Search results for: Caspase 4, human recombinant
#28992627 2017/10/09 Save this To Up
H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.Apoptosis, fibrosis and NLRP3 inflammasome activation are involved in the development of diabetic cardiomyopathy (DCM). Human recombinant relaxin-3 (H3 relaxin) is a novel bioactive peptide that inhibits cardiac injury; however, whether H3 relaxin prevents cardiac injury in rats with DCM and the underlying mechanisms are unknown.
2504 related Products with: H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.Influenza A H3N2 Viral Ly Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Mouse Anti-Influenza-A HA Mouse Anti-Influenza-A He Mouse Anti-Influenza-A He Native Influenza A Virus Native Influenza A Virus Native Influenza A Virus Recombinant Influenza A V Recombinant Influenza A V
#28990932 2017/10/09 Save this To Up
Uromodulin p.Cys147Trp mutation drives kidney disease by activating ER stress and apoptosis.Uromodulin-associated kidney disease (UAKD) is caused by mutations in the uromodulin (UMOD) gene that result in a misfolded form of UMOD protein, which is normally secreted by nephrons. In UAKD patients, mutant UMOD is poorly secreted and accumulates in the ER of distal kidney epithelium, but its role in disease progression is largely unknown. Here, we modeled UMOD accumulation in mice by expressing the murine equivalent of the human UMOD p.Cys148Trp point mutation (UmodC147W/+ mice). Like affected humans, these UmodC147W/+ mice developed spontaneous and progressive kidney disease with organ failure over 24 weeks. Analysis of diseased kidneys and purified UMOD-producing cells revealed early activation of the PKR-like ER kinase/activating transcription factor 4 (PERK/ATF4) ER stress pathway, innate immune mediators, and increased apoptotic signaling, including caspase-3 activation. Unexpectedly, we also detected autophagy deficiency. Human cells expressing UMOD p.Cys147Trp recapitulated the findings in UmodC147W/+ mice, and autophagy activation with mTOR inhibitors stimulated the intracellular removal of aggregated mutant UMOD. Human cells producing mutant UMOD were susceptible to TNF-α- and TRAIL-mediated apoptosis due to increased expression of the ER stress mediator tribbles-3. Blocking TNF-α in vivo with the soluble recombinant fusion protein TNFR:Fc slowed disease progression in UmodC147W/+ mice by reducing active caspase-3, thereby preventing tubule cell death and loss of epithelial function. These findings reveal a targetable mechanism for disease processes involved in UAKD.
1481 related Products with: Uromodulin p.Cys147Trp mutation drives kidney disease by activating ER stress and apoptosis.Kidney disease spectrum ( ENZYMATIC ASSAY KITS (CH ENZYMATIC ASSAY KITS (CH ENZYMATIC ASSAY KITS (CH Breast disease spectrum t Kidney disease spectrum ( Apoptosis Protease Activa Apoptosis Protease Activa Apoptosis Protease Activa Apoptosis Protease Activa c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein
#28902369 2017/09/13 Save this To Up
Synergistic inhibitory effects on hepatocellular carcinoma with recombinant human adenovirus Aspp2 and oxaliplatin via p53-independent pathway in vitro and in vivo.The present study was designed to investigate the synergistic inhibitory effects on hepatocellular carcinoma with recombinant human adenovirus Aspp2 (Aspp2-ad) and oxaliplatin via p53-independent pathway in vitro and in vivo. After being treated with Aspp2-ad and/or oxaliplatin for 24-48 h, HepG2P53-/- and Hep3B cells showed a significant growth inhibition compared with vehicle control. Combination group showed a synergetic effect, the inhibitory rates were all above 80% at 48 h point in HepG2P53-/- and Hep3B cells. The apoptotic cell numbers of Aspp2-ad and/or oxaliplatin treatment groups were increased remarkably, especially for the combined therapy group in the liver cancer cells. The Hep3B xenograft experiment also showed similar inhibition of Aspp2-ad and/or oxaliplatin to the in vitro experiment. H&E results showed that combination group had the least mitotic indexes and the most necrosis. The immunohistochemistry results showed that PCNA, CD31 expression decreased greatly in treatment groups. These results suggested that Aspp2-ad might inhibit proliferation and vascular growth of hepatocarcinoma. Aspp2 induced apoptosis protein expression in Aspp2-ad and combination groups, the Aspp2, Bax and activation of caspase-3 expression increased greatly both in vitro and in vivo. But interestingly, the autophagy proteins showed different responses not only in HepG2P53-/- and Hep3B cells but also in vitro and in vivo. We found that Aspp2-ad downregulated the p-ERK, p-STAT3 expression, the synergistic effects were observed in combination group, while there was not response of mTOR to Aspp2-ad. In conclusion, Aspp2-ad, in P53-independent manner, regulated ERK and STAT3 signal moleculars to inhibit hepatocarcinoma in coordination with oxaliplatin by influencing the protein expression of proliferation, apoptosis, autophagy and vascular growth. Aspp2-ad has the potential to be developed in gene therapy for HCC, especially for P53 deletion or mutation in HCC.
