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           Search results for: MOUSE ANTI HUMAN EPITHELIAL MEMBRANE ANTIGEN-MONOCLONAL ANTIBODY   

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#28910443   2017/09/14 Save this To Up

Spatiotemporally Controlled Ablation of Klf5 Results in Dysregulated Epithelial Homeostasis in Adult Mouse Corneas.

Corneal epithelial (CE) homeostasis requires coordination between proliferation and differentiation. Here we examine the role of cell proliferation regulator Krüppel-like factor 5 (Klf5) in adult mouse CE homeostasis.

2569 related Products with: Spatiotemporally Controlled Ablation of Klf5 Results in Dysregulated Epithelial Homeostasis in Adult Mouse Corneas.

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#28668253   2017/07/02 Save this To Up

Expression and secretion of the Giardia duodenalis variant surface protein 9B10A by transfected trophozoites causes damage to epithelial cell monolayers mediated by protease activity.

Giardia duodenalis is the protozoan parasite responsible for most cases of parasitic diarrhea worldwide. The pathogenic mechanisms of giardiasis have not yet been fully characterized. In this context parasite's excretory/secretory products have been related to the damage induced by the parasite on enterocytes. Among these is the Variable Surface Proteins (VSPs) family involved in antigenic variation and in the induction of protective response. In proteomic analyses carried out to identify the proteases with high molecular weight secreted by Giardia trophozoites during the initial phase of interaction with IEC-6 cell monolayers we identified the VSP9B10A protein. In silico bioinformatics analyses predicted a central region in residues 324-684 displaying the catalytic triad and the substrate binding pocket of cysteine proteases. The analysis of the effect of the VSP9B10A protein on epithelial cell monolayers using trophozoites that were transfected with a plasmid carrying the vsp9b10a gene sequence under the control of a constitutive promoter showed that transfected trophozoites expressing the VSP9B10A protein caused cytotoxic damages on IEC-6 and MDCK cell monolayers. This was characterized by loss of cell-cell contacts and cell detachment from the substrate while no damage was observed with trophozoites that did not express the VSP9B10A protein. The same cytotoxic effect was detected when IEC-6 cell monolayers were incubated only with supernatants from co-cultures of IEC-6 cell monolayers with VSP9B10A transfected trophozoites and this effect was not observed when transfected trophozoites were incubated with a monospecific polyclonal antibody anti-VSP9B10A previous to interaction with IEC-6 monolayers. These results demonstrate that the VSP9B10A protein secreted upon interaction with epithelial cells caused damage in these cells. Thus this protein might be considered as a conditional virulence factor candidate. To our knowledge this is the first report on the proteolytic activity from a Giardia VSP opening new research lines on these proteins.

2822 related Products with: Expression and secretion of the Giardia duodenalis variant surface protein 9B10A by transfected trophozoites causes damage to epithelial cell monolayers mediated by protease activity.

Fluorescein 5 thiosemicar Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri AccuRapid™ Cell Free Pr MarkerGene™ â Galactos Anti C Reactive Protein A Amplite™ Universal Fluo Amplite™ Universal Fluo MOUSE ANTI BORRELIA BURGD cell cycle progression 2 TOM1-like protein 2 antib Cell Meter™ Caspase 3 7

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#28552668   2017/05/29 Save this To Up

β1-Integrin Accumulates in Cystic Fibrosis Luminal Airway Epithelial Membranes and Decreases Sphingosine, Promoting Bacterial Infections.

Chronic pulmonary colonization with bacterial pathogens, particularly Pseudomonas aeruginosa, is the primary cause of morbidity and mortality in patients with cystic fibrosis (CF). We observed that β1-integrins accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with CF. β1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap β1-integrins on the luminal pole of bronchial epithelial cells. β1-integrins downregulate acid ceramidase expression, resulting in further accumulation of ceramide and consequent reduction of surface sphingosine, a lipid that kills bacteria. Interrupting this vicious cycle by triggering surface β1-integrin internalization via anti-β1-integrin antibodies or the RGD peptide ligand-or by genetic or pharmacological correction of ceramide levels-normalizes β1-integrin distribution and sphingosine levels in CF epithelial cells and prevents P. aeruginosa infection in CF mice. These findings suggest a therapeutic avenue to ameliorate CF-associated bacterial infections.

