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Attaching-and-Effacing Pathogens Exploit Junction Regulatory Activities of N-WASP and SNX9 to Disrupt the Intestinal Barrier.

Neural Wiskott-Aldrich Syndrome protein (N-WASP) is a key regulator of the actin cytoskeleton in epithelial tissues and is poised to mediate cytoskeletal-dependent aspects of apical junction complex (AJC) homeostasis. Attaching-and-effacing (AE) pathogens disrupt this homeostasis through translocation of the effector molecule early secreted antigenic target-6 (ESX)-1 secretion-associated protein F (EspF). Although the mechanisms underlying AJC disruption by EspF are unknown, EspF contains putative binding sites for N-WASP and the endocytic regulator sorting nexin 9 (SNX9). We hypothesized that N-WASP regulates AJC integrity and AE pathogens use EspF to induce junction disassembly through an N-WASP- and SNX9-dependent pathway.

1788 related Products with: Attaching-and-Effacing Pathogens Exploit Junction Regulatory Activities of N-WASP and SNX9 to Disrupt the Intestinal Barrier.

FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Topoisomerase II; Clone Topoisomerase II; Clone Topoisomerase II; Clone Toludine Blue Solution Toludine Blue Solution Toludine Blue Solution Toxoplasma gondii MIC 3 r Toxoplasma gondii P24 (GR

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Surface-Modification of RIPL Peptide-Conjugated Liposomes to Achieve Steric Stabilization and pH Sensitivity.

We have previously demonstrated that RIPL peptide-conjugated liposomes (RIPL-L) exhibited high hepsin (HPN) selectivity and enhanced intracellular drug delivery. In this study, surface modification of RIPL-L was performed to reduce plasma protein adsorption and off-target effects. For steric stabilization, distearoyl phosphatidylethanolamine (DSPE)-polyethylene glycol (PEG)2000 was used (5% molar ratio to total lipid) to prepare PEG-RIPL-L. Further, pH-sensitive oligopeptides [(HD)4 or (HE)4] were coupled to shield the RIPL polyarginine moiety, yielding (HD)4/PEG-RIPL-L and (HE)4/PEG-RIPL-L. All liposomal vesicles had a narrow and homogenous size distribution of approximately 140–150 nm, with zeta potentials varying from −15 to 36 mV. Increased plasma stability was observed upon quantifying the protein adsorbed onto liposomes by using a micro bicinchoninic acid assay. The (HD)4- and (HE)4-coupling capacity of PEG-RIPL-L was investigated by measuring the amount of oligopeptide involved in transient ionic complexation (TIC-oligopep) and zeta potential changes. As the molar ratio of (HD)4 and (HE)4 increased, TIC-oligopep increased and zeta potential decreased. (HE)4/PEG-RIPL-L were pH-sensitive, producing 1.6-fold greater cellular uptake of FITC-dextran by LNCaP cells at pH 6.8 than at pH 7.4. This result suggested that (HE)4/PEG-RIPL-L might provide a sterically stabilized, pH-sensitive drug carrier for HPN-specific cancer targeting.

2858 related Products with: Surface-Modification of RIPL Peptide-Conjugated Liposomes to Achieve Steric Stabilization and pH Sensitivity.

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Ursodeoxycholic acid protects against intestinal barrier breakdown by promoting enterocyte migration via EGFR- and COX-2-dependent mechanisms.

The intestinal barrier is often disrupted in disease states, and intestinal barrier failure leads to sepsis. Ursodeoxycholic acid (UDCA) is a bile acid that may protect the intestinal barrier. We hypothesized that UDCA would protect the intestinal epithelium in injury models. To test this hypothesis, we utilized an in vitro wound healing assay and a mouse model of intestinal barrier injury. We found that UDCA stimulates intestinal epithelial cell migration in vitro, and this migration was blocked by inhibition of COX-2, EGFR, or ERK. Furthermore, UDCA stimulated both COX-2 induction and EGFR phosphorylation. In vivo, UDCA protected the intestinal barrier from LPS-induced injury as measured by FITC dextran leakage into the serum. Using BrdU and EdU injections, we found that UDCA stimulated intestinal epithelial cell migration in these animals. These effects were blocked with either administration of Rofecoxib, a COX-2 inhibitor, or in EGFR dominant negative Velvet mice, where UDCA had no effect on LPS-induced injury. Finally, we found increased COX-2 and phosphorylated ERK levels in LPS animals also treated with UDCA. Taken together, these data suggest that UDCA can stimulate intestinal epithelial cell migration and protect against acute intestinal injury via an EGFR- and COX-2-dependent mechanism. UDCA may be an effective treatment to prevent the early onset of gut origin sepsis.

