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  • Normal and prostate cancer cells display distinct molecular profiles of alpha-tubulin posttranslational modifications. 16541425

    BACKGROUND: Multiple diverse posttranslational modifications of alpha-tubulin such as detyrosination, further cleavage of the penultimate glutamate residue (Delta2-tubulin), acetylation, and polyglutamylation increase the structural and functional diversity of microtubules. METHODS: Herein, we characterized the molecular profile of alpha-tubulin posttranslational modifications in normal human prostate epithelial cells (PrEC), immortalized normal prostate epithelial cells (PZ-HPV-7), androgen-dependent prostate cancer cells (LNCaP), transitional androgen-independent prostate cancer cells (LNCaP-cds and CWR22Rv1), and androgen-independent prostate cancer cells (PC3). RESULTS: Compared to PrEC and PZ-HPV-7 cells, all cancer cells exhibited elevated levels of detyrosinated and polyglutamylated alpha-tubulin, that was paralleled by decreased protein levels of tubulin tyrosine ligase (TTL). In contrast, PrEC and PZ-HPV-7 cells expressed markedly higher levels of Delta2-tubulin. Whereas alpha-tubulin acetylation levels were generally equivalent in all the cell lines, PC3 cells did not display detectable levels of Ac-tubulin. CONCLUSION: These data may reveal novel biomarkers of prostate cancer and new therapeutic targets.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Species differences in the expression of Ahi1, a protein implicated in the neurodevelopmental disorder Joubert syndrome, with preferential accumulation to stigmoid bodies ... 18785627

    Joubert syndrome (JBTS) is an autosomal recessive disorder characterized by cerebellum and brainstem malformations. Individuals with JBTS have abnormal breathing and eye movements, ataxia, hypotonia, and cognitive difficulty, and they display mirror movements. Mutations in the Abelson-helper integration site-1 gene (AHI1) cause JBTS in humans, suggesting that AHI1 is required for hindbrain development; however AHI1 may also be required for neuronal function. Support for this idea comes from studies demonstrating that the AHI1 locus is associated with schizophrenia. To gain further insight into the function of AHI1 in both the developing and mature central nervous system, we determined the spatial and temporal expression patterns of the gene products of AHI1 orthologs throughout development, in human, mouse, and zebrafish. Murine Ahi1 was distributed throughout the cytoplasm, dendrites, and axons of neurons, but was absent in glial cells. Ahi1 expression in the mouse brain was observed as early as embryonic day 10.5 and persisted into adulthood, with peak expression during the first postnatal week. Murine Ahi1 was observed in neurons of the hindbrain, midbrain, and ventral forebrain. Generally, the AHI1/Ahi1/ahi1 orthologs had a conserved distribution pattern in human, mouse, and zebrafish, but mouse Ahi1 was not present in the developing and mature cerebellum. Ahi1 was also observed consistently in the stigmoid body, a poorly characterized cytoplasmic organelle found in neurons. Overall, these results suggest roles for AHI1 in neurodevelopmental processes that underlie most of the neuroanatomical defects in JBTS, and perhaps in neuronal functions that contribute to schizophrenia.
    Tipo de documento:
    Referencia
    Referencia del producto:
    Múltiplo
    Nombre del producto:
    Múltiplo

  • Thrombospondin-1 promotes cellular adherence of gram-positive pathogens via recognition of peptidoglycan. 17507668

    Thrombospondin-1 (TSP1) is a matricellular glycoprotein that has key roles in interactions between human cells and components of the extracellular matrix. Here we report a novel role for the lectin TSP1 in pathogen-host interactions. Binding assays and flow cytometric analysis demonstrate that Streptococcus pneumoniae and other gram-positive pathogens including S. pyogenes, Staphylococcus aureus, and Listeria monocytogenes interact specifically with human TSP1. We also show for the first time that host cell-bound TSP1 promotes adherence of gram-positive pathogens to human epithelial and endothelial cell lines. Pretreatment of bacteria with sodium periodate but not Pronase E substantially reduced TSP1-mediated bacterial adherence to host cells, suggesting that a glycoconjugate on the bacterial cell surface functions as the receptor for TSP1. Lipoteichoic acids did not affect TSP1-mediated adherence of S. pneumoniae to host cells. In contrast, attachment of S. pneumoniae and other gram-positive pathogens to host cells via TSP1 was blocked by soluble peptidoglycan, indicating recognition of bacterial peptidoglycan by TSP1. In conclusion, our results demonstrate that recognition of gram-positive pathogens by TSP1 promotes bacterial colonization of host tissue cells. In this scenario, peptidoglycan functions as adhesin and TSP1 acts as a molecular bridge linking gram-positive bacteria with receptors on the host cell.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB1980