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Integrin β1 (CD29) Antib Integrin â3 (Phospho Tyr Integrin â3 (Phospho Tyr Integrin â3 (Ab 773) Ant Integrin â3 (Ab 785) Ant LPAM-1(Integrin α4, CD49 Integrin alphaX antibody CD41 Integrin alpha 2b an Integrin alpha6 antibody Human integrin aVb3, affi Angiogenesis (Human) Anti Angiogenesis (Human) Anti

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#28476558   2017/05/06 Save this To Up

Low expression of complement inhibitory protein CD59 contributes to humoral autoimmunity against astrocytes.

Neuromyelitis optica spectrum disorder is primarily an anti-aquaporin 4 autoantibody-mediated, central nervous system-restricted channelopathy. Patients frequently develop central nervous system-restricted lesions even though autoantigen aquaporin 4 in neuromyelitis optica spectrum disorder is broadly distributed in the central nervous system and peripheral organs. The cause of such tissue-specific immune response remains largely unknown. We confirmed here that CD59, an inhibitory regulator of the complement membrane attack complex, is expressed and co-localized with aquaporin 4 in peripheral organs but is only minimally expressed in astrocytes in the central nervous system. In addition, we further found that CD59 overexpression in mouse brains decreased demyelination, blocked the loss of astrocytes and aquaporin 4, and inhibited membrane attack complex formation and infiltration of inflammatory cells. Inactivation of CD59 in mouse peripheral aquaporin 4-expressing cells and tissues led to complement-dependent cytotoxicity. In accordance with the mouse data, human samples presented higher expression of CD59 in many aquaporin 4-expressing peripheral tissues but not in astrocytes. Silencing or blocking CD59 in aquaporin 4-expressing human tracheal epithelial and skeletal muscle cells induced membrane attack complex formation and cytotoxicity, which suggests a protective role of CD59 in anti-aquaporin 4 antibodies-mediated complement toxicity. Our findings suggest that low CD59 expression in astrocytes may contribute to central nervous system-restricted lesions in neuromyelitis optica spectrum disorder. Restoring CD59 expression in astrocytes may serve as a novel therapeutic target of neuromyelitis optica spectrum disorder.

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#28456612   2017/04/30 Save this To Up

Experimental Laminin 332 Mucous Membrane Pemphigoid Critically Involves C5aR1 and Reflects Clinical and Immunopathological Characteristics of the Human Disease.

Mucous membrane pemphigoid is an autoantibody-mediated disease predominantly affecting the oral cavity, pharynx, and conjunctiva. Conjunctival lesions may lead to impaired vision and, finally, blindness. About 25% of mucous membrane pemphigoid patients generate autoantibodies against the α3 chain of laminin 332 (LAMα3), a structural protein of epidermal/epithelial basement membranes. Here, we established a mouse model by the passive transfer of rabbit IgG against the murine homologs of two immunodominant fragments in adult C57BL/6 mice (mLAMα3). After repeated subcutaneous injections of anti-mLAMα3 IgG erosions and crusts occurred predominantly around the snout, eyes, and on ears. Conjunctival and oral/pharyngeal lesions with subepithelial splitting were found in 80% and 100% of mice, respectively. In contrast, disease development was abrogated in FcRγ chain-deficient mice and markedly reduced in C5aR1-deficient mice. Furthermore, wild-type mice injected with anti-mLAMα3 F(ab')2 were completely protected. Our findings suggest a crucial codominant role of FcRγ and complement activation of the anti-mLAMα3 IgG-induced mouse model of mucous membrane pemphigoid. This model will help further discover the pathomechanisms of this devastating disease. Furthermore, it may be of use to explore the effect of urgently needed more specific anti-inflammatory mediators on mucosal and skin lesions in autoantibody-mediated diseases.

