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  • Proceedings of the National Academy of Sciences  (26)
  • 1
    Online-Ressource
    Online-Ressource
    Isolation of a rat liver delta-aminolevulinate dehydrase (ALAD) cDNA clone: evidence for unequal ALAD gene dosage among inbred mouse strains.
    Proceedings of the National Academy of Sciences ; 1986
    In:  Proceedings of the National Academy of Sciences Vol. 83, No. 15 ( 1986-08), p. 5568-5572
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 83, No. 15 ( 1986-08), p. 5568-5572
    Kurzfassung: We have isolated several cDNA clones encoding delta-aminolevulinate dehydrase [ALAD; porphobilinogen synthase; 5-aminolevulinate hydro-lyase (adding 5-aminolevulinate and cyclizing), EC 4.2.1.24], the second enzyme in the heme biosynthetic pathway. We used a rabbit polyclonal antibody developed against the purified 35-kDa subunit of rat liver ALAD to screen a lambda gt11 cDNA expression library constructed from rat liver mRNA. A prototype clone (ALAD-1) contained a 680-base-pair insert and expressed a 140-kDa beta-galactosidase gene cDNA insert fusion protein immunoreactive with both polyclonal and monoclonal anti-ALAD. Identity of ALAD-1 was verified by hydridization to ALAD mRNA that had been enriched via immunopurification of rat liver polysomes with anti-ALAD. Intensity of such hybridization to a 1500-nucleotide-long mRNA was approximately equal to 200-fold greater than that realized with whole liver mRNA, a result consistent with the degree of immunoenrichment of ALAD mRNA found independently by analysis of cell-free translation products. A second ALAD cDNA clone (ALAD-3) was isolated when the rat liver cDNA expression library was rescreened with ALAD-1. The identity of both ALAD cDNA clones was established by correspondence between their nucleotide sequence and the reported amino-terminal protein sequence of bovine ALAD. Hybridization of ALAD cDNA to mouse genomic DNA indicates that the previously unexplained incremental differences in ALAD enzymatic activity among inbred mouse strains has arisen through alterations in ALAD gene dose.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.83.15.5568
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1986
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    Joint analysis of stressors and ecosystem services to enhance restoration effectiveness
    Proceedings of the National Academy of Sciences ; 2013
    In:  Proceedings of the National Academy of Sciences Vol. 110, No. 1 ( 2013-01-02), p. 372-377
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 110, No. 1 ( 2013-01-02), p. 372-377
    Kurzfassung: With increasing pressure placed on natural systems by growing human populations, both scientists and resource managers need a better understanding of the relationships between cumulative stress from human activities and valued ecosystem services. Societies often seek to mitigate threats to these services through large-scale, costly restoration projects, such as the over one billion dollar Great Lakes Restoration Initiative currently underway. To help inform these efforts, we merged high-resolution spatial analyses of environmental stressors with mapping of ecosystem services for all five Great Lakes. Cumulative ecosystem stress is highest in near-shore habitats, but also extends offshore in Lakes Erie, Ontario, and Michigan. Variation in cumulative stress is driven largely by spatial concordance among multiple stressors, indicating the importance of considering all stressors when planning restoration activities. In addition, highly stressed areas reflect numerous different combinations of stressors rather than a single suite of problems, suggesting that a detailed understanding of the stressors needing alleviation could improve restoration planning. We also find that many important areas for fisheries and recreation are subject to high stress, indicating that ecosystem degradation could be threatening key services. Current restoration efforts have targeted high-stress sites almost exclusively, but generally without knowledge of the full range of stressors affecting these locations or differences among sites in service provisioning. Our results demonstrate that joint spatial analysis of stressors and ecosystem services can provide a critical foundation for maximizing social and ecological benefits from restoration investments.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1213841110
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2013
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    Tracing of the In Vivo Path from Amino Acid to Protein
    Proceedings of the National Academy of Sciences ; 1958
    In:  Proceedings of the National Academy of Sciences Vol. 44, No. 2 ( 1958-02), p. 92-97
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 44, No. 2 ( 1958-02), p. 92-97
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.44.2.92
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1958
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    The maximum rate of mammal evolution
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 11 ( 2012-03-13), p. 4187-4190
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 11 ( 2012-03-13), p. 4187-4190
    Kurzfassung: How fast can a mammal evolve from the size of a mouse to the size of an elephant? Achieving such a large transformation calls for major biological reorganization. Thus, the speed at which this occurs has important implications for extensive faunal changes, including adaptive radiations and recovery from mass extinctions. To quantify the pace of large-scale evolution we developed a metric, clade maximum rate, which represents the maximum evolutionary rate of a trait within a clade. We applied this metric to body mass evolution in mammals over the last 70 million years, during which multiple large evolutionary transitions occurred in oceans and on continents and islands. Our computations suggest that it took a minimum of 1.6, 5.1, and 10 million generations for terrestrial mammal mass to increase 100-, and 1,000-, and 5,000-fold, respectively. Values for whales were down to half the length (i.e., 1.1, 3, and 5 million generations), perhaps due to the reduced mechanical constraints of living in an aquatic environment. When differences in generation time are considered, we find an exponential increase in maximum mammal body mass during the 35 million years following the Cretaceous–Paleogene (K–Pg) extinction event. Our results also indicate a basic asymmetry in macroevolution: very large decreases (such as extreme insular dwarfism) can happen at more than 10 times the rate of increases. Our findings allow more rigorous comparisons of microevolutionary and macroevolutionary patterns and processes.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1120774109
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2012
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    Fusion of influenza virus membranes with liposomes at pH 7.5.
