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1.
In general, invasive plants are assumed to behave more aggressively in their invasive ranges than in their native range, and studies of the mechanisms of invasion often assume these differences. However, comparisons of abundances between native and invasive ranges are rarely carried out. We compared density and dispersion of the invasive plant, Centaurea melitensis (Asteraceae) in its native range and two invasive ranges of similar mediterranean-climate type. The objective was to quantify the differences in its abundance among three distant regions. We surveyed six sites in the native range (Spain) and in each of two invaded ranges (California and central Chile) for population density, relative dominance and spatial distribution of Centaurea. Centaurea occurred at higher densities in invasive sites than in native ones, with a median of 100 plants per m2 and 70 plants per m2 in California and Chile, respectively, compared to only 4 plants per m2 in Spain. Centaurea was more dominant in both invasive ranges than in the native range. Centaurea density and relative dominance were highly variable within regions. Plants in Spain were randomly dispersed, while those in both invasive ranges were more aggregated. Annual precipitation and mean annual temperature were the best predictors of Centaurea density. In California sites, density was negatively correlated with soil nutrients. The presence of at least one high-density population with near total dominance in Spain suggests that there might be ecological mechanisms for invasiveness in Centuarea that are not unique to invaded ranges. 相似文献
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Legacies of Prehistoric Agricultural Practices Within Plant and Soil Properties Across an Arid Ecosystem 总被引:1,自引:0,他引:1
Sharon J. Hall Jolene Trujillo Dana Nakase Colleen Strawhacker Melissa Kruse-Peeples Hoski Schaafsma John Briggs 《Ecosystems》2013,16(7):1273-1293
Closely integrated research between archaeologists and ecologists provides a long-term view of human land use that is rare in the ecological literature, allowing for investigation of activities that lead to enduring environmental outcomes. This extended temporal perspective is particularly important in aridlands where succession occurs slowly and ecosystem processes are mediated by abiotic, geomorphic factors. Numerous studies show that impacts from ancient human actions can persist, but few have explored the types of practices or mechanisms that lead to either transient or long-term environmental change. We compared plant and soil properties and processes from a range of landscape patch types in the Sonoran Desert of the US Southwest that supported different, well-documented prehistoric farming practices from AD 750–1300. Our results show that the types of ancient human activities that leave long-term ecological legacies in aridlands are those that fundamentally alter “slow variables” such as soil properties that regulate the timing and supply of water. Prehistoric Hohokam floodwater-irrigation practices, but not dryland farming techniques, substantially altered soil texture, which was strongly associated with desert plant community and functional composition. However, prehistoric agriculture did not consistently alter long-term nutrient availability and thus had no impact on “fast variables” such as production of seasonal annual plants that are restricted to periods of ample rainfall. In this arid ecosystem, the inverse texture model explained patterns in plant functional composition at large scales, but is less predictive of production of short-lived desert annuals that experience a more mesic precipitation regime. 相似文献
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Anna V. Miller Mark A. Hicks Wataru Nakajima Amanda C. Richardson Jolene J. Windle Hisashi Harada 《PloS one》2013,8(4)
Paclitaxel (Taxol)-induced cell death requires the intrinsic cell death pathway, but the specific participants and the precise mechanisms are poorly understood. Previous studies indicate that a BH3-only protein BIM (BCL-2 Interacting Mediator of cell death) plays a role in paclitaxel-induced apoptosis. We show here that BIM is dispensable in apoptosis with paclitaxel treatment using bim−/− MEFs (mouse embryonic fibroblasts), the bim−/− mouse breast tumor model, and shRNA-mediated down-regulation of BIM in human breast cancer cells. In contrast, both bak
