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  • CHO cells adhering to nitrogen-rich plasma-polymerised ethylene exhibit high production of a specific recombinant protein. 19623580

    In many industrial applications, inadequate cell attachment can be a limitation, especially when serum-free media are used. Nitrogen-rich plasma-polymerised ethylene (PPE:N) exhibits high concentrations of polar groups that can help to promote the attachment of weakly adherent cell types. Tissue plasminogen activator-producing Chinese hamster ovary (CHO) cells, adapted to suspension, were grown in the presence PPE:N flakes and were found to adhere to them. The growth rate was reduced, but cell viability was enhanced and their metabolism was more efficient, with generally higher recombinant protein productivity. Finally, cell adhesion on PPE:N surfaces was found to be independent of integrins, and was probably mediated by certain non-specific interactions with the PPE:N surface.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB1952
    Nombre del producto:
    Anti-Integrin beta1 Antibody, Cytosolic

  • Cholinergic deafferentation exacerbates seizure-induced loss of somatostatin-immunoreactive neurons in the rat hippocampus. 9284343

    The loss of somatostatin-immunoreactive neurons and the sprouting of mossy fibers are typical histopathological abnormalities in the hippocampus in experimental and human temporal lobe epilepsy. To investigate whether the development of seizure-induced alterations is regulated by the subcortical afferent pathways to the hippocampus, we lesioned cholinergic, noradrenergic or serotonergic afferent pathways in rats two days after seizures were induced with kainate. Two months later, somatostatin-immunoreactive neurons were counted in the hilus to assess the severity of neuronal damage. Mossy fiber sprouting was analysed from adjacent Timm-stained sections. Kainate-induced seizures caused a loss of hilar somatostatin-immunoreactive neurons in the septal end of the hippocampus, where 63% of the somatostatin-immunoreactive neurons survived. Even more severe damage was found in the temporal end of the hippocampus (only 21% surviving). Cholinergic deafferentation of the hippocampus (using 192-IgG saporin) decreased the overall number of hilar somatostatin-immunoreactive neurons. In control rats that did not receive kainate, 87% (septal end) and 74% (temporal end) of the hilar somatostatin-immunoreactive neurons remained after cholinergic deafferentation. Moreover, seizure-induced damage to hilar somatostatin-immunoreactive neurons was further exacerbated by 192-IgG-saporin, with only 35% of the neurons remaining in the septal end and 14% in the temporal end of the hippocampus. Noradrenergic [using N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine] or serotonergic (using 5,7-dihydroxytryptamine) lesions did not affect the number of hilar somatostatin-immunoreactive neurons either in control or in kainate-treated rats. The severity and distribution of seizure-induced mossy fiber sprouting were also not affected by any of the lesions. These data suggest that various subcortical afferent pathways may differentially modulate seizure-induced damage to the hippocampus. Damage to cholinergic neurons results in the loss of hilar somatostatin-immunoreactive neurons and exacerbates the seizure-induced loss of somatostatin-immunoreactive neurons.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB308
    Nombre del producto:
    Anti-Dopamine β Hydroxylase Antibody, clone 4F10.2

  • Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2. 18417716

    Apoptosis plays a critical role during development and in the maintenance of the vascular system. B-cell leukemia lymphoma 2 (bcl-2) protects endothelial cells (EC) from apoptosis in response to a variety of stimuli. Previous work from this laboratory demonstrated attenuation of postnatal retinal vascular development and retinal neovascularization during oxygen-induced ischemic retinopathy in bcl-2-deficient (bcl-2-/-) mice. To gain further insight into the function of bcl-2 in the endothelium, we isolated retinal EC from bcl-2+/+ and bcl-2-/- mice. Retinal EC lacking bcl-2 demonstrated reduced cell migration, tenascin-C expression, and adhesion to vitronectin and fibronectin. The bcl-2-/- retinal EC also failed to undergo capillary morphogenesis in Matrigel. In addition, using an ex vivo angiogenesis assay, we observed reduced sprouting from aortic rings grown in culture from bcl-2-/- mice compared with bcl-2+/+ mice. Furthermore, reexpression of bcl-2 was sufficient to restore migration and capillary morphogenesis defects observed in bcl-2-/- retinal EC. Mechanistically, bcl-2-/- cells expressed significantly less endothelial nitric oxide synthase, an important downstream effecter of proangiogenic signaling. This may be attributed to increased oxidative stress in the absence of bcl-2. In fact, incubation of retinal EC or aortic rings from bcl-2-/- mice with the antioxidant N-acetylcysteine rescued their capillary morphogenesis and sprouting defects. Thus, bcl-2-mediated cellular functions play important roles not only in survival but also in proangiogenic phenotype of EC with a significant impact on vascular development and angiogenesis.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • SPARC mediates early extracellular matrix remodeling following myocardial infarction. 21602472