1265 related Products with: Synergistic inhibitory effects on hepatocellular carcinoma with recombinant human adenovirus Aspp2 and oxaliplatin via p53-independent pathway in vitro and in vivo.Recombinant Human WNT Inh Recombinant Human WNT Inh Recombinant Human WNT Inh Inhibitory Mouse Monoclon Inhibitory Mouse Monoclon Human Migration Inhibitor Macrophage Colony Stimula Macrophage Colony Stimula anti H inh human blood an Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe
#28873083 2017/09/05 Save this To Up
SKLB188 inhibits the growth of head and neck squamous cell carcinoma by suppressing EGFR signalling.Overexpression of epidermal growth factor receptor (EGFR) occurs in approximately 90% of head and neck squamous cell carcinoma (HNSCC), and is correlated with poor prognosis. Thus, targeting EGFR is a promising strategy for treatment of HNSCC. Several small molecule EGFR inhibitors have been tested in clinical trials for treatment of HNSCC, but none of them are more effective than the current chemotherapeutic drugs. Thus, it is urgently needed to develop novel EGFR inhibitors for HNSCC treatment.
1204 related Products with: SKLB188 inhibits the growth of head and neck squamous cell carcinoma by suppressing EGFR signalling.Head and neck squamous ce Multiple head and neck sq Multiple organ squamous c Esophagus squamous cell c Esophagus squamous cell c Lung squamous cell carcin Skin malignant tumor tiss Esophagus squamous cell c Esophagus squamous cell c Esophagus squamous cell c Lung squamous cell carcin Lung squamous cell carcin
#28784797 2017/08/08 Save this To Up
Cytotoxic protein from the mushroom Coprinus comatus possesses a unique mode for glycan binding and specificity.Glycans possess significant chemical diversity; glycan binding proteins (GBPs) recognize specific glycans to translate their structures to functions in various physiological and pathological processes. Therefore, the discovery and characterization of novel GBPs and characterization of glycan-GBP interactions are significant to provide potential targets for therapeutic intervention of many diseases. Here, we report the biochemical, functional, and structural characterization of a 130-amino-acid protein, Y3, from the mushroom Coprinus comatus Biochemical studies of recombinant Y3 from a yeast expression system demonstrated the protein is a unique GBP. Additionally, we show that Y3 exhibits selective and potent cytotoxicity toward human T-cell leukemia Jurkat cells compared with a panel of cancer cell lines via inducing caspase-dependent apoptosis. Screening of a glycan array demonstrated GalNAcβ1-4(Fucα1-3)GlcNAc (LDNF) as a specific Y3-binding ligand. To provide a structural basis for function, the crystal structure was solved to a resolution of 1.2 Å, revealing a single-domain αβα-sandwich motif. Two monomers were dimerized to form a large 10-stranded, antiparallel β-sheet flanked by α-helices on each side, representing a unique oligomerization mode among GBPs. A large glycan binding pocket extends into the dimeric interface, and docking of LDNF identified key residues for glycan interactions. Disruption of residues predicted to be involved in LDNF/Y3 interactions resulted in the significant loss of binding to Jurkat T-cells and severely impaired their cytotoxicity. Collectively, these results demonstrate Y3 to be a GBP with selective cytotoxicity toward human T-cell leukemia cells and indicate its potential use in cancer diagnosis and treatment.
