1,728,429 research outputs found
Knowledge-aided STAP in heterogeneous clutter using a hierarchical bayesian algorithm
No full textThis paper addresses the problem of estimating the covariance matrix of a primary vector from heterogeneous samples and some prior knowledge, under the framework of knowledge-aided space-time adaptive processing (KA-STAP). More precisely, a Gaussian scenario is considered where the covariance matrix of the secondary data may differ from the one of interest. Additionally, some knowledge on the primary data is supposed to be available and summarized into a prior matrix. Two KA-estimation schemes are presented in a Bayesian framework whereby the minimum mean square error (MMSE) estimates are derived. The first scheme is an extension of a previous work and takes into account the non-homogeneity via an original relation. {In search of simplicity and to reduce the computational load, a second estimation scheme, less complex, is proposed and omits the fact that the environment may be heterogeneous.} Along the estimation process, not only the covariance matrix is estimated but also some parameters representing the degree of \emph{a priori} and/or the degree of heterogeneity. Performance of the two approaches are then compared using STAP synthetic data. STAP filter shapes are analyzed and also compared with a colored loading technique
STAP
No full text<p>The comparative analysis of ss-rRNA sequences is one of the most powerful approaches for studying phylogenetic relationships among all organisms. Our ss-rRNA Taxonomy Assigning Pipeline (STAP) combines publicly available packages such as, PHYML, BLASTN, and CLUSTALW with our own automatic alignment masking and tree parsing programs. STAP makes automatic taxonomic assignments for ss-rRNAs based on neighbor-joining or maximum likelihood phylogenetic trees rather than on the top BLASTN hits, and thus its results are more reliable and accurate. Most importantly, the automation yields results comparable to those achievable by manual analysis, yet offers speed and capacity that are unattainable by manual efforts.</p>
<p>First, ss-rRNA sequences obtained either by PCR of environmental samples or by metagenomic shotgun sequencing are searched against our ss-rRNA database by BLASTN to select a related data set. STAP then automatically generates, masks, and trims the multiple sequence alignments. Next, it builds a phylogenetic tree by either the maximum likelihood or neighbor-joining method. Automated analysis of the tree yields taxonomic assignments for each query sequence.</p>
<p>A paper describing STAP has been published (7/2/08) in PLoS One.</p>
<p>• Wu D, Hartman A, Ward N, Eisen JA (2008) An Automated Phylogenetic Tree-Based Small Subunit rRNA Taxonomy and Alignment Pipeline (STAP). PLoS ONE 3(7): e2566. doi:10.1371/ journal.pone.0002566</p>
<p> </p>
<p>There is only one file (STAP.zip) in this package, unzip it and the README.pdf file explains how to install STAP.</p
Brk phosphorylates and regulates STAP-2 functions
No full textSignal transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein that contains Pleckstrin and Src homology 2 (SH2)-like domains as well as a YXXQ motif in its C-terminal region. STAP-2 is also known as breast tumor kinase (Brk) substrate (BKS). Our previous studies revealed that STAP-2 binds to signal transducer and activator of transcription 3 (STAT3) and STAT5, and regulates the signaling pathways downstream of them. In the present study, we identified tyrosine-250 (Tyr250) in STAP-2 as a major site of phosphorylation by Brk, using a series of STAP-2 YF mutants and anti-phospho-STAP-2 Tyr250 antibody. Furthermore, overexpression of the STAP-2 Y250F mutant protein affected Brk-mediated STAT3 activation. Importantly, small-interfering RNA-mediated reduction of endogenous STAP-2 expression decreased Brk-mediated STAT3 activation. Taken together, our findings demonstrate that STAP-2 is phosphorylated at Tyr250 by Brk, and plays an important role in Brk-mediated STAT3 activation
Joint allocation of transmit-receive resource for MIMO-STAP
No full textAiming to address the issue of target detection performance degradation due to limited resources of airborne multiple-in multiple-out (MIMO) radar, a joint allocation method of transmit-receive spatial-temporal resources is developed to ameliorate the detection performance of MIMO radar-based space-time adaptive processing (STAP). A MIMO-STAP model containing space-time resources to be configured is firstly constructed. Then, with the criterion of maximizing the output signal-to-clutter-noise ratio (SCNR), a problem to jointly design the transmitting and receiving elements, transmitting pulses, baseband waveform, and receiving weight is formulated. To tackle the resultant complex nonlinear joint optimization issue, it is decomposed into four independent sub-problems based on the alternating iteration strategy, then the sub-problems are efficiently solved by corresponding optimization techniques, i.e., the optimal antenna pulse subset can be selected by employing the sequential convex approximation (SCA) method, the transmitting waveform is optimized using the semi-positive definite program (SDP) and randomization method, and the receiving weight is designed under the minimum variance distortionless response (MVDR) criteria, which work iteratively to achieve an effective solution to the joint optimization problem. Extensive simulation results verify the effectiveness of the developed algorithm
Cbl controls STAP-2 activity through protein degradation