    Secreted protein, acidic, and rich in cysteine (SPARC) is a matricellular protein that functions in the extracellular processing of newly synthesized collagen. Collagen deposition to form a scar is a key event following a myocardial infarction (MI). Because the roles of SPARC in the early post-MI setting have not been defined, we examined age-matched wild-type (WT; n=22) and SPARC-deficient (null; n=25) mice at day 3 post-MI. Day 0 WT (n=28) and null (n=20) mice served as controls. Infarct size was 52 ± 2% for WT and 47 ± 2% for SPARC null (P=NS), indicating that the MI injury was comparable in the two groups. By echocardiography, WT mice increased end-diastolic volumes from 45 ± 2 to 83 ± 5 μl (P less than 0.05). SPARC null mice also increased end-diastolic volumes but to a lesser extent than WT (39 ± 3 to 63 ± 5 μl; P less than 0.05 vs. day 0 controls and vs. WT day 3 MI). Ejection fraction fell post-MI in WT mice from 57 ± 2 to 19 ± 1%. The decrease in ejection fraction was attenuated in the absence of SPARC (65 ± 2 to 28 ± 2%). Fibroblasts isolated from SPARC null left ventricle (LV) showed differences in the expression of 22 genes encoding extracellular matrix and adhesion molecule genes, including fibronectin, connective tissue growth factor (CTGF; CCN2), matrix metalloproteinase-3 (MMP-3), and tissue inhibitor of metalloproteinase-2 (TIMP-2). The change in fibroblast gene expression levels was mirrored in tissue protein extracts for fibronectin, CTGF, and MMP-3 but not TIMP-2. Combined, the results of this study indicate that SPARC deletion preserves LV function at day 3 post-MI but may be detrimental for the long-term response due to impaired fibroblast activation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB1954
    Nombre del producto:
    Anti-Fibronectin Antibody

  • Adverse effects of reduced oxygen tension on the proliferative capacity of rat kidney and insulin-secreting cell lines involve DNA damage and stress responses. 18692496

    Standard cell culture conditions do not reflect the physiological environment in terms of oxygen tension (20% vs 3%). The effects of lowering oxygen tension on cell proliferation in culture can be beneficial as well as detrimental depending on the cell line studied, but the molecular mechanism underlying such effects is not fully understood. We observed that the proliferative capacity of the rat cell lines NRK and INS-1 was inhibited when cultured under 3% oxygen as compared to 20% oxygen. Suppression of proliferation in NRK cells was accompanied by induction of DNA double strand breaks whereas in INS-1 cells it was accompanied by up-regulation of p53 and p27. Although Sirt1 was up-regulated in both cell lines by 3% oxygen the effects on antioxidant enzymes (MnSOD, CuZnSOD and catalase) were cell line specific. Marked up-regulation of heme oxygenase-1 (HO-1) was detected in both NRK and INS-1 cells when cultured in 3% oxygen. HO-1 expression can be readily induced by exposure to hydrogen peroxide in culture. These results suggest that reduced oxygen tension suppresses the proliferative capacity of these two cell lines through a stress response that is similar to an oxidative stress response but the molecular events that lead to the reduced cell proliferation are cell line specific.
    Tipo de documento:
    Referencia
    Referencia del producto:
    07-131
    Nombre del producto:
    Anti-Sirt1(Sir2) Antibody

  • Retinoblastoma tumor-suppressor protein phosphorylation and inactivation depend on direct interaction with Pin1. 22322860

    Inactivation of the retinoblastoma protein (pRb) by phosphorylation triggers uncontrolled cell proliferation. Accordingly, activation of cyclin-dependent kinase (CDK)/cyclin complexes or downregulation of CDK inhibitors appears as a common event in human cancer. Here we show that Pin1 (protein interacting with NIMA (never in mitosis A)-1), a peptidylprolyl isomerase involved in the control of protein phosphorylation, is an essential mediator for inactivation of the pRb. Our results indicate that Pin1 controls cell proliferation by altering pRb phosphorylation without affecting CDK and protein phosphatase 1 and 2 activity. We demonstrated that Pin1 regulates tumor cell proliferation through direct interaction with the spacer domain of the pRb protein, and allows the interaction between CDK/cyclin complexes and pRb in mid/late G1. Phosphorylation of pRb Ser 608/612 is the crucial motif for Pin1 binding. We propose that Pin1 selectively boosts the switch from hypo- to hyper-phosphorylation of pRb in tumor cells. In addition, we demonstrate that the CDK pathway is responsible for the interaction of Pin1 and pRb. Prospectively, our findings therefore suggest that the synergism among CDK and Pin1 inhibitors holds great promise for targeted pharmacological treatment of cancer patients, with the possibility of reaching high effectiveness at tolerated doses.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-379
    Nombre del producto:
    Anti-E2F-1 Antibody, clones KH20 and KH95

