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  • COA 125042

    Document Type:
    Certificate of Analysis
    Product Catalog Number:
    125042

  • Increased atherosclerosis in streptozotocin-induced diabetic mice. 8601643

    Premature and extensive atheroscleroses involving renal, peripheral, and cardiovascular sites remain major complications of diabetes mellitus. Controversy exists as to the contribution of hyperglycemia versus elevated local or systemic concentrations of insulin to atherosclerosis risk. In this report, we developed the first murine model susceptible to both atherosclerosis and diabetes to determine which diabetogenic factors contribute to vascular disease. C57BL/6 and BALB/c mice were treated with multiple low-dose streptozotocin (STZ) or control citrate buffer and fed rodent chow or an atherogenic-promoting (Ath) diet for 12-20 wk. STZ treatment resulted in sustained hyperglycemia (250-420 mg/dl) and a modest reduction in plasma insulin levels for both strains regardless of diet. Citrate-treated C57BL/6 mice fed the Ath diet showed extensive oil red O-staining fatty streak aortic sinus lesions (20,537+/-2,957 micron2), the size of which did not differ for Ath-fed mice treated with STZ (16,836+/-2,136 micron2). In contrast, hyperglycemic BALB/c mice fed the Ath diet showed a 17-fold increase in atherosclerotic lesion area (7,922+/-2,096 micron2) as compared with citrate-treated mice fed the Ath diet (467+/-318 micron2). Correlations between lesion size and plasma glucose levels were significant for BALB/c (r = 0.741, P 0.009), but not C57BL/6 (r = 0.314, P0.3) mice. Lesion size correlated significantly with plasma cholesterol for C57BL/6 (r = 0.612, P0.03) but not BALB/c (r = 0.630, P0.1) mice. Immunohistochemistry showed that aortic sinus lesions from both strains contained macrophages, but smooth muscle cells were clearly present in lesions of BALB/c mice. In summary, we present the first small animal model showing accelerated atherosclerosis in response to hyperglycemia. Fatty streaks resembled those of human type II lesions in that both macrophages and smooth muscle cells were evident. In addition, our results support the concept that hyperglycemia as opposed to hyperinsulinemia contributes heavily to risk of atherosclerosis.
    Document Type:
    Reference
    Product Catalog Number:
    RI-13K
    Product Catalog Name:
    Rat Insulin RIA

  • Effects of JC virus infection on anti-apoptotic protein survivin in progressive multifocal leukoencephalopathy. 17392168

    Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease of the central nervous system resulting from the productive infection of oligodendrocytes by the opportunistic polyomavirus JC virus (JCV). Apoptosis is a host defense mechanism to dispose of damaged cells; however, certain viruses have the ability to deregulate apoptotic pathways to complete their life cycles. One such pathway involves survivin, a member of the inhibitor of apoptosis family, which is abundantly expressed during development in proliferating tissues but should be absent in normal, terminally differentiated cells. Immunohistochemistry performed in 20 cases of PML revealed the presence of survivin in JCV-infected oligodendrocytes and bizarre astrocytes within demyelinated plaques. Survivin up-regulation was also found in oligodendroglial and astrocytic cultures infected with JCV. Cell cycle analysis and DNA laddering demonstrated a significantly lower number of cells undergoing apoptosis on JCV infection compared with noninfected cultures; small interfering RNA inhibition of survivin resulted in a dramatic increase in apoptotic cells in JCV-infected cultures. This is the first report describing the activation of survivin by JCV infection in vitro and in PML clinical cases. These observations provide new insights into the anti-apoptotic mechanisms used by JCV to complete its lytic cycle and may suggest new therapeutic targets for PML.
    Document Type:
    Reference
    Product Catalog Number:
    MAB342
    Product Catalog Name:
    Anti-Galactocerebroside Antibody, clone mGalC

  • Fibrillin-2, tenascin-C, matrilin-2, and matrilin-4 are strongly expressed in the epithelium of human granular and lattice type I corneal dystrophies. 22876117