1633 related Products with: Ursodeoxycholic acid protects against intestinal barrier breakdown by promoting enterocyte migration via EGFR- and COX-2-dependent mechanisms.

BIBW-2992 (Afatinib) Mech BYL-719 Mechanisms: PI3K- AZD-3514 Mechanisms: Andr Dacomitinib (PF-00299804) Androst-4-ene-3,17-dion-1 Rat intestinal fatty acid Ursodeoxycholic acid CAS PSAP (Prostate Specific PSAP (Prostate Specific Cytokeratin AE1 (Acidic) Cytokeratin AE1 (Acidic) Glial Fibrillary Acidic

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Hexadecylated linear PEI self-assembled nanostructures as efficient vectors for neuronal gene delivery.

Development of efficient and safe nucleic acid carriers is one of the most challenging requirements to improve the success of gene therapy. Here, we synthesized a linker, 3-(hexadecyloxy)-1-chloropropan-2-ol, and grafted it onto linear polyethylenimine in varying amounts to obtain a series of HD-lPEI polymers that were able to form self-assembled nanoparticles (SN). H-NMR spectrometry was used to determine the extent of grafting of the linker, HD, on to the lPEI backbone. We further complexed the SN of HD-lPEI with plasmid DNA (pDNA) and the resultant nanoplexes were characterized by their size and zeta potential and further evaluated for their transfection ability and cytotoxicity in MCF-7 cells. In the series, the SN of HD-lPEI-3 (ca. 15% substitution) showed the highest transfection efficiency (~ 91%) with non-significant cytotoxicity in comparison to the commercial transfection reagents. The in vitro gene knockdown study displayed ~ 80% suppression of GFP gene expression by SN of HD-lPEI-3/pDNA/siRNA complex, whereas Lipofectamine™/pDNA/siRNA complex could suppress the expression by only ~ 48%. The enhanced expression of luciferase gene using SN of HD-lPEI-3 in different vital organs of Balb/c mice also demonstrated the potential of the projected formulation for gene delivery. The encouraging results of SN of HD-lPEI-3 polymer for delivery of nucleic acids in vitro and in vivo paved the way to evaluate the potential of the same for neuronal siRNA delivery. The safe and efficient stereotaxic delivery of FITC-labeled siRNA against α-synuclein gene also confirms the potential applicability of HD-lEPI-3 SN as a vector for neuronal delivery.

1910 related Products with: Hexadecylated linear PEI self-assembled nanostructures as efficient vectors for neuronal gene delivery.

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Prolonged phonation impairs the integrity and barrier function of porcine vocal fold epithelium: a preliminary study.

Voice abuse is known to be a common risk factor of voice disorders and prolonged; high-intensity phonation has been shown to damage the vocal fold epithelium. We aim to evaluate the effects of phonation on the integrity and barrier function of vocal fold epithelium using a porcine laryngeal model.

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Active Porcine PAI-1 Func Active porcine tPA functi ACTH (1 24) (Human, Rat, ELMGPI Mouse IgG anti por Mouse anti-porcine type I Mouse anti-porcine type I ELRGPI Rat IgG anti porci Rat anti-porcine type I c Rat anti-porcine type I c ELHGPI Human Monkey IgG a Human monkey anti-porcine Human monkey anti-porcine

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Cinobufagin Induces Apoptosis in Osteosarcoma Cells Via the Mitochondria-Mediated Apoptotic Pathway.

Osteosarcoma is a common primary malignant bone tumor that mainly occurs in childhood and adolescence. Despite developments in the diagnosis and treatment of osteosarcoma, the prognosis is still very poor. Cinobufagin is an active component in the anti-tumor Chinese medicine called "Chan Su", and we previously revealed that cinobufagin induced apoptosis and reduced the viability of osteosarcoma cells; however, the underlying mechanism remains to be elucidated. Herein, the present study was undertaken to illuminate the molecular mechanism of cinobufagin-induced apoptosis of osteosarcoma cell.

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Apoptosis antibody array Cancer Apoptosis Phospho- anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Macrophage Colony Stimula Macrophage Colony Stimula anti H inh human blood an GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep

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Bubbles Induce Endothelial Microparticle Formation via a Calcium-Dependent Pathway Involving Flippase Inactivation and Rho Kinase Activation.