  • Polo-like kinase 1 enhances survival and mutagenesis after genotoxic stress in normal cells through cell cycle checkpoint bypass. 20089605

    Polo-like kinase 1 (Plk1) is a key regulator of mitosis. Aberrant Plk1 activity is found in tumors, but little is known regarding its role in the DNA damage response of normal cells and its potential contribution to the early stages of carcinogenesis. Inappropriate survival signaling after DNA damage may facilitate clonal expansion of genetically compromised cells, and it is known that protein tyrosine phosphatase (PTP) inhibitors activate key survival pathways. In this study we employed hexavalent chromium [Cr(VI)], a well-documented genotoxicant, to investigate the mechanism by which survival pathway activation could lead to loss of checkpoint control via a mechanism involving Plk1. We recently reported that PTP inhibition enhances clonogenic survival and mutagenesis after Cr(VI) exposure by overriding Cr-induced growth arrest. Here, we report that checkpoint bypass, facilitated by PTP inhibition, was associated with decreased Cdk1 Tyr15 phosphorylation, as well as increased Plk1 activity and nuclear localization. Plk1 was necessary for increased survival after PTP inhibition and Cr(VI) exposure in normal human fibroblasts via enhanced mitotic progression. In addition, pharmacological inhibition of Plk1 abolished the PTP inhibitor-induced bypass of the G2/M checkpoint. Notably, Plk1 overexpression increased survival and mutagenesis after Cr(VI) exposure in wild-type S. cerevisiae. Taken together, our data indicate that Plk1 activation and nuclear localization are necessary for PTP-regulated mitotic progression after DNA damage. Our studies highlight a role for Plk1 in the loss of checkpoint control, increased survival, and mutagenesis after genotoxic exposure in normal cells, which in turn may lead to genomic instability and carcinogenesis.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-740
    Nombre del producto:
    Anti-phospho-ATM (Ser1981) Antibody, clone 10H11.E12

  • Atorvastatin inhibits ABCA1 expression and cholesterol efflux in THP-1 macrophages by an LXR-dependent pathway. 18427282

    The effect of atorvastatin on adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) expression and cholesterol efflux remains controversial. In an effort to clarify this issue, ABCA1 expression and apolipoprotein AI (apoAI)-mediated cholesterol efflux after atorvastatin treatment were investigated in THP-1 macrophages. Atorvastatin from 2 microM to 40 microM dose-dependently inhibited ABCA1 expression in human monocyte-derived macrophages and phorbol 12-myristate 13-acetate (PMA)-stimulated THP-1 monocytes. ApoAI-mediated cholesterol efflux was reduced in PMA-stimulated THP-1 cells treated with atorvastatin, this effect was abolished with acetylated low-density lipoprotein (LDL) pretreatment. Atorvastatin treatment also dose-dependently reduced liver X receptor alpha (LXRalpha) expression and Rho activation. Rho activation by farnysylpyophosphate (FPP) and lysophosphatidic acid (LPA) did not salvage, but further depressed, the cholesterol efflux and ABCA1 expression in the presence of atorvastatin. Without atorvastatin, Rho activation by mevalonate, FPP, and LPA diminished apoAI-mediated cholesterol efflux, and Rho activation by GTPgammaS also decreased ABCA1 messenger ribonucleic acid (mRNA) by 16%. Furthermore, Rho inhibition by C3 exoenzyme increased ABCA1 mRNA by 48% despite a 17% decrease in apoAI-mediated cholesterol efflux. LXRalpha agonists (T01901317 and 22(R)-hydroxycholesterol) prevented any reductions in cholesterol efflux or ABCA1 expression associated with atorvastatin treatment. Furthermore, Western blot analysis demonstrated the reciprocal inhibition of Rho and LXRalpha. In conclusion, atorvastatin decreases ABCA1 expression in noncholesterol-loaded macrophages in an LXRalpha- but not Rho-dependent pathway; this effect can be compromised after acetylated LDL cholesterol loading.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-778
    Nombre del producto:
    Anti-Rho (-A Antibody, -B, -C), clone 55