2693 related Products with: Experimental Laminin 332 Mucous Membrane Pemphigoid Critically Involves C5aR1 and Reflects Clinical and Immunopathological Characteristics of the Human Disease.

Rabbit Anti-Human Androge Rabbit Anti-Human Androge Rabbit Anti-Human Androge Goat Anti-Human Androgen CAR,CAR,Constitutive acti Recombinant Human Androge Androgen Receptor (Phosph Androgen Receptor (Phosph Androgen Receptor (Ab 650 translocation associated Laminin gamma-2 antibody Breast cancer membrane pr

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#27550944   2016/08/23 Save this To Up

The Discovery and Preclinical Development of ASG-5ME, an Antibody-Drug Conjugate Targeting SLC44A4-Positive Epithelial Tumors Including Pancreatic and Prostate Cancer.

Here, we report the development of an antibody-drug conjugate, ASG-5ME, which targets the solute carrier receptor SLC44A4. SLC44A4 is a member of a family of putative choline transporters that we show to be markedly upregulated in a variety of epithelial tumors, most notably prostate and pancreatic cancer. SLC44A4 is normally expressed on the apical surface of secretory epithelial cells, but in cancer we show expression is not restricted to the luminal surface in advanced and undifferentiated tumors. ASG-5ME consists of a human IgG2 anti-SLC44A4 antibody conjugated through a cleavable linker to the microtubule-disrupting agent monomethylauristatin E. It has potent antitumor activity in both cell line - and patient-derived xenograft models of pancreatic and prostate cancers. Combination studies with ASG-5ME and nab-paclitaxel demonstrated combination effect in both pancreatic and prostate tumor models. Altogether, the data presented here suggest that ASG-5ME may have the potential to offer a new therapeutic option for the treatment of pancreatic and prostate cancers. Mol Cancer Ther; 15(11); 2679-87. ©2016 AACR.

2349 related Products with: The Discovery and Preclinical Development of ASG-5ME, an Antibody-Drug Conjugate Targeting SLC44A4-Positive Epithelial Tumors Including Pancreatic and Prostate Cancer.

Androgen Receptor (Phosph Androgen Receptor (Phosph Androgen Receptor (Ab 650 Bladder cancer tissue arr Breast cancer tissue arra Breast cancer tissue arra Cervix cancer tissue arra Esophagus cancer tissue a Esophageal cancer tissue Kidney cancer tissue arra Kidney cancer tissue arra Liver cancer antibody scr

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#27780843   2016/10/26 Save this To Up

Binding of anti-dsDNA antibodies to proximal tubular epithelial cells contributes to renal tubulointerstitial inflammation.

Immune deposits are often observed along the tubular basement membrane in patients with lupus nephritis, but the role of anti-dsDNA antibody (Ab) deposition on tubulointerstitial inflammation remains to be investigated. We examined the effect of human polyclonal anti-dsDNA Abs on inflammatory processes in cultured proximal renal tubular epithelial cells (PTEC, HK-2 cells) and their association with serum levels of interleukin (IL)-6, IL-8 and monocyte chemoattractant protein-1 (MCP-1) in patients. Binding of anti-dsDNA Abs to HK-2 cells was investigated by cellular ELISA, flow cytometry and immunohistochemistry. IL-6, IL-8 and MCP-1 secretion, mitogen-activated protein kinase (MAPK) activation and the effect of mycophenolic acid (MPA) were investigated by ELISAs and Western blot analysis. NZBWF1/J mice with active nephritis were randomized to receive either mycophenolate mofetil (MMF) (100 mg/kg per day) or vehicle for up to 12 weeks to study renal histopathology focusing on tubulointerstitial changes. Our results demonstrated that anti-dsDNA Abs bound to HK-2 cell surface and induced IL-6, IL-8 and MCP-1 secretion through distinct MAPK pathways. MPA inhibited anti-dsDNA Ab binding to HK-2 cells and suppressed apical and basolateral IL-6 and IL-8, but not MCP-1, secretion. Anti-dsDNA Ab level correlated with serum and tubulointerstitial expression of IL-6, IL-8 and MCP-1. MMF treatment in NZBWF1/J mice reduced anti-dsDNA Ab production and MAPK activation in the renal tubulointerstitium, together with decreased IL-6 and MCP-1 expression. Our data demonstrate that anti-dsDNA Abs contribute to inflammatory processes in the tubulointerstitium in lupus nephritis through their binding to proximal renal tubular epithelial cells and induction of pro-inflammatory mediators, and MPA ameliorates anti-dsDNA Ab induced IL-6 and IL-8 secretion in these cells.