Intravascular bubbles can exert pleiotropic detrimental effects, partly by inducing endothelial microparticles (EMPs) production, which play critical roles in cell communication and vascular inflammation cascades. However, the underlying mechanisms remain unclear. This study aimed to delineate the possible mechanisms involving bubble-induced EMPs formation.

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anti RhoD human antigen I voltage-dependent calcium Rho Kinase Alpha Antibody Endothelial Tube Formatio Anti-CACNA1b(Voltage-depe Anti CACNA1b(Voltage depe Anti-AICDA(Activation-ind Anti AICDA(Activation ind Primary Antibody Dropper HCV core recombinant anti HCV NS4 recombinant antig Recombinant Viral Antige

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The mechanism of lauric acid-modified protein nanocapsules escape from intercellular trafficking vesicles and its implication for drug delivery.

Protein nanocapsules have exhibited promising potential applications in the field of protein drug delivery. A major issue with various promising nano-sized biotherapeutics including protein nanocapsules is that owing to their particle size they are subject to cellular uptake via endocytosis, and become entrapped and then degraded within endolysosomes, which can significantly impair their therapeutic efficacy. In addition, many nano-sized biotherapeutics could be also sequestered by autophagosomes and degraded through the autolysosomal pathway. Thus, a limiting step in achieving an effective protein therapy is to facilitate the endosomal escape and auto-lysosomal escape to ensure cytosolic delivery of the protein drugs. Here, we prepared a protein nanocapsule based on BSA (nBSA) and the BSA nanocapsules modified with a bilayer of lauric acid (LA-nBSA) to investigate the escape effects from the endosome and autophagosome. The size distribution of nBSA and LA-nBSA analyzed using DLS presents a uniform diameter centered at 10 nm and 16 nm. The data also showed that FITC-labeled nBSA and LA-nBSA were taken up by the cells mainly through Arf-6-dependent endocytosis and Rab34-mediated macropinocytosis. In addition, LA-nBSA could efficiently escape from endosomal before the degradation in endo-lysosomes. Autophagy could also sequester the LA-nBSA through p62 autophagosome vesicles. These two types of nanocapsules underwent different intracellular destinies and lauric acid (LA) coating played a vital role in intracellular particle retention. In conclusion, the protein nanocapsules modified with LA could enhance the protein nanocapsules escape from intercellular trafficking vesicles, and protect the protein from degradation by the lysosomes.

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Bone Morphogenetic Protei Recombinant Human PKC the Recombinant Human PKC the Recombinant Human PKC the Protein A (Liquid form) Protein A (Liquid form) Protein A (Liquid form) Protein A (Liquid form) NATIVE HUMAN PROLACTIN, P AZD-3514 Mechanisms: Andr (5Z)-7-[(5-Acetyloxy-2-fo (5Z)-7-[(5-Acetyloxy-2-fo

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A first-in-class inhibitor, MLN4924 (pevonedistat), induces cell-cycle arrest, senescence, and apoptosis in human renal cell carcinoma by suppressing UBE2M-dependent neddylation modification.

MLN4924 is a second-generation inhibitor that targets ubiquitin-proteasome system by inhibiting neddylation activation enzyme (NAE), and subsequently blocking the neddylation-dependent activation of Cullin-RING E3 ligases (CRLs), which leads to the accumulation of CRLs substrates and hence, suppressing diverse tumor development. In this study, we investigated the potential application of this first-in-class inhibitor MLN4924 in the treatment of human renal cell carcinoma both in vitro and in vivo.

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cell cycle progression 2 Cell cycle antibody array Cell Cycle Control Phosph Cell Cycle Phospho-Specif Lung squamous cell carcin Kidney clear cell carcino Kidney clear cell carcino Rabbit Anti-Cell death in Rabbit Anti-Cell death in Cervix squamous cell carc Human Squamous Cell Carci Human squamous cell carci

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[Expression of MiR-296-5p in Diffuse Large B-Cell Lymphoma and Its Influence on Biological Behavior of Tumor Cells].

To detect the expression of miRNA-296-5p in diffuse large B cell lymphoma (DLBCL) cells and study the proliferation, migration and apoptosis of DLBCL cells after interfering the expression of miRNA-296-5p.

2481 related Products with: [Expression of MiR-296-5p in Diffuse Large B-Cell Lymphoma and Its Influence on Biological Behavior of Tumor Cells].

Macrophage Colony Stimula Macrophage Colony Stimula Human Large Intestine Mic Diffuse large B cell lymp Diffuse large-B cell lymp Diffuse large B cell lymp Diffuse large B-cell lymp 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

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