  • Myocyte apoptosis and reduced SR gene expression precede the transition from chronically stunned to hibernating myocardium. 11708839

    A systematic transition from chronic stunning to hibernation occurs as coronary flow reserve decreases to a critical level. Hibernating myocardium exhibits apoptosis-induced myocyte loss and a reduction in the expression of the sarcoplasmic reticulum (SR) Ca2+ ATPase but whether similar cellular changes occur in chronic stunning is unknown. Pigs with a chronic left anterior descending coronary artery (LAD) stenosis were studied one (n=9) or two (n=10) months after instrumentation. Anterior hypokinesis with normal levels of resting perfusion developed at each time-point, consistent with chronic stunning. After 1 month, sub-endocardial flow reserve was moderately reduced (adenosine/rest, LAD: 3.60+/-0.91 v Remote: 6.00+/-0.54, P0.01) with no regional differences in SR protein expression, no increase in apoptosis (32+/-6 v 21+/-5 nuclei/10(6) myocyte nuclei, p-ns) and no regional myocyte loss (1976+/-44 v 1955+/-30 nuclei/mm2, p-ns). After 2 months, sub-endocardial flow reserve in chronically stunned myocardium was severely impaired (LAD: 1.41+/-0.21 v Remote: 5.59+/-0.96, P0.01). There were small but significant reductions in LAD mRNA and protein levels for the SRCa2+ ATPase and phospholamban whereas calsequestrin was unchanged. In addition, regional myocyte apoptosis increased (127+/-24 v 55+/-9 nuclei/10(6) myocyte nuclei, P0.01), resulting in the onset of myocyte loss (1293+/-50 v 1394+/-32 nuclei/mm2, P0.01). Apoptosis-induced myocyte loss and reductions in SR protein expression are not invariably present in viable chronically dysfunctional myocardium. They are induced as the propensity of a region to develop reversible ischemia increases (as reflected by coronary flow reserve). The temporal progression indicates that alterations in SR protein expression and myocyte apoptosis precede the transition from chronically stunned to hibernating myocardium.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-205

  • Complete set of orthogonal 21st aminoacyl-tRNA synthetase-amber, ochre and opal suppressor tRNA pairs: concomitant suppression of three different termination codons in an ... 15576346

    We describe the generation of a complete set of orthogonal 21st synthetase-amber, ochre and opal suppressor tRNA pairs including the first report of a 21st synthetase-ochre suppressor tRNA pair. We show that amber, ochre and opal suppressor tRNAs, derived from Escherichia coli glutamine tRNA, suppress UAG, UAA and UGA termination codons, respectively, in a reporter mRNA in mammalian cells. Activity of each suppressor tRNA is dependent upon the expression of E.coli glutaminyl-tRNA synthetase, indicating that none of the suppressor tRNAs are aminoacylated by any of the twenty aminoacyl-tRNA synthetases in the mammalian cytoplasm. Amber, ochre and opal suppressor tRNAs with a wide range of activities in suppression (increases of up to 36, 156 and 200-fold, respectively) have been generated by introducing further mutations into the suppressor tRNA genes. The most active suppressor tRNAs have been used in combination to concomitantly suppress two or three termination codons in an mRNA. We discuss the potential use of these 21st synthetase-suppressor tRNA pairs for the site-specific incorporation of two or, possibly, even three different unnatural amino acids into proteins and for the regulated suppression of amber, ochre and opal termination codons in mammalian cells.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB4410