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Mouse Anti-B. pertussis T Mouse Anti-C. difficile T Mouse Anti-C. difficile T Mouse Anti-Diphtheria Tox Mouse Anti-Diphtheria Tox Mouse Anti-E. coli Labile Mouse Anti-E. coli Labile Mouse Anti-Human Fibrobla Mouse Anti-Human Fibrobla Goat Anti-C. botulinum To Sheep Anti-C. perfringens Goat Anti-Diphtheria Toxi

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#27524237   2016/09/25 Save this To Up

Siglec-F is a novel intestinal M cell marker.

Intestinal microfold (M) cells are epithelial cells primarily present on Peyer's patches (PPs) in the small intestine. The ability of M cells to shuttle antigens into the PP for appropriate immune responses makes M cells a target for next-generation oral vaccine delivery. In this regard, discovery of M cell-specific receptors are of great interest, which could act as molecular tags for targeted delivery of cargo to M cells. Here, using a monoclonal antibody we generated to the Sialic acid-binding immunoglobulin-like lectin F (Siglec-F), we show that Siglec-F is expressed on mouse M cells in the small intestine. Immunohistochemical analysis of the PP tissue sections shows that Siglec-F is expressed on the surface of the M cell membrane exposed to the intestinal lumen. Anti-Siglec-F antibody injected into the mouse small intestine bound to M cells, demonstrating the potential to target M cells via Siglec-F.

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#27251132   2016/06/02 Save this To Up

Multi-walled carbon nanotubes directly induce epithelial-mesenchymal transition in human bronchial epithelial cells via the TGF-β-mediated Akt/GSK-3β/SNAIL-1 signalling pathway.

Multi-walled carbon nanotubes (MWCNT) are currently under intense toxicological investigation due to concern on their potential health effects. Current in vitro and in vivo data indicate that MWCNT exposure is strongly associated with lung toxicity (inflammation, fibrosis, granuloma, cancer and airway injury) and their effects might be comparable to asbestos-induced carcinogenesis. Although fibrosis is a multi-origin disease, epithelial-mesenchymal transition (EMT) is recently recognized as an important pathway in cell transformation. It is known that MWCNT exposure induces EMT through the activation of the TGF-β/Smad signalling pathway thus promoting pulmonary fibrosis, but the molecular mechanisms involved are not fully understood. In the present work we propose a new mechanism involving a TGF-β-mediated signalling pathway.

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TGF beta induced factor 2 Anti AGO2 Human, Monoclon Macrophage Colony Stimula anti H inh human blood an anti CD7 All T cells Reco anti Transferrin receptor AKT Phospho-Specific Arra TGF-Beta Signaling Phosph Mouse Anti-Human Fibrobla Mouse Anti-Human Fibrobla Goat Anti-Human Tissue Fa Rat Mesenchymal Stem Cell

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#27219015   2016/05/25 Save this To Up

Autophagy Induced by Intracellular Infection of Propionibacterium acnes.

Sarcoidosis is caused by Th1-type immune responses to unknown agents, and is linked to the infectious agent Propionibacterium acnes. Many strains of P. acnes isolated from sarcoid lesions cause intracellular infection and autophagy may contribute to the pathogenesis of sarcoidosis. We examined whether P. acnes induces autophagy.

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