−/− MEFs and human breast cancer cells in which BAK was down-regulated by shRNA were more resistant to paclitaxel. However, paclitaxel sensitivity was not affected in bax−/− MEFs or in human breast cancer cells in which BAX was down-regulated, suggesting that paclitaxel-induced apoptosis is BAK-dependent, but BAX-independent. In human breast cancer cells, paclitaxel treatment resulted in MCL-1 degradation which was prevented by a proteasome inhibitor, MG132. A Cdk inhibitor, roscovitine, blocked paclitaxel-induced MCL-1 degradation and apoptosis, suggesting that Cdk activation at mitotic arrest could induce subsequent MCL-1 degradation in a proteasome-dependent manner. BAK was associated with MCL-1 in untreated cells and became activated in concert with loss of MCL-1 expression and its release from the complex. Our data suggest that BAK is the mediator of paclitaxel-induced apoptosis and could be an alternative target for overcoming paclitaxel resistance. 相似文献
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Cao C Bai Y Holloway MJ Edgeworth RL Jackson EA Cotropia J Ugen KE 《DNA and cell biology》2004,23(12):836-841
Human monoclonal antibodies (HuMAbs) demonstrate great potential for passive immunotherapy against HIV-1. The gp41 transmembrane envelope glycoprotein of HIV has an important role in the pathogenicity of AIDS and importantly displays considerably less hypervariability than the gp120 surface envelope HIV glycoprotein, which makes it particularly a better candidate for the development of passive and active immunotherapies. The general aim of this study was to develop HuMAbs to HIV surface glycoproteins and particularly gp41. Peripheral blood mononuclear cells (PBMCs) were isolated from an HIV-seropositive long-term nondisease progressing patient. B-cells from this individual were then immortalized by Epstein-Barr virus (EBV) transformation, and antibody production was stabilized by fusion of transformed cells with a heteromyeloma. Subsets of the human heterohybridomas so generated were analyzed by ELISA. The hybridoma with the highest binding by immunoassay against gp160 was further analyzed. This hybridoma, designated as clone 37 (C37), was determined to be an IgM Kappa antibody and overlapping peptides of HIV envelope proteins (derived from the MN tissue culture line adapted HIV isolate) were used to map the specific binding domain of this HuMAb. Overlapping peptides designated 2026 (SWSNKSLDDIWNN, AA614-626), and 2027 (DDIWNNMTWMQWEREIDNYT, AA621-640) within the HIV-1 gp41 transmembrane glycoprotein were demonstrated to bind to C37 indicating that the specific binding domain for the antibody was DDIWNN. High affinity binding of C37 by ELISA to recombinant gp41 was demonstrated as well. Few IgM HuMAbs against HIV have been generated and characterized. Theoretically, because of the pentameric binding nature of IgM antibodies as well as their very efficient ability to activate complement, such reagents could have potential as anti-HIV agents. 相似文献
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MAPK signaling up-regulates the activity of hypoxia-inducible factors by its effects on p300 总被引:23,自引:0,他引:23
Sang N Stiehl DP Bohensky J Leshchinsky I Srinivas V Caro J 《The Journal of biological chemistry》2003,278(16):14013-14019
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A Farnesyltransferase Inhibitor Induces Tumor Regression in Transgenic Mice Harboring Multiple Oncogenic Mutations by Mediating Alterations in Both Cell Cycle Control and Apoptosis 总被引:6,自引:2,他引:4 下载免费PDF全文
Rebecca E. Barrington Mark A. Subler Elaine Rands Charles A. Omer Patricia J. Miller Jeffrey E. Hundley Steven K. Koester Dean A. Troyer David J. Bearss Michael W. Conner Jackson B. Gibbs Kelly Hamilton Kenneth S. Koblan Scott D. Mosser Timothy J. ONeill Michael D. Schaber Edith T. Senderak Jolene J. Windle Allen Oliff Nancy E. Kohl 《Molecular and cellular biology》1998,18(1):85-92