  • Complex assembly and metabolic profiling of Arabidopsis thaliana plants overexpressing vitamin B₆ biosynthesis proteins. 20675613

    In plants, vitamin B₆ biosynthesis requires the activity of PDX1 and PDX2 proteins. Arabidopsis thaliana encodes for three PDX1 proteins, named PDX1.1, 1.2, and 1.3, but only one PDX2. Here, we show in planta complex assembly of PDX proteins, based on split-YFP and FPLC assays, and can demonstrate their presence in higher complexes of around 750 kDa. Metabolic profiling of plants ectopically expressing the different PDX proteins indicates a negative influence of PDX1.2 on vitamin B₆ biosynthesis and a correlation between aberrant vitamin B6 content, PDX1 gene expression, and light sensitivity specifically for PDX1.3. These findings provide first insights into in planta vitamin B₆ synthase complex assembly and new information on how the different PDX proteins affect plant metabolism.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-724
    Nombre del producto:
    Anti-Myc Tag Antibody, clone 4A6

  • Down syndrome fibroblasts and mouse Prep1-overexpressing cells display increased sensitivity to genotoxic stress. 20110257

    PREP1 (PKNOX1) maps in the Down syndrome (DS) critical region of chromosome 21, is overexpressed in some DS tissues and might be involved in the DS phenotype. By using fibroblasts from DS patients and by overexpressing Prep1 in F9 teratocarcinoma and Prep1(i/i) MEF to single out the role of the protein, we report that excess Prep1 increases the sensitivity of cells to genotoxic stress and the extent of the apoptosis directly correlates with the level of Prep1. The apoptotic response of Prep1-overexpressing cells is mediated by the pro-apoptotic p53 protein that we show is a direct target of Prep1, as its depletion reverts the apoptotic phenotype. The induction of p53 overcomes the anti-apoptotic role of Bcl-X(L), previously shown to be also a Prep1 target, the levels of which are increased in Prep1-overexpressing cells as well. Our results provide a rationale for the involvement of PREP1 in the apoptotic phenotype of DS tissues and indicate that differences in Prep1 level can have drastic effects.
    Tipo de documento:
    Referencia
    Referencia del producto:
    05-766

  • Changes in Hsp60 level of the failing heart following acute myocardial infarction and the effect of long-term treatment with trandolapril. 17202668

    Changes in heat shock protein (Hsp) 60 of the viable left ventricular muscle (viable LV) after myocardial infarction in rats and the effect of the angiotensin I-converting enzyme inhibitor (ACEI) trandolapril were examined. Myocardial infarction was induced in rats by ligation of the left coronary artery. The coronary artery-ligated (CAL) and sham-operated (Sham) rats were orally treated with 3 mg/kg/d trandolapril from the 2nd to 8th week after surgery. Hemodynamic parameters and tissue weights of the left and right ventricles of the animals at the 8th week after CAL (8w-CAL rats) showed signs indicating chronic heart failure. An increase in Hsp60 content, a decrease in mitochondrial oxygen consumption rate (OCR), and an increase in the mitochondrial thiobarbiturate-reacting substance (TRS) of the viable LV were detected. Eight weeks after CAL. Long-term treatment of the CAL rats with trandolapril improved the hemodynamic parameters, attenuated the CAL-induced increase in Hsp60 content, the decrease in mitochondrial OCR, and the increase in the mitochondrial TRS content of the viable LV at the 8th week after myocardial infarction. The increase in Hsp60 content was closely related to the decrease in the mitochondrial OCR and to a rise in the LVEDP of the CAL animal at the 8th week after myocardial infarction. These results suggest that a series of pathophysiological alterations, including a reduction in mitochondrial function, appearance of reactive oxygen stress, and production of Hsp60 is involved in the development of cardiac failure and that trandolapril is beneficial for preventing these alterations.
    Tipo de documento:
    Referencia
    Referencia del producto:
    MAB3104
    Nombre del producto:
    Anti-Calpain I Antibody, large subunit, clone P9