precursor Pr Anti-Amyloid Precursor Pr Anti Amyloid Precursor Pr Anti-Bone Morphogenetic P Anti Bone Morphogenetic P Anti-Bone Morphogenetic P Anti Bone Morphogenetic P Amyloid Precursor Protein Amyloid Precursor Protein
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Generation and characterization of a novel candidate gene therapy and vaccination vector based on human species D adenovirus type 56.The vectorization of rare human adenovirus (HAdV) types will widen our knowledge of this family and their interaction with cells, tissues and organs. In this study we focus on HAdV-56, a member of human Ad species D, and create ease-of-use cloning systems to generate recombinant HAdV-56 vectors carrying foreign genes. We present in vitro transduction profiles for HAdV-56 in direct comparison to the most commonly used HAdV-5-based vector. In vivo characterizations demonstrate that when it is delivered intravenously (i.v.) HAdV-56 mainly targets the spleen and, to a lesser extent, the lungs, whilst largely bypassing liver transduction in mice. HAdV-56 triggered robust inflammatory and cellular immune responses, with higher induction of IFNγ, TNFα, IL5, IL6, IP10, MCP1 and MIG1 compared to HAdV-5 following i.v. administration. We also investigated its potential as a vaccine vector candidate by performing prime immunizations in mice with HAdV-56 encoding luciferase (HAdV-56-Luc). Direct comparisons were made to HAdV-26, a highly potent human vaccine vector currently in phase II clinical trials. HAdV-56-Luc induced luciferase 'antigen'-specific IFNγ-producing cells and anti-HAdV-56 neutralizing antibodies in Balb/c mice, demonstrating a near identical profile to that of HAdV-26. Taken together, the data presented provides further insight into human Ad receptor/co-receptor usage, and the first report on HAdV-56 vectors and their potential for gene therapy and vaccine applications.
2490 related Products with: Generation and characterization of a novel candidate gene therapy and vaccination vector based on human species D adenovirus type 56.fibronectin type III and Bovine Androstenedione,AS Androgen Receptor (Phosph Androgen Receptor (Phosph Interferon-a Receptor Typ Histone H3 (Di-Methyl-Lys Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 DLK1 Antibody Source Rabb CD209 (DC-SIGN) Antibody Doublecortin Antibody Sou
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Recombinant human GLP-1(rhGLP-1) alleviating renal tubulointestitial injury in diabetic STZ-induced rats.GLP-1-based treatment improves glycemia through stimulation of insulin secretion and inhibition of glucagon secretion. Recently, more and more findings showed that GLP-1 could also protect kidney from diabetic nephropathy. Most of these studies focused on glomeruli, but the effect of GLP-1 on tubulointerstitial and tubule is not clear yet. In this study, we examined the renoprotective effect of recombinant human GLP-1 (rhGLP-1), and investigated the influence of GLP-1 on inflammation and tubulointerstitial injury using diabetic nephropathy rats model of STZ-induced. The results showed that rhGLP-1 reduced urinary albumin without influencing the body weight and food intake. rhGLP-1 could increased the serum C-peptide slightly but not lower fasting blood glucose significantly. In diabetic nephropathy rats, beside glomerular sclerosis, tubulointerstitial fibrosis was very serious. These lesions could be alleviated by rhGLP-1. rhGLP-1 decreased the expression of profibrotic factors collagen I, α-SMA, fibronectin, and inflammation factors MCP-1 and TNFα in tubular tissue and human proximal tubular cells (HK-2 cells). Furthermore, rhGLP-1 significantly inhibited the phosphorylation of NF-κB, MAPK in both diabetic tubular tissue and HK-2 cells. The inhibition of the expression of TNFα, MCP-1, collagen I and α-SMA in HK-2 cells by GLP-1 could be mimicked by blocking NF-κB or MAPK. These results indicate that rhGLP-1 exhibit renoprotective effect by alleviation of tubulointerstitial injury via inhibiting phosphorylation of MAPK and NF-κB. Therefore, rhGLP-1 may be a potential drug for treatment of diabetic nephropathy.