The farnesyltransferase inhibitor L-744,832 selectively blocks the transformed phenotype of cultured cells expressing a mutated H-ras gene and induces dramatic regression of mammary and salivary carcinomas in mouse mammary tumor virus (MMTV)–v-Ha-ras transgenic mice. To better understand how the farnesyltransferase inhibitors might be used in the treatment of human tumors, we have further explored the mechanisms by which L-744,832 induces tumor regression in a variety of transgenic mouse tumor models. We assessed whether L-744,832 induces apoptosis or alterations in cell cycle distribution and found that the tumor regression in MMTV–v-Ha-ras mice could be attributed entirely to elevation of apoptosis levels. In contrast, treatment with doxorubicin, which induces apoptosis in many tumor types, had a minimal effect on apoptosis in these tumors and resulted in a less dramatic tumor response. To determine whether functional p53 is required for L-744,832-induced apoptosis and the resultant tumor regression, MMTV–v-Ha-ras mice were interbred with p53−/− mice. Tumors in ras/p53−/− mice treated with L-744,832 regressed as efficiently as MMTV–v-Ha-ras tumors, although this response was found to be mediated by both the induction of apoptosis and an increase in G1 with a corresponding decrease in the S-phase fraction. MMTV–v-Ha-ras mice were also interbred with MMTV–c-myc mice to determine whether ras/myc tumors, which possess high levels of spontaneous apoptosis, have the potential to regress through a further increase in apoptosis levels. The ras/myc tumors were found to respond nearly as efficiently to L-744,832 treatment as the MMTV–v-Ha-ras tumors, although no induction of apoptosis was observed. Rather, the tumor regression in the ras/myc mice was found to be mediated by a large reduction in the S-phase fraction. In contrast, treatment of transgenic mice harboring an activated MMTV–c-neu gene did not result in tumor regression. These results demonstrate that a farnesyltransferase inhibitor can induce regression of v-Ha-ras-bearing tumors by multiple mechanisms, including the activation of a suppressed apoptotic pathway, which is largely p53 independent, or by cell cycle alterations, depending upon the presence of various other oncogenic genetic alterations. 相似文献
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Dadi Jiang Catherine I. Dumur H. Davis Massey Viswanathan Ramakrishnan Mark A. Subler Jolene J. Windle 《PloS one》2015,10(2)
p53 is an important tumor suppressor gene which is mutated in ~50% of all human cancers. Some of these mutants appear to have acquired novel functions beyond merely losing wild-type functions. To investigate these gain-of-function effects in vivo, we generated mice of three different genotypes: MMTV-Hras/p53+/+, MMTV-Hras/p53-/-, and MMTV-Hras/p53R172H/R172H. Salivary tumors from these mice were characterized with regard to age of tumor onset, tumor growth rates, cell cycle distribution, apoptotic levels, tumor histopathology, as well as response to doxorubicin treatment. Microarray analysis was also performed to profile gene expression. The MMTV-Hras/p53-/- and MMTV-Hras/p53R172H/R172H mice displayed similar properties with regard to age of tumor onset, tumor growth rates, tumor histopathology, and response to doxorubicin, while both groups were clearly distinct from the MMTV-Hras/p53+/+ mice by these measurements. In addition, the gene expression profiles of the MMTV-Hras/p53-/- and MMTV-Hras/p53R172H/R172H tumors were tightly clustered, and clearly distinct from the profiles of the MMTV-Hras/p53+/+ tumors. Only a small group of genes showing differential expression between the MMTV-Hras/p53-/- and MMTV-Hras/p53R172H/R172H tumors, that did not appear to be regulated by wild-type p53, were identified. Taken together, these results indicate that in this MMTV-Hras-driven salivary tumor model, the major effect of the p53 R172H mutant is due to the loss of wild-type p53 function, with little or no gain-of-function effect on tumorigenesis, which may be explained by the tissue- and tumor type-specific properties of this gain-of-function mutant of p53. 相似文献
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Braden Kuo Manoj Bhasin Jolene Jacquart Matthew A. Scult Lauren Slipp Eric Isaac Kagan Riklin Veronique Lepoutre Nicole Comosa Beth-Ann Norton Allison Dassatti Jessica Rosenblum Andrea H. Thurler Brian C. Surjanhata Nicole N. Hasheminejad Leslee Kagan Ellen Slawsby Sowmya R. Rao Eric A. Macklin Gregory L. Fricchione Herbert Benson Towia A. Libermann Joshua Korzenik John W. Denninger 《PloS one》2015,10(4)