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- Codilean, A. T., et al.
(författare)
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OCTOPUS database (v.2)
- 2022
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Ingår i: Earth System Science Data. - : Copernicus GmbH. - 1866-3508 .- 1866-3516. ; 14:8, s. 3695-3713
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Tidskriftsartikel (refereegranskat)abstract
- OCTOPUS v.2 is an Open Geospatial Consortium (OGC) compliant web-enabled database that allows users to visualise, query, and download cosmogenic radionuclide, luminescence, and radiocarbon ages and denudation rates associated with erosional landscapes, Quaternary depositional landforms, and archaeological records, along with ancillary geospatial (vector and raster) data layers. The database follows the FAIR (Findability, Accessibility, Interoperability, and Reuse) data principles and is based on open-source software deployed on the Google Cloud Platform. Data stored in the database can be accessed via a custom-built web interface and via desktop geographic information system (GIS) applications that support OGC data access protocols. OCTOPUS v.2 hosts five major data collections. CRN Denudation and ExpAge consist of published cosmogenic Be-10 and Al-26 measurements in modern fluvial sediment and glacial samples respectively. Both collections have a global extent; however, in addition to geospatial vector layers, CRN Denudation also incorporates raster layers, including a digital elevation model, gradient raster, flow direction and flow accumulation rasters, atmospheric pressure raster, and CRN production scaling and topographic shielding factor rasters. SahulSed consists of published optically stimulated luminescence (OSL) and thermoluminescence (TL) ages for fluvial, aeolian, and lacustrine sedimentary records across the Australian mainland and Tasmania. SahulArch consists of published OSL, TL, and radiocarbon ages for archaeological records, and FosSahul consists of published late-Quaternary records of direct and indirect non-human vertebrate (mega)fauna fossil ages that have been systematically quality rated. Supporting data are comprehensive and include bibliographic, contextual, and sample-preparation- and measurement-related information. In the case of cosmogenic radionuclide data, OCTOPUS also includes all necessary information and input files for the recalculation of denudation rates using the open-source program CAIRN. OCTOPUS v.2 and its associated data curation framework allow for valuable legacy data to be harnessed that would otherwise be lost to the research community. The database can be accessed at https://octopusdata.org (last access: 1 July 2022). The individual data collections can also be accessed via their respective digital object identifiers (DOIs) (see Table 1).
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| 2. |
- Arsura, Marcello, et al.
(författare)
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Transient activation of NF-kappaB through a TAK1/IKK kinase pathway by TGF-beta1 inhibits AP-1/SMAD signaling and apoptosis : implications in liver tumor formation.
- 2003
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 22:3, s. 412-425
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Tidskriftsartikel (refereegranskat)abstract
- NF-kappaB has been implicated in the regulation of apoptosis, a key mechanism of normal and malignant growth control. Previously, we demonstrated that inhibition of NF-kappaB activity by TGF-beta1 leads directly to induction of apoptosis of murine B-cell lymphomas and hepatocytes. Thus, we were surprised to determine that NF-kappaB is transiently activated in response to TGF-beta1 treatment. Here we elucidate the mechanism of TGF-beta1-mediated regulation of NF-kappaB and induction of apoptosis in epithelial cells. We report that TGF-beta1 activates IKK kinase, which mediates IkappaB-alpha phosphorylation. In turn, the activation of IKK following TGF-beta1 treatment is mediated by the TAK1 kinase. As a result of NF-kappaB activation, IkappaB-alpha mRNA and protein levels are increased leading to postrepression of NF-kappaB and induction of cell death. Inhibition of NF-kappaB following TGF-beta1 treatment increased AP-1 complex transcriptional activity through sustained c-Jun phosphorylation, thereby potentiating AP-1/SMADs-mediated cell killing. Furthermore, TGF-beta1-mediated upregulation of Smad7 appeared independent of NF-kappaB. In hepatocellular carcinomas of TGF-beta1 or TGF-alpha/c-myc transgenic mice, we observed constitutive activation of NF-kappaB that led to inhibition of JNK signaling. Overall, our data illustrate an autocrine mechanism based on the ability of IKK/NF-kappaB/IkappaB-alpha signaling to negatively regulate NF-kappaB levels thereby permitting TGF-beta1-induced apoptosis through AP-1 activity.
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