2168 related Products with: Recombinant human GLP-1(rhGLP-1) alleviating renal tubulointestitial injury in diabetic STZ-induced rats.Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Human Epstein-Barr Virus Macrophage Colony Stimula Macrophage Colony Stimula TGF beta induced factor 2 Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe
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In vitro modeling of HIV proviral activity in microglia.Microglia, the resident macrophages of the brain, play a key role in the pathogenesis of HIV-associated neurocognitive disorders (HAND) due to their productive infection by HIV. This results in the release of neurotoxic viral proteins and pro-inflammatory compounds which negatively affect the functionality of surrounding neurons. Because models of HIV infection within the brain are limited, we aimed to create a novel microglia cell line with an integrated HIV provirus capable of recreating several hallmarks of HIV infection. We utilized clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing technology and integrated a modified HIV provirus into CHME-5 immortalized microglia to create HIV-NanoLuc CHME-5. In the modified provirus, the Gag-Pol region is replaced with the coding region for NanoLuciferase (NanoLuc), which allows for the rapid assay of HIV long terminal repeat activity using a luminescent substrate, while still containing the necessary genetic material to produce established neurotoxic viral proteins (e.g. tat, nef, gp120). We confirmed that HIV-NanoLuc CHME-5 microglia express NanoLuc, along with the HIV viral protein Nef. We subsequently exposed these cells to a battery of experiments to modulate the activity of the provirus. Proviral activity was enhanced by treating the cells with pro-inflammatory factors lipopolysaccharide (LPS) and tumor necrosis factor alpha and by overexpressing the viral regulatory protein Tat. Conversely, genetic modification of the toll-like receptor-4 gene by CRISPR/Cas9 reduced LPS-mediated proviral activation, and pharmacological application of NF-κB inhibitor sulfasalazine similarly diminished proviral activity. Overall, these data suggest that HIV-NanoLuc CHME-5 may be a useful tool in the study of HIV-mediated neuropathology and proviral regulation.
Resorufin Oleate, Fluorog HIV 1 intergase antigen. HIV1 integrase antibody, HIV Self Test Kit, 1Test HIV I&II test strip, Infe Recombinant HIV-1 pol Int Recombinant HIV-1 pol Int Recombinant HIV-1 pol Int Recombinant HIV-1 p31 Int Recombinant HIV-1 p31 Int Recombinant HIV-1 p31 Int Cell Meter™ Fluorimetri
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A novel engineered interchain disulfide bond in the constant region enhances the thermostability of adalimumab Fab.We constructed a system for expressing the Fab of the therapeutic human monoclonal antibody adalimumab at a yield of 20 mg/L in the methylotrophic yeast Pichia pastoris. To examine the contribution of interchain disulfide bonds to conformational stability, we prepared adalimumab Fab from which the interchain disulfide bond at the C-terminal region at both the CHand CL domains was deleted by substitution of Cys with Ala (Fab). DSC measurements showed that the Tm values of Fabwere approximately 5 °C lower than those of wild-type Fab, suggesting that the interchain disulfide bond contributes to conformational thermostability. Using computer simulations, we designed a novel interchain disulfide bond outside the C-terminal region to increase the stability of Fab. The resulting Fab (mutSS Fab) had the mutations H:V177C and L:Q160C in Fab, confirming the formation of the disulfide bond between CHand CL. The thermostability of mutSS Fabwas approximately 5 °C higher than that of Fab. Therefore, the introduction of the designed interchain disulfide bond enhanced the thermostability of Faband mitigated the destabilization caused by partial reduction of the interchain disulfide bond at the C-terminal region, which occurs in site-specific modification such as PEGylation.
1961 related Products with: A novel engineered interchain disulfide bond in the constant region enhances the thermostability of adalimumab Fab.Thermal Shaker with cooli FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Multiple organ tumor tiss HIV 1 intergase antigen. Goat Anti- TRPM8, (intern Goat Anti- TFAP2D, (inter Goat Anti- T1R3, (interna
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Purification of target proteins from intracellular inclusions mediated by intein cleavable polyhydroxyalkanoate synthase fusions.Recombinant protein production and purification from Escherichia coli is often accompanied with expensive and complicated procedures, especially for therapeutic proteins. Here it was demonstrated that, by using an intein cleavable polyhydroxyalkanoate synthase fusion, recombinant proteins can be first produced and sequestered on a natural resin, the polyhydroxyalkanoate (PHA) inclusions, then separated from contaminating host proteins via simple PHA bead isolation steps, and finally purified by specific release into the soluble fraction induced by a pH reduction.
