Millipore Sigma Vibrant Logo
 

+antibody


10494 Results Búsqueda avanzada  
Mostrar
Productos (215)
Documentos (10,000)
Páginas (279)

Acote sus resultados Utilice los filtros siguientes para refinar su búsqueda

Tipo de documento

  • (7,552)
  • (2,201)
  • (211)
  • (19)
  • (9)
  • Mostrar más
¿No encuentra lo que está buscando?
Póngase en contacto con
el Servicio de Atención
al Cliente

 
¿Necesita ayuda para encontrar un documento?

  • Ligation of endothelial alpha v beta 3 integrin increases capillary hydraulic conductivity of rat lung. 7554109

    Complement-mediated pulmonary edema results from increases in lung capillary hydraulic conductivity (Lp), possibly by receptor-mediated mechanisms. We considered the Lp effects of vitronectin and the vitronectin-containing complement complex SC5b-9, which ligate the integrin alpha v beta 3. Vitronectin, SC5b-9, and SC5b-9-enriched zymosan-activated serum all rapidly increased Lp, as determined by the split-drop technique in single lung capillaries of rat lung. The Lp increases were inhibited by a monospecific (LM609) and a polyclonal (R838) antibody against the alpha v beta 3 integrin but not by an irrelevant monoclonal antibody isotype matched with LM609, by a monoclonal antibody against the alpha v beta 5 integrin, or by preimmune rabbit serum. Vitronectin monomers failed to increase Lp. The tyrosine kinase blockers genistein and methyl 2,5-dihydroxycinnamate caused significant concentration-dependent inhibitions of Lp increases due to vitronectin and zymosan-activated serum. By contrast, the protein kinase C blocker calphostin C had no major effect. We conclude that (1) multivalent ligation of the luminally located alpha v beta 3 integrin of lung capillary endothelium increases transcapillary liquid flux, and (2) the dominant signal transduction pathway for this effect occurs through tyrosine kinase activation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB88917
    Nombre del producto:
    Anti-Vitronectin Antibody, clone 8E6(LJ8)

  • Alpha-synuclein deficiency in the C57BL/6JOlaHsd strain does not modify disease progression in the ME7-model of prion disease. 19879926

    We previously detailed how intrahippocampal inoculation of C57BL/6J mice with murine modified scrapie (ME7) leads to chronic neurodegeneration (Cunningham C, Deacon R, Wells H, Boche D, Waters S, Diniz CP, Scott H, Rawlins JN, Perry VH (2003) Eur J Neurosci 17:2147-2155.). Our characterization of the ME7-model is based on inoculation of this murine modified scrapie agent into C57BL/6J mice from Harlan laboratories. This agent in the C57BL/6J host generates a disease that spans a 24-week time course. The hippocampal pathology shows progressive misfolded prion (PrP(Sc)) deposition, astrogliosis and leads to behavioural dysfunction underpinned by the early synaptic loss that precedes neuronal death. The Harlan C57BL/6J, although widely used as a wild type mouse, are a sub-strain harbouring a spontaneous deletion of alpha-synuclein with the full description C57BL/6JOlaHsd. Recently alpha-synuclein has been shown to ameliorate the synaptic loss in a mouse model lacking the synaptic chaperone CSP-alpha. This opens a potential confound of the ME7-model, particularly with respect to the signature synaptic loss that underpin the physiological and behavioural dysfunction. To investigate if this strain-selective loss of a candidate disease modifier impacts on signature ME7 pathology, we compared cohorts of C57BL/6JOlaHsd (alpha-synuclein negative) with the founder strain from Charles Rivers (C57BL/6JCrl, alpha-synuclein positive). There were subtle changes in behaviour when comparing control animals from the two sub-strains indicating potentially significant consequences for studies assuming neurobiogical identity of both strains. However, there was no evidence that the absence of alpha-synuclein modifies disease. Indeed, accumulation of PrP(Sc), synaptic loss and the behavioural dysfunction associated with the ME7-agent was the same in both genetic backgrounds. Our data suggest that alpha-synuclein deficiency does not contribute to the compartment specific processes that give rise to prion disease mediated synaptotoxicity and neurodegeneration.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB368

  • Identification of orexins and cognate receptors in the lacrimal gland of sheep. 22465661