    To determine the extracellular matrix proteins involved in the formation of human granular and lattice type I corneal stromal dystrophies, the expression patterns of fibrillin-2, tenascin-C, matrilin-2, and matrilin-4 were compared in human corneal stromal dystrophy samples.Ten cases of granular dystrophy, 7 cases of lattice dystrophy, and 6 normal corneal buttons collected during corneal transplantation were examined for their expression patterns of fibrillin-2, tenascin-C, matrilin-2, and matrilin-4 by immunohistochemistry.Highly elevated fibrillin-2, tenascin-C, matrilin-2, and matrilin-4 were observed in the epithelial layer of both granular and lattice type I dystrophies. Fibrillin-2, tenascin-C, and matrilin-4 in the granular dystrophy and all antibodies in the lattice dystrophy showed statistically significant staining in the corneal stroma (pless than 0.05). Interestingly, fibrillin-2, matrilin-2, and matrilin-4 stained significantly in amyloid plaques of lattice type 1 dystrophy.Fibrillin-2, tenascin-C, matrilin-2, and matrilin-4 may be markers of the pathogenesis of either granular or lattice type I corneal dystrophy, as revealed by immunohistochemical analysis. Each molecule seems to be involved in the regeneration and reorganization of the corneal matrix in granular and lattice type I dystrophies.
    Document Type:
    Reference
    Product Catalog Number:
    MAB2642
    Product Catalog Name:
    Anti-Fibrillin-2 Antibody, clone 48

  • Neuronal precursor-specific activity of a human doublecortin regulatory sequence. 15663475

    The doublecortin (DCX) gene encodes a 40-kDa microtubule-associated protein specifically expressed in neuronal precursors of the developing and adult CNS. Due to its specific expression pattern, attention was drawn to DCX as a marker for neuronal precursors and neurogenesis, thereby underscoring the importance of its promoter identification and promoter analysis. Here, we analysed the human DCX regulatory sequence and confined it to a 3.5-kb fragment upstream of the ATG start codon. We demonstrate by transient transfection experiments that this fragment is sufficient and specific to drive expression of reporter genes in embryonic and adult neuronal precursors. The activity of this regulatory fragment overlapped with the expression of endogenous DCX and with the young neuronal markers class III beta-tubulin isotype and microtubule-associated protein Map2ab but not with glial or oligodendroglial markers. Electrophysiological data further confirmed the immature neuronal nature of these cells. Deletions within the 3.5-kb region demonstrated the relevance of specific regions containing transcription factor-binding sites. Moreover, application of neurogenesis-related growth factors in the neuronal precursor cultures suggested the lack of direct signalling of these factors on the DCX promoter construct.
    Document Type:
    Reference
    Product Catalog Number:
    AB142

  • Protein Phosphatase 2a and glycogen synthase kinase 3 signaling modulate prepulse inhibition of the acoustic startle response by altering cortical M-Type potassium channe ... 20592205

    There is considerable interest in the regulation of sensorimotor gating, since deficits in this process could play a critical role in the symptoms of schizophrenia and other psychiatric disorders. Sensorimotor gating is often studied in humans and rodents using the prepulse inhibition of the acoustic startle response (PPI) model, in which an acoustic prepulse suppresses behavioral output to a startle-inducing stimulus. However, the molecular and neural mechanisms underlying PPI are poorly understood. Here, we show that a regulatory pathway involving protein phosphatase 2A (PP2A), glycogen synthase kinase 3 beta (GSK3beta), and their downstream target, the M-type potassium channel, regulates PPI. Mice (Mus musculus) carrying a hypomorphic allele of Ppp2r5delta, encoding a regulatory subunit of PP2A, show attenuated PPI. This PPP2R5delta reduction increases the phosphorylation of GSK3beta at serine 9, which inactivates GSK3beta, indicating that PPP2R5delta positively regulates GSK3beta activity in the brain. Consistently, genetic and pharmacological manipulations that reduce GSK3beta function attenuate PPI. The M-type potassium channel subunit, KCNQ2, is a putative GSK3beta substrate. Genetic reduction of Kcnq2 also reduces PPI, as does systemic inhibition of M-channels with linopirdine. Importantly, both the GSK3 inhibitor 3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)1H-pyrrole-2,5-dione (SB216763) and linopirdine reduce PPI when directly infused into the medial prefrontal cortex (mPFC). Whole-cell electrophysiological recordings of mPFC neurons show that SB216763 and linopirdine have similar effects on firing, and GSK3 inhibition occludes the effects of M-channel inhibition. These data support a previously uncharacterized mechanism by which PP2A/GSK3beta signaling regulates M-type potassium channel activity in the mPFC to modulate sensorimotor gating.
    Document Type:
    Reference
    Product Catalog Number:
    AB15452
    Product Catalog Name:
    Anti-MAP2 Antibody