2201 related Products with: Purification of target proteins from intracellular inclusions mediated by intein cleavable polyhydroxyalkanoate synthase fusions.Octyl â D 1 thioglucopyr Acyl CoA Synthase NDFIP1 (siRNA target site mFGF 21 (siRNA target sit LacZ (siRNA target site) MOUSE ANTI BOVINE ROTAVIR Amplite™ Intracellular Mouse Anti-RSV 33kDa & 19 MOUSE ANTI BORRELIA BURGD Proteins: Mouse CD40 Lig Proteins: Mouse CD40 Lig Proteins: Mouse Activin-
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MicroRNA-155 induction via TNF-α and IFN-γ suppresses expression of programmed death ligand-1 (PD-L1) in human primary cells.Programmed death ligand-1 (PD-L1) is a critical regulator of T cell function contributing to peripheral immune tolerance. Although it has been shown that posttranscriptional regulatory mechanisms control PD-L1 expression in cancer, it remains unknown whether such regulatory loops operate also in non-transformed cells. Here we studied PD-L1 expression in human dermal lymphatic endothelial cells (HDLECs), which play key roles in immunity and cancer. Treatment of HDLECs with the pro-inflammatory cytokines IFN-γ and TNF-α synergistically up-regulated PD-L1 expression. IFN-γ and TNF-α also affected expression of several microRNAs (miRNAs) that have the potential to suppress PD-L1 expression. The most highly up-regulated miRNA following IFN-γ and TNF-α treatment in HDLECs was miR-155, which has a central role in the immune system and cancer. Induction of miR-155 was driven by TNF-α, the effect of which was significantly enhanced by IFN-γ. The PD-L1 3'-UTR contains two functional miR-155-binding sites. Endogenous miR-155 controlled the kinetics and maximal levels of PD-L1 induction upon IFN-γ and TNF-α treatments. We obtained similar findings in dermal fibroblasts, demonstrating that the IFN-γ/TNF-α/miR-155/PD-L1 pathway is not restricted to HDLECs. These results reveal miR-155 as a critical component of an inflammation-induced regulatory loop controlling PD-L1 expression in primary cells.
2173 related Products with: MicroRNA-155 induction via TNF-α and IFN-γ suppresses expression of programmed death ligand-1 (PD-L1) in human primary cells.Anti AGO2 Human, Monoclon Macrophage Colony Stimula anti H inh human blood an RANK Ligand Soluble, Huma anti CD7 All T cells Reco anti Transferrin receptor Rabbit Anti-Cell death in Rabbit Anti-Cell death in Goat Anti-Human CD274 PD- Recombinant Human Flt3-Li Recombinant Human IFN-γ Anti C Reactive Protein A
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In vitro studies on the role of recombinant human soluble thrombomodulin in the context of retinoic acid mediated APL differentiation syndrome.Recombinant human soluble thrombomodulin (rTM) is a newly developed anti-coagulant approved for treatment of disseminated intravascular coagulation (DIC) in Japan. rTM exerts anti-inflammatory and cytoprotective functions via its lectin-like and epidermal growth factor-like domains, respectively. In this study, we retrospectively reviewed the treatment of 21 consecutive patients with coagulopathy, complicated by acute promyelocytic leukemia (APL), with all-trans retinoic acid (ATRA) with or without combination with rTM. Surprisingly, none of the 14 rTM-treated patients developed retinoic acid (RA)-related differentiation syndrome (DS). The co-culture of vascular endothelial cell-derived EA.hy926 and APL-derived NB4 cells in the presence of RA increased production of tumor necrosis factor alpha (TNF-α) in culture media, in parallel with activation of p38 mitogen-activated protein kinase and increased levels of intracellular adhesion molecule 1 (ICAM1) in EA.hy926 cells. This was also associated with increased levels of the phosphorylated forms of VE-cadherin and enhanced vascular permeability of EA.hy926 monolayers. Importantly, addition of rTM to this co-culture system inhibited the RA-induced phosphorylation of p38 and VE-cadherin and decreased ICAM1 and vascular permeability in EA.hy926 cells, without a decrease inthe levels of TNF-α. Taken together, use of rTM may be a promising treatment strategy to prevent DS in APL patients who receive ATRA.
1373 related Products with: In vitro studies on the role of recombinant human soluble thrombomodulin in the context of retinoic acid mediated APL differentiation syndrome.Macrophage Colony Stimula Macrophage Colony Stimula Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle
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