    The aim of the present work was to study, by means of immunohistochemical and RT-PCR techniques, the presence and distribution of immunopositivity for orexin A and B (OXA and OXB) and orexin type 1 and 2 receptors (OX(1)R and OX(2)R) in the lacrimal gland of sheep as well as the gene expressions for prepro-orexin (PPOX) and cognate receptors. In serial sections, positive staining for OXA and OXB were localized in the same nervous fibers within the connective tissue septa. Positive staining for OX(1)R was evidenced in the wall of small arteries while that for OX(2)R was observed in the secretory portion of the acinar gland cells with a characteristic localization in the apical cytoplasm. RT-PCR analysis showed the presence of transcripts for PPOX, OX(1)R and OX(2)R in the sheep lacrimal gland; the gene expression of OX(1)R was two-fold greater (p<0.01) than that of OX(2)R. Taken together the present findings raise intriguing questions on the potential role of the orexinergic system in the regulation of lacrimal gland functions that require further investigations.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AP132B
    Nombre del producto:
    Goat Anti-Rabbit IgG Antibody, biotin-SP conjugate

  • Novel role for amphiregulin in protection from liver injury. 15753092

    Clinically, the Fas and Fas ligand system plays a central role in the development of hepatocyte apoptosis, a process contributing to a broad spectrum of liver diseases. Therefore, the development of therapies aimed at the inhibition of hepatocyte apoptosis is a major issue. Activation of the epidermal growth factor receptor has been shown to convey survival signals to the hepatocyte. To learn about the endogenous response of epidermal growth factor receptor ligands during Fas-mediated liver injury we investigated the expression of epidermal growth factor, transforming growth factor alpha, heparin-binding epidermal growth factor-like growth factor, betacellulin, epiregulin, and amphiregulin in the liver of mice challenged with Fas-agonist antibody. Amphiregulin expression, barely detectable in healthy liver, was significantly up-regulated. Amphiregulin administration abrogated Fas-mediated liver injury in mice and showed direct anti-apoptotic effects in primary hepatocytes. Amphiregulin activated the Akt and signal transducer and activator of transcription-3 survival pathways, and up-regulated Bcl-xL expression. Amphiregulin knock-out mice showed signs of chronic liver damage in the absence of any noxious treatment, and died faster than wild type mice in response to lethal doses of Fas-agonist antibody. In contrast, these mice were more resistant against sublethal liver damage, supporting the hypothesis that chronic liver injury can precondition hepatocytes inducing resistance to subsequent cell death. These results show that amphiregulin is a protective factor induced in response to liver damage and that it may be therapeutic in liver diseases.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Anti-GluR4 Polyclonal Antibody

    Tipo de documento:
    Certificado de análisis
    Número de lote:
    2872462
    Referencia del producto:
    AB1508
    Nombre del producto:
    Anti-Glutamate Receptor 4 Antibody

  • IGF-I enhances ?5?1 integrin expression and cell motility in human chondrosarcoma cells. 21344385

    Chondrosarcoma is a type of highly malignant tumor with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Integrins are the major adhesive molecules in mammalian cells and have been associated with metastasis of cancer cells. Insulin-like growth factor-I (IGF)-I plays an important role in regulating cell growth, proliferation, survival, and metabolism. However, the effects of IGF-I in migration and integrin expression in chondrosarcoma cells are largely unknown. In this study, we found that IGF-I increased the migration and the expression of ?5?1 integrin in human chondrosarcoma cells. Pretreatment of cells with IGF-I receptor antibody reduced IGF-I-induced cell migration and integrin expression. Activations of phosphatidylinositol 3-kinase (PI3K), Akt, and nuclear factor-?B (NF-?B) pathways after IGF-I treatment were demonstrated, and IGF-I-induced expression of integrin and migration activity was inhibited by the specific inhibitor and mutant of PI3K, Akt, and NF-?B cascades. Taken together, our results indicated that IGF-I enhances the migration of chondrosarcoma cells by increasing ?5?1 integrin expression through the IGF-I receptor/PI3K/Akt/NF-?B signal transduction pathway.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB2637
    Nombre del producto:
    Anti-Integrin beta-3 (CD61) Antibody, clone HMb3-1