1045 related Products with: Cytotoxic protein from the mushroom Coprinus comatus possesses a unique mode for glycan binding and specificity.NATIVE HUMAN PROLACTIN, P Rabbit Anti-Rat Androgen NATIVE HUMAN PROLACTIN, P Acyl CoA binding Protein MOUSE ANTI BOVINE ROTAVIR Bone Morphogenetic Protei Mouse Anti-Human Retinol MOUSE ANTI BORRELIA BURGD S100 alpha - Rabbit polyc Human S100 Calcium Bindin ribosome binding protein ribosome binding protein
#28526746 2017/05/20 Save this To Up
Region-specific proteolysis differentially regulates type 1 inositol 1,4,5-trisphosphate receptor activity.The inositol 1,4,5 trisphosphate receptor (IP3R) is an intracellular Ca(2+) release channel expressed predominately on the membranes of the endoplasmic reticulum. IP3R1 can be cleaved by caspase or calpain into at least two receptor fragments. However, the functional consequences of receptor fragmentation are poorly understood. Our previous work has demonstrated that IP3R1 channels, formed following either enzymatic fragmentation or expression of the corresponding complementary polypeptide chains, retain tetrameric architecture and are still activated by IP3 binding despite the loss of peptide continuity. In this study, we demonstrate that region-specific receptor fragmentation modifies channel regulation. Specifically, the agonist-evoked temporal Ca(2+) release profile and protein kinase A modulation of Ca(2+) release are markedly altered. Moreover, we also demonstrate that activation of fragmented IP3R1 can result in a distinct functional outcome. Our work suggests that proteolysis of IP3R1 may represent a novel form of modulation of IP3R1 channel function and increases the repertoire of Ca(2+) signals achievable through this channel.
1042 related Products with: Region-specific proteolysis differentially regulates type 1 inositol 1,4,5-trisphosphate receptor activity.Primary antibody IL-1RAc Primary antibody IL-1RAc IGF-1R Signaling Phospho- T-Cell Receptor Signaling 10x ELISA WASH BUFFER, Pr 10X PHOSPHATE BUFFERED SA ELISA p55,p60,Pig,Sus scr Goat Anti-Human Bradykini Goat Anti-Human, Mouse Ca Goat Anti-Rat CCKA Recept Goat Anti- collagen type Goat Anti-Rat Collagen, t
#28463985 2017/05/02 Save this To Up
Palmitic acid is a toll-like receptor 4 ligand that induces human dendritic cell secretion of IL-1β.Palmitic acid (PA) and other saturated fatty acids are known to stimulate pro-inflammatory responses in human immune cells via Toll-like receptor 4 (TLR4). However, the molecular mechanism responsible for fatty acid stimulation of TLR4 remains unknown. Here, we demonstrate that PA functions as a ligand for TLR4 on human monocyte derived dendritic cells (MoDCs). Hydrophobicity protein modeling indicated PA can associate with the hydrophobic binding pocket of TLR4 adaptor protein MD-2. Isothermal titration calorimetry quantified heat absorption that occurred during PA titration into TLR4/MD2, indicating that PA binds to TLR4/MD2. Treatment of human MoDCs with PA resulted in endocytosis of TLR4, further supporting the function of PA as a TLR4 agonist. In addition, PA stimulated DC maturation and activation based on the upregulation of DC costimulatory factors CD86 and CD83. Further experiments showed that PA induced TLR4 dependent secretion of the pro-inflammatory cytokine IL-1β. Lastly, our experimental data show that PA stimulation of NF-κB canonical pathway activation is regulated by TLR4 signaling and that reactive oxygen species may be important in upregulating this pro-inflammatory response. Our experiments demonstrate for the first time that PA activation of TLR4 occurs in response to direct molecular interactions between PA and MD-2. In summary, our findings suggest a likely molecular mechanism for PA induction of pro-inflammatory immune responses in human dendritic cells expressing TLR4.