    Proceedings of the National Academy of Sciences ; 1985
    In:  Proceedings of the National Academy of Sciences Vol. 82, No. 14 ( 1985-07), p. 4611-4615
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 82, No. 14 ( 1985-07), p. 4611-4615
    Kurzfassung: Influenza virus X-31 (H3N2) membranes fuse with liposomes containing ganglioside GD1a at pH 7.5. Fusion was demonstrated by electron microscopy and also can be measured by counting the labeled virus proteins incorporated into liposomes after bound virus has been removed. Liposomes composed of lipids that have no net charge behave as reported by other investigators and do not fuse with influenza X-31 membranes at neutral pH, but they do fuse at low pH. Therefore, the liposomal composition is a factor in whether liposomes fuse with influenza virus membranes at neutral pH, probably by determining whether binding occurs. The liposomal composition necessary for fusion at neutral pH needs to be individualized for each influenza subtype. To establish that a virus requires low pH for membrane fusion, it is first necessary to establish that fusion does not occur at neutral pH under conditions where adequate binding occurs.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.82.14.4611
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1985
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Subunit interaction during catalysis: alternating site cooperativity in photophosphorylation shown by substrate modulation of [18O]ATP species formation.
    Proceedings of the National Academy of Sciences ; 1979
    In:  Proceedings of the National Academy of Sciences Vol. 76, No. 8 ( 1979-08), p. 3646-3650
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 76, No. 8 ( 1979-08), p. 3646-3650
    Kurzfassung: Pronounced substrate modulation of incorporation of water oxygen into ATP formed by photophosphorylation is observed, as measured by 31P NMR analysis of products formed from ADP and highly 18O-labeled Pi. A marked increase occurs in oxygen exchange per ATP formed as ADP or Pi concentration is decreased. This is explainable by the binding-change mechanism for ATP synthesis, in which the energy-linked release of ATP from one site requires the binding of ADP and Pi at an alternate site. Analysis of the distribution of 18O-labeled species arising from the ATP formed eliminates explanations for substrate modulation based on preexisting or induced enzyme heterogeneity. Furthermore, the results, together with other related findings, make participation of control sites unlikely. The occurrence of alternating site catalysis cooperativity in ATP synthesis by chloroplasts thus appears to be reasonably well established.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.76.8.3646
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1979
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    Modulation of stoichiometry of the sarcoplasmic reticulum calcium pump may enhance thermodynamic efficiency.
    Proceedings of the National Academy of Sciences ; 1985
    In:  Proceedings of the National Academy of Sciences Vol. 82, No. 1 ( 1985-01), p. 98-101
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 82, No. 1 ( 1985-01), p. 98-101
    Kurzfassung: The coupling of calcium transport to ATP hydrolysis in rabbit muscle sarcoplasmic reticulum vesicles was determined under steady-state conditions in the presence of 5 mM oxalate and using various concentrations of vesicles to modulate the concentration of free Ca2+ in the medium. This experimental approach takes advantage of the fact that at high concentrations of vesicles the slow rate of liberation of Ca2+ from its oxalate complex becomes rate limiting for pumping, therefore pushing the steady-state levels of this cation to very low values. A reduction in the number of calcium ions transported per ATP cleaved from a value near 2 at a low concentration of vesicles (high medium Ca2+ concentration) to a limiting value of about 1 at a very high concentration of vesicles (low medium Ca2+ concentration) was observed. A marked decrease in the specific ATPase activity was also found to take place as the concentration of the sarcoplasmic reticulum vesicles was increased to high levels and the concentration of medium Ca2+ declined. The data presented indicate that binding of 1 Ca2+ to the sarcoplasmic reticulum ATPase is sufficient to activate the pump. Furthermore, these findings support the existence of a control mechanism for the calcium pump that helps to avoid a futile cycle of ATP cleavage with no net transport of calcium and that increases the pumping capability at low concentrations of free Ca2+.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.82.1.98
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1985
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Online-Ressource
    Cyclic AMP mediates the direct antiproliferative action of mismatched double-stranded RNA.