  • Scutellaria baicalensis attenuates blood-brain barrier disruption after intracerebral hemorrhage in rats. 22298450

    Disruption of the blood-brain barrier (BBB) contributes to the inflammatory response and edema formation in the brain, exacerbating brain damage. The present study evaluated the effects of Scutellaria baicalensis (SR) water extracts on BBB disruption after intracerebral hemorrhage (ICH) in rats. ICH was induced by stereotaxic intrastriatal injection of bacterial type VII collagenase, and SR was administrated orally three times (50 mg/ml/kg) during the 48 h after ICH onset. SR treatment significantly reduced the degree of (1) hemorrhage volume and edema percentage of the ipsilateral hemisphere, (2) brain water content, (3) MPO-positive neutrophil infiltration in the peri-hematoma, and (4) BBB permeability measured by Evans blue leakage. In addition, expression of matrix metalloproteinase (MMP)-9, MMP-12, and tissue inhibitor of MMPs (TIMP)-1 were investigated with immunohistochemistry. SR treatment reduced MMP-9 and MMP-12 expression in the peri-hematoma after ICH. These results indicate that SR attenuates the BBB disruption through anti-inflammatory effects and suppression of MMP expression. These findings provide a pharmacological basis for the use of SR in the treatment of the BBB disruption following stroke and trauma.
    Tipo de documento:
    Referencia
    Referencia del producto:
    AB19016
    Nombre del producto:
    Anti-MMP-9 Antibody, Catalytic domain

  • Procedures for derivation and characterisation of human embryonic stem cells from Odense, Denmark. 22528347

    In 1998, a development occurred in stem cell biology with the first report of the derivation of a human embryonic stem cell (hESC) line. Since then a number of techniques have been used to derive and characterise hESCs. Here, we describe the derivation methods used by our laboratory for isolation of the ICM by immunosurgery and outgrowth of the whole blastocyst. We have added protocols for routine culture, passaging and cryopreservation of our hESC lines as well as the methods we have used for characterisation (flow cytometry, karyotyping, immunocytochemistry, in vitro and in vivo differentiation). Additionally, we have included gene sequences for PCR and an antibody list for immunocytochemistry.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB4381
    Nombre del producto:
    Anti-TRA-1-81 Antibody, clone TRA-1-81

  • Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway. 11520989

    In mammals, the canonical nuclear factor kappaB (NF-kappaB) signaling pathway activated in response to infections is based on degradation of IkappaB inhibitors. This pathway depends on the IkappaB kinase (IKK), which contains two catalytic subunits, IKKalpha and IKKbeta. IKKbeta is essential for inducible IkappaB phosphorylation and degradation, whereas IKKalpha is not. Here we show that IKKalpha is required for B cell maturation, formation of secondary lymphoid organs, increased expression of certain NF-kappaB target genes, and processing of the NF-kappaB2 (p100) precursor. IKKalpha preferentially phosphorylates NF-kappaB2, and this activity requires its phosphorylation by upstream kinases, one of which may be NF-kappaB-inducing kinase (NIK). IKKalpha is therefore a pivotal component of a second NF-kappaB activation pathway based on regulated NF-kappaB2 processing rather than IkappaB degradation.
    Tipo de documento:
    Referencia
    Referencia del producto:
    06-413
    Nombre del producto:
    Anti-NFκB p52 Antibody

  • A small molecule that directs differentiation of human ESCs into the pancreatic lineage. 19287398

    Stepwise differentiation from embryonic stem cells (ESCs) to functional insulin-secreting beta cells will identify key steps in beta-cell development and may yet prove useful for transplantation therapy for diabetics. An essential step in this schema is the generation of pancreatic progenitors--cells that express Pdx1 and produce all the cell types of the pancreas. High-content chemical screening identified a small molecule, (-)-indolactam V, that induces differentiation of a substantial number of Pdx1-expressing cells from human ESCs. The Pdx1-expressing cells express other pancreatic markers and contribute to endocrine, exocrine and duct cells, in vitro and in vivo. Further analyses showed that (-)-indolactam V works specifically at one stage of pancreatic development, inducing pancreatic progenitors from definitive endoderm. This study describes a chemical screening platform to investigate human ESC differentiation and demonstrates the generation of a cell population that is a key milepost on the path to making beta cells.
    Tipo de documento:
    Referencia
    Referencia del producto:
    07-633
    Nombre del producto: