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  • Oncogene-induced senescence as an initial barrier in lymphoma development. 16079837

    Acute induction of oncogenic Ras provokes cellular senescence involving the retinoblastoma (Rb) pathway, but the tumour suppressive potential of senescence in vivo remains elusive. Recently, Rb-mediated silencing of growth-promoting genes by heterochromatin formation associated with methylation of histone H3 lysine 9 (H3K9me) was identified as a critical feature of cellular senescence, which may depend on the histone methyltransferase Suv39h1. Here we show that Emicro-N-Ras transgenic mice harbouring targeted heterozygous lesions at the Suv39h1, or the p53 locus for comparison, succumb to invasive T-cell lymphomas that lack expression of Suv39h1 or p53, respectively. By contrast, most N-Ras-transgenic wild-type ('control') animals develop a non-lymphoid neoplasia significantly later. Proliferation of primary lymphocytes is directly stalled by a Suv39h1-dependent, H3K9me-related senescent growth arrest in response to oncogenic Ras, thereby cancelling lymphomagenesis at an initial step. Suv39h1-deficient lymphoma cells grow rapidly but, unlike p53-deficient cells, remain highly susceptible to adriamycin-induced apoptosis. In contrast, only control, but not Suv39h1-deficient or p53-deficient, lymphomas senesce after drug therapy when apoptosis is blocked. These results identify H3K9me-mediated senescence as a novel Suv39h1-dependent tumour suppressor mechanism whose inactivation permits the formation of aggressive but apoptosis-competent lymphomas in response to oncogenic Ras.
    Document Type:
    Reference
    Product Catalog Number:
    07-332
    Product Catalog Name:
    Anti-HP1γ Antibody

  • Clinical and biochemical correlates of insoluble alpha-synuclein in dementia with Lewy bodies. 16482476

    Alpha-synuclein is a major constituent of Lewy bodies, the fibrillar aggregates that form within neurons in Parkinson's disease and dementia with Lewy bodies (DLB). Recent biochemical data show that alpha-synuclein accumulates in Parkinson's disease in a detergent insoluble form. We now examine the relationship between detergent insoluble alpha-synuclein and the presence of Lewy bodies, clinical measures of dementia and biochemical parameters in a series of individuals with DLB. We found that Triton X-100 insoluble alpha-synuclein enriched nearly twofold in the temporal cortex of patients with DLB compared to age-matched controls. By contrast the total amount of alpha-synuclein protein was unchanged. Surprisingly, the degree of Triton X-100 insoluble alpha-synuclein did not correlate with either the duration of illness or the number of Lewy bodies counted using stereological methods from an adjacent block of tissue. However, the Triton X-100 soluble fraction of alpha-synuclein did correlate strongly with the expression of several heat shock proteins (HSPs) in DLB but not control cases, suggesting a coordinated HSP response in DLB neocortex.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • HLJ1 is a novel caspase-3 substrate and its expression enhances UV-induced apoptosis in non-small cell lung carcinoma. 20494979

    Carcinogenesis is determined based on both cell proliferation and death rates. Recent studies demonstrate that heat shock proteins (HSPs) regulate apoptosis. HLJ1, a member of the DnaJ-like Hsp40 family, is a newly identified tumor suppressor protein closely related to relapse and survival in non-small cell lung cancer (NSCLC) patients. However, its role in apoptosis is currently unknown. In this study, NSCLC cell lines displaying varying HLJ1 expression levels were subjected to ultraviolet (UV) irradiation, followed by flow cytometry. Interestingly, the percentages of apoptotic cells in the seven cell lines examined were positively correlated with HLJ1 expression. Enforcing expression of HLJ1 in low-HLJ1 expressing highly invasive cells promoted UV-induced apoptosis through enhancing JNK and caspase-3 activation in NSCLC. Additionally, UV irradiation led to reduced levels of HLJ1 predominantly in apoptotic cells. The pan-caspase inhibitor, zVAD-fmk and caspase-3-specific inhibitor, DEVD-fmk, prevented UV-induced degradation of HLJ1 by the late stage of apoptosis. Further experiments revealed a non-typical caspase-3 cleavage site (MEID) at amino acid 125-128 of HLJ1. Our results collectively suggest that HLJ1 is a novel substrate of caspase-3 during the UV-induced apoptotic process.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple

  • Gastrin-producing endocrine cells: a novel source of histamine in the rat stomach. 9751525

    Gastrin and histamine both potently stimulate secretion of acid into the gastric lumen. How these agents interact and how their release is controlled is poorly understood. Therefore, we decided to look for histamine in the antral portion of the rat stomach where the gastrin-producing G cells are located. We used immunocytochemical methods to visualize histamine, histidine decarboxylase (HDC, the enzyme that converts histidine to histamine), and the type 1 vesicular monoamine transporter (VMAT1, the protein responsible for moving histamine into vesicles for storage and release). We were surprised to find that histamine, HDC, and VMAT1 were all present in G cells. Our results suggest that G cells synthesize and secrete gastrin and histamine. Whether histamine acts in concert with gastrin to stimulate acid secretion, or functions as an autocrine inhibitor of gastrin release remains to be seen.
    Document Type:
    Reference
    Product Catalog Number:
    AB1569
    Product Catalog Name:
    Anti-Dopa Decarboxylase Antibody

  • The role of hyperglycemia in FAT/CD36 expression and function. 16838191

    FAT/CD36 is a long-chain fatty acid transporter and scavenger receptor for oxidized LDL. Defects in FAT/CD36 have been linked to the hypertriglyceridemia and insulin resistance. Expression of FAT/CD36 was reported increase in type 1 diabetes; however, it remains unclear whether serum glucose or insulin plays an important role in this regulation. To elucidate the individual contribution of plasma glucose and insulin in the regulation of FAT/CD36 mRNA expression, we induced type 1 diabetes in male Sprague-Dawley rats using streptozotocin (STZ) and compared traditional insulin treatment with administration of the orally absorbed chemical agent vanadate, which reduces blood glucose levels via mechanisms that bypass insulin receptor action. STZ-exposed animals showed significant decreases in body weight (285.5 +/- 2.8 vs. 233.1 +/- 3.5 g, P 0.001) and serum insulin levels (9.7 +/- 0.7 vs. 2.8 +/- 0.6 microU/ml, P 0.05), accompanied by significant increases in blood glucose (71 +/- 3 vs. 433 +/- 11 mg/dl, P 0.001), water intake (38.9 +/- 0.9 vs. 205.9 +/- 3.3 ml/day, P 0.001) and food intake (22.0 +/- 0.4 vs. 36.9 +/- 1.0 g/day, P 0.001). Diabetic animals demonstrated significant increases in FAT/CD36 mRNA levels in duodenum (2.2-fold), jejunum (1.8-fold), ileum (1.5-fold), adipose tissue (1.7-fold), and heart (2.5-fold) (P 0.05). Insulin treatment reversed body weight loss and corrected hyperglycemia at diabetic rats as expected. Insulin treatment also corrected increased FAT/CD36 mRNA expression at diabetic rats. Vanadate significantly reduced serum glucose levels without increasing serum insulin or affecting body weight but reversed increased FAT/CD36 mRNA expression in diabetic rats. These data suggest that plasma glucose levels play more important role in the regulation of FAT/CD36 expression than concurrent changes in plasma insulin.
    Document Type:
    Reference
    Product Catalog Number:
    SRI-13K
    Product Catalog Name:
    Sensitive Rat Insulin RIA

  • A family of Ca2+-dependent activator proteins for secretion: comparative analysis of structure, expression, localization, and function. 14530279