    Proceedings of the National Academy of Sciences ; 1991
    In:  Proceedings of the National Academy of Sciences Vol. 88, No. 3 ( 1991-02), p. 906-910
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 88, No. 3 ( 1991-02), p. 906-910
    Kurzfassung: Previous experiments have demonstrated that double-stranded RNAs (dsRNAs) can exert an antiproliferative effect on human tumor cells, independent of interferon (IFN) induction. However, the mechanism by which dsRNAs inhibit tumor growth has not been elucidated. As a first step in determining the molecular events responsible for growth arrest, we have explored the role of signal transduction through the cAMP system in the antiproliferative effect of the mismatched dsRNA, r(I)n.r(C12,U)n (Ampligen). These studies utilized the human glioma cell line A1235, which does not produce detectable levels of IFN-alpha, -beta, or -gamma in response to mismatched dsRNA treatment. Treatment of A1235 cells with mismatched dsRNA in combination with either 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), which inhibits cAMP-dependent protein kinase and protein kinase C, or N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA1004), which preferentially inhibits the cAMP-dependent protein kinase, yielded an antagonism of the mismatched dsRNA-induced antiproliferative effect. Measurement of adenylate cyclase activation showed a dose-dependent increase in activity at antiproliferative mismatched dsRNA concentrations, but not at lower, nonantiproliferative doses. This increase in activity was rapid, seen as early as 30 sec after initiation of treatment, and it was sustained at peak levels for 1-2 hr. Analysis of the intracellular cAMP concentration gave similar kinetics of induction. Exposure of cells to the stable cAMP analogue dibutyryl cAMP yielded dose-dependent inhibition of cell growth. The cAMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine also inhibited proliferation. In contrast, neither H-7 nor HA1004 had an effect on growth inhibition induced by human natural IFN-alpha treatment. In addition, antiproliferative doses of IFN-alpha did not increase cAMP concentrations. These results indicate that the cAMP system is utilized by mismatched dsRNA as an early signal transduction mechanism for growth control. Furthermore, the antiproliferative effects induced by mismatched dsRNA and IFN can occur by different mechanisms of action.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.88.3.906
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 1991
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Online-Ressource
    The α-synuclein hereditary mutation E46K unlocks a more stable, pathogenic fibril structure
    Proceedings of the National Academy of Sciences ; 2020
    In:  Proceedings of the National Academy of Sciences Vol. 117, No. 7 ( 2020-02-18), p. 3592-3602
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 117, No. 7 ( 2020-02-18), p. 3592-3602
    Kurzfassung: Aggregation of α-synuclein is a defining molecular feature of Parkinson’s disease, Lewy body dementia, and multiple systems atrophy. Hereditary mutations in α-synuclein are linked to both Parkinson’s disease and Lewy body dementia; in particular, patients bearing the E46K disease mutation manifest a clinical picture of parkinsonism and Lewy body dementia, and E46K creates more pathogenic fibrils in vitro. Understanding the effect of these hereditary mutations on α-synuclein fibril structure is fundamental to α-synuclein biology. We therefore determined the cryo-electron microscopy (cryo-EM) structure of α-synuclein fibrils containing the hereditary E46K mutation. The 2.5-Å structure reveals a symmetric double protofilament in which the molecules adopt a vastly rearranged, lower energy fold compared to wild-type fibrils. We propose that the E46K misfolding pathway avoids electrostatic repulsion between K46 and K80, a residue pair which form the E46-K80 salt bridge in the wild-type fibril structure. We hypothesize that, under our conditions, the wild-type fold does not reach this deeper energy well of the E46K fold because the E46-K80 salt bridge diverts α-synuclein into a kinetic trap—a shallower, more accessible energy minimum. The E46K mutation apparently unlocks a more stable and pathogenic fibril structure.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1917914117
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2020
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Drivers and hotspots of extinction risk in marine mammals
    Proceedings of the National Academy of Sciences ; 2012
    In:  Proceedings of the National Academy of Sciences Vol. 109, No. 9 ( 2012-02-28), p. 3395-3400
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 109, No. 9 ( 2012-02-28), p. 3395-3400
    Kurzfassung: The world's oceans are undergoing profound changes as a result of human activities. However, the consequences of escalating human impacts on marine mammal biodiversity remain poorly understood. The International Union for the Conservation of Nature (IUCN) identifies 25% of marine mammals as at risk of extinction, but the conservation status of nearly 40% of marine mammals remains unknown due to insufficient data. Predictive models of extinction risk are crucial to informing present and future conservation needs, yet such models have not been developed for marine mammals. In this paper, we: ( i ) used powerful machine-learning and spatial-modeling approaches to understand the intrinsic and extrinsic drivers of marine mammal extinction risk; ( ii ) used this information to predict risk across all marine mammals, including IUCN “Data Deficient” species; and ( iii ) conducted a spatially explicit assessment of these results to understand how risk is distributed across the world's oceans. Rate of offspring production was the most important predictor of risk. Additional predictors included taxonomic group, small geographic range area, and small social group size. Although the interaction of both intrinsic and extrinsic variables was important in predicting risk, overall, intrinsic traits were more important than extrinsic variables. In addition to the 32 species already on the IUCN Red List, our model identified 15 more species, suggesting that 37% of all marine mammals are at risk of extinction. Most at-risk species occur in coastal areas and in productive regions of the high seas. We identify 13 global hotspots of risk and show how they overlap with human impacts and Marine Protected Areas.
    Materialart: Online-Ressource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1121469109
    RVK:
    TA 1000
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Proceedings of the National Academy of Sciences
    Publikationsdatum: 2012
    ZDB Id: 209104-5
    ZDB Id: 1461794-8
    SSG: 11
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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