2489 related Products with: Palmitic acid is a toll-like receptor 4 ligand that induces human dendritic cell secretion of IL-1β.Rabbit Anti-Nociceptin re Rabbit Anti-Nociceptin re Rabbit Anti-Nociceptin re Rabbit Anti-Nociceptin re Rabbit Anti-VIP Receptor Rabbit Anti-IL-4I1 Polycl Rabbit Anti-IL-4I1 Polycl Monoclonal antibody: Hum Anti C Reactive Protein A Mouse Anti-Human Interleu RANK Ligand Soluble, Huma IL-12 Receptor beta2 anti
#28409545 2017/04/14 Save this To Up
High-affinity caspase-4 binding to LPS presented as high molecular mass aggregates or in outer membrane vesicles.Caspases of the non-canonical inflammasome (caspases -4, -5, and -11) directly bind endotoxin (LOS/LPS) and can be activated in the absence of any co-factors. Models of LPS-induced caspase activation have postulated that 1:1 binding of endotoxin monomers to caspase trigger caspase oligomerization and activation, analogous to that established for endotoxin-induced activation of MD-2/TLR4. However, using metabolically radiolabeled LOS and LPS, we now show high affinity and selective binding of caspase-4 to high molecular mass aggregates of purified endotoxin and to endotoxin-rich outer membrane vesicles without formation of 1:1 endotoxin:caspase complexes. Thus, our findings demonstrate markedly different endotoxin recognition properties of caspase-4 from that of MD-2/TLR4 and strongly suggest that activation of caspase-4 (and presumably caspase-5 and caspase-11) are mediated by interactions with activating endotoxin-rich membrane interfaces rather than by endotoxin monomers.
2611 related Products with: High-affinity caspase-4 binding to LPS presented as high molecular mass aggregates or in outer membrane vesicles.EnzyChrom™ Kinase Assay High density (495 cases 5 Cell Meter™ Annexin V B Cell Meter™ Fluorimetri Apoptosis (Human) Antibod Cytokine (Human) Antibody Cytokine (Human) Antibody Cytokine (Mouse) Antibody Growth Factor (Human) Ant Inflammation (Human) Anti Inflammation (Mouse) Anti High density multiple org
#28391633 2017/04/09 Save this To Up
Comparisons of cardioprotective efficacy between fibroblast growth factor 21 and dipeptidyl peptidase-4 inhibitor in prediabetic rats.Comparative efficacy between fibroblast growth factor 21 (FGF21) and vildagliptin on metabolic regulation, cardiac mitochondrial function, heart rate variability (HRV), and left ventricular (LV) function is not known. We hypothesized that FGF21 and vildagliptin share a similar efficacy in improving these parameters in high fat diet (HFD)-induced obese-insulin resistant rats.
2006 related Products with: Comparisons of cardioprotective efficacy between fibroblast growth factor 21 and dipeptidyl peptidase-4 inhibitor in prediabetic rats.Goat Anti-Human Fibroblas Human Fibroblast Growth F Growth Factor (Human) Ant Human, Fibroblast Growth Human, Fibroblast Growth Rabbit Polyclonal Antibod Sheep Polyclonal Antibody ELISA Human , Fibroblast Mouse, Fibroblast Growth Mouse, Fibroblast Growth Rabbit Polyclonal Antibod ELISA Mouse Rat , Fibrobl
#28216966 2017/02/20 Save this To Up
Suppression of colorectal tumorigenesis by recombinant Bacteroides fragilis enterotoxin-2 in vivo.To evaluate the impact of recombinant Bacteroides fragilis enterotoxin-2 (BFT-2, or Fragilysin) on colorectal tumorigenesis in mice induced by azoxymethane/dextran sulfate sodium (AOM/DSS).
1533 related Products with: Suppression of colorectal tumorigenesis by recombinant Bacteroides fragilis enterotoxin-2 in vivo.Recombinant Influenza HA Recombinant Influenza HA Recombinant Influenza HA Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interle Recombinant Ra Interleuki Recombinant Mouse Interle
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