    Ca2+-dependent activator protein for secretion (CAPS) 1 is an essential cytosolic component of the protein machinery involved in large dense-core vesicle (LDCV) exocytosis and in the secretion of a subset of neurotransmitters. In the present study, we report the identification, cloning, and comparative characterization of a second mammalian CAPS isoform, CAPS2. The structure of CAPS2 and its function in LDCV exocytosis from PC12 cells are very similar to those of CAPS1. Both isoforms are strongly expressed in neuroendocrine cells and in the brain. In subcellular fractions of the brain, both CAPS isoforms are enriched in synaptic cytosol fractions and also present on vesicular fractions. In contrast to CAPS1, which is expressed almost exclusively in brain and neuroendocrine tissues, CAPS2 is also expressed in lung, liver, and testis. Within the brain, CAPS2 expression seems to be restricted to certain brain regions and cell populations, whereas CAPS1 expression is strong in all neurons. During development, CAPS2 expression is constant between embryonic day 10 and postnatal day 60, whereas CAPS1 expression is very low before birth and increases after postnatal day 0 to reach a plateau at postnatal day 21. Light microscopic data indicate that both CAPS isoforms are specifically enriched in synaptic terminals. Ultrastructural analyses show that CAPS1 is specifically localized to glutamatergic nerve terminals. We conclude that at the functional level, CAPS2 is largely redundant with CAPS1. Differences in the spatial and temporal expression patterns of the two CAPS isoforms most likely reflect as yet unidentified subtle functional differences required in particular cell types or during a particular developmental period. The abundance of CAPS proteins in synaptic terminals indicates that they may also be important for neuronal functions that are not exclusively related to LDCV exocytosis.
    Document Type:
    Reference
    Product Catalog Number:
    LP1
    Product Catalog Name:
    VLDL, human

  • Biochemical assays for multiple activation states of protein kinase C. 17406536

    This protocol describes biochemical procedures to monitor the activation of the protein kinase C (PKC) family using PKCdelta as the representative. The PKC family is composed of ten isoforms divided into cPKC, nPKC and aPKC groups, and their catalytic activity is regulated by multiple mechanisms. For example, PKCdelta in the nPKC group is activated by diacylglycerol as a second messenger in the receptor-coupled manner, through tyrosine phosphorylation and protein complex formation in stress-stimulated cells, and by the caspase-catalyzed cleavage during apoptosis. The isoform is immunoprecipitated from cultured cells, the protein kinase activity is measured by in vitro kinase assay and the tyrosine phosphorylation and protein complex formation are characterized by immunoblot, whereas the generation of the catalytic fragment is detected by immunoblot in the cell extract. The combination of these procedures is useful to evaluate the activation states of the PKC family in cells. This protocol can be completed in 3-5 d.
    Document Type:
    Reference
    Product Catalog Number:
    AP132A
    Product Catalog Name:
    Goat Anti-Rabbit IgG Antibody, Alkaline Phosphatase conjugate

  • When using Immobilon-P in a slot blot unit, the membrane is sticking to the plastic part of the devi…

    The sticking of the membrane is due to the type of plastic used in the blotting unit.

    One way to address this issue is to silicanize the surface of the plastic. This can be done using a product like Sigmacote (Sigma # SL-2). [The coating should be tested on a noncritical area of the unit, such as a small area on the exterior, to make sure that the solution is compatible with the type of plastic used in the device. The solvent for the silicone is heptane.] Pour a small amount of Sigmacote onto a kimwipe and then wipe across the surface that will be in contact with the membrane. Let the solvent dry off completely, and then wipe the surface with a clean kimwipe to remove any residue. Wash the unit thoroughly in Milli-Q water, and then proceed with the binding.

    Another potential problem is that the unit may be closed too tightly. To address this issue, close the unit with just enough pressure to obtain a seal; additional pressure is of no benefit.
    Document Type:
    FAQ
    Product Catalog Number:
    C3117
    Product Catalog Name:
    Immobilon® Membranes, Sandwiches and Blotting Filter Paper

  • Chronic treatment with a novel ?-secretase modulator, JNJ-40418677, inhibits amyloid plaque formation in a mouse model of Alzheimer's disease. 21232036

    ?-Secretase modulators represent a promising therapeutic approach for Alzheimer's disease (AD) because they selectively decrease amyloid ? 42 (A?42), a particularly neurotoxic A? species that accumulates in plaques in the brains of patients with AD. In the present study, we describe the in vitro and in vivo pharmacological properties of a potent novel ?-secretase modulator, 2-(S)-(3,5-bis(4-(trifluoromethyl)phenyl)phenyl)-4-methylpentanoic acid (JNJ-40418677).
    Document Type:
    Reference
    Product Catalog Number:
    AB5352
    Product Catalog Name:
    Anti-Amyloid Precursor Protein Antibody, CT

  • 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.
    Document Type:
    Reference
    Product Catalog Number:
    05-205