  • Amyloid precursor-like protein 2 cleavage contributes to neuronal intranuclear inclusions and cytotoxicity in spinocerebellar ataxia-7 (SCA7). 20732423

    In spinocerebellar ataxia-7 (SCA7), a polyglutamine (polyQ) expansion in the ataxin-7 protein leads to the formation of neuronal intranuclear inclusions (NIIs) and neurodegeneration. In this study, amyloid precursor-like protein 2 (APLP2) was identified as a partner protein for ataxin-7. APLP2, belonging to the APP gene family, undergoes secretase and caspase cleavages and has been implicated in the pathogenesis of Alzheimer's disease (AD). Activated caspase-3 cleaves APP family proteins to release N-terminal fragments (NTFs) and intracellular C-terminal domains (ICDs), which can translocate into the nucleus and induce neurotoxicity in AD. Here, we report abnormal nuclear relocation of APLP2 and detection of NTFs in NIIs in SCA7. The ICDs generated by caspase-3 cleavage of APLP2 accumulate in nuclei and contribute to a cumulative toxicity when coexpressed with mutated ataxin-7. Our data suggest that the interaction between APLP2 and ataxin-7 and proteolytic processing of APLP2 may contribute to the pathogenesis of SCA7.
    Document Type:
    Reference
    Product Catalog Number:
    MAB342
    Product Catalog Name:
    Anti-Galactocerebroside Antibody, clone mGalC

  • Tau accumulation in astrocytes in progressive supranuclear palsy is a degenerative rather than a reactive process. 12200627

    Tau-immunoreactive astrocytes in progressive supranuclear palsy (PSP) have a distinctive morphology and are referred to as tufted astrocytes (TA). We hypothesized that TA may be a degenerative change in reactive astrocytes. To test this hypothesis we examined the relationship of TA to gliosis in PSP. We first examined the distribution of gliosis [glial fibrillary acid protein (GFAP)-positive astrocytes], TA, neurofibrillary tangles (NFT) and pretangles in brain sections of neuropathologically pure PSP cases. Second, we examined PSP cases complicated by infarcts or Alzheimer's disease, since these cases would have reactive astrocytes associated with lesions. We used double immunostaining for GFAP and tau for cases with vascular lesions, and triple immunostaining for GFAP, tau and beta-amyloid protein for sections with senile plaques. There was no correlation between the distribution of gliosis and TA, with gliosis prominent in globus pallidus and subthalamic nucleus, and TA prominent in motor cortex and striatum. On the other hand, gliosis paralleled the distribution of NFT, but not the distribution of pretangles, suggesting that NFT contributes to gliosis in PSP. Although reactive astrocytes were present around infarcts and senile plaques, TA were not associated with these lesions. Tau accumulation in astrocytes in PSP was not preferential to (and was actually independent of) reactive astrocytes. This is consistent with the notion that tau accumulation in astrocytes is a degenerative rather than reactive process. Unlike NFT, astrocytic degeneration does not seem to contribute to gliosis or neuronal loss in PSP, and its clinical significance remains unclear.
    Document Type:
    Reference
    Product Catalog Number:
    AB5306
    Product Catalog Name:
    Anti-Amyloid Antibody, β 37-42, aβ