No full textSignal transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein that contains pleckstrin and Src homology 2 (SH2)-like domains as well as a YXXQ motif in its C-terminal region. Our previous study in T cells demonstrated that STAP-2 influences FAK protein levels through recruitment of E3 ubiquitin ligase, Cbl, to FAK. In the present study, we found that Cbl directly controls the protein levels and activity of STAP-2. STAP-2 physically interacted with Cbl through its PH and SH2-like domains. Small-interfering RNA-mediated reduction of endogenous Cbl restored STAP-2 protein levels. In contrast, over-expression of Cbl induced STAP-2 degradation. Importantly, Cbl-mediated regulation of STAP-2 protein levels affected Brk/STAP-2-induced STAT3 activation. These results indicate that Cbl regulates STAP-2 protein levels and Brk/STAP-2-mediated STAT3 activation
STAP-2 interacts with and modulates BCR-ABL-mediated tumorigenesis
No full textIn chronic myeloid leukemia (CML), the BCR-ABL fusion oncoprotein activates multiple pathways involved in cell survival, growth promotion and disease progression. In this report, we show that the signal transducing adaptor protein-2 (STAP-2) is involved in BCR-ABL activity. We demonstrate that STAP-2 bound to BCR-ABL, and BCR and ABL proteins, depending on the STAP-2 Src homology 2-like domain. BCR-ABL phosphorylates STAP-2 Tyr250 and the phosphorylated STAP-2 in turn up-regulated BCR-ABL phosphorylation, leading to enhanced activation of downstream signaling molecules including ERK, STAT5, BCL-xL and BCL-2. In addition, STAP-2 interacts with BCR-ABL to alter chemokine receptor expression leading to downregulation of CXCR4 and upregulation of CCR7. The interaction between STAP-2 and BCR-ABL plays a crucial role in conferring a growth advantage and resistance to imatinib, a BCR-ABL inhibitor, as well as tumor progression. Notably, mice injected with BCR-ABL/STAP-2-expressing Ba/F3 cells developed lymph node enlargement and hepatosplenomegaly. Moreover, suppression of STAP-2 in K562 CML cells resulted in no tumor formation in mice. Our results demonstrate a critical contribution of STAP-2 in BCR-ABL activity, and suggest that STAP-2 might be an important candidate for drug development for patients with CML. Further, the expression of STAP-2 provides useful information for estimating the characteristics of individual CML clones
Physical and functional interactions between STAP-2/BKS and STAT5.
No full textSignal-transducing adaptor protein family of proteins (STAPs), which currently contains two members, are proposed to be adaptor molecules because of their pleckstrin homology (PH) and Src-homology 2 (SH2)-like domains. STAP-1 has been shown to interact with STAT5 and the tyrosine kinase Tec. With regard to STAP-2/BKS functions, immunoprecipitation experiments and intracellular stainings revealed STAP-2/BKS binds STAT5 in several types of cells. Mutational studies revealed that the PH- and SH2-like domains of STAP-2/BKS interacted with the C-terminal region of STAT5. STAP-2/BKS and STAT5 were found to constitutively co-localize in the cytoplasm of resting cells, but STAP-2/BKS was found to dissociate upon STAT5 phosphorylation, suggesting a role in regulating signaling of STAT5. The physiological role of these interactions is not fully understood, but in studies of overexpression of STAP-2/BKS, cytokine-induced tyrosine phosphorylation and transcriptional activation of STAT5 was diminished. In addition, thymocytes from STAP-2/BKS-deficient mice showed the enhanced interleukin-2-dependent cell growth. Taken together, STAP-2/BKS is an additional modulator of STAT5-mediated signaling
STAP-2 interacts with Pyk2 and enhances Pyk2 activity in T-cells
No full textSTAP-2 is an adaptor molecule regulating several signaling pathways, including TLRs and cytokine/chemokine receptors in immune cells. We previously reported that STAP-2 enhances SDF-1 a-induced Vavl/Racl-mediated T-cell chemotaxis. However, the detailed mechanisms of STAP-2 involvement in enhancing T-cell chemotaxis remain unknown. In the present study, we demonstrate that STAP-2 directly interacts with Pyk2, which is a key molecule in the regulation of SDF-la/CXCR4-mediated T-cell chemotaxis, and increases phosphorylation of Pyk2. Pyk2 itself can induce STAP-2 Y250 phosphorylation, and this phosphorylation is critical for maximal interactions between STAP-2 and Pyk2. Finally, SDF-1 a induced T-cell chemotaxis is inhibited by treatment with Pyk2 siRNA or AG17, an inhibitor of Pyk2, in Jurkat cells overexpressing STAP-2. Taken together, the Pyk2/STAP-2 interaction is a novel mechanism to regulate SDF-1 alpha-dependent T-cell chemotaxis
Positive interactions between STAP-1 and BCR-ABL influence chronic myeloid leukemia cell proliferation and survival
No full textChronic myeloid leukemia (CML) is a clonal disease characterized by the presence of the Philadelphia chromosome and its oncogenic product, BCR-ABL, which activates multiple pathways involved in cell survival, growth promotion, and disease progression. We recently reported that signal-transducing adaptor protein 1 (STAP-1) is upregulated in CML stem cells (LSCs) and functions to reduce the apoptosis of CML LSCs by upregulating the STAT5-downstream anti-apoptotic genes. In this study, we demonstrate the detailed molecular interactions among BCR-ABL, STAP-1, and signal transducer and activator of transcription 5 (STAT5). Studies with deletion mutants have revealed that STAP-1 interacts with BCR-ABL and STAT5a through its SH2 and PH domains, respectively, suggesting the possible role of STAP-1 as a scaffold protein. Furthermore, the binding of STAP-1 to BCR-ABL stabilizes the BCR-ABL protein in CML cells. Since STAP-1 is highly expressed in CML cells, we also analyzed the STAP-1 promoter activity using a luciferase reporter construct and found that NFATc1 is involved in activating the STAP-1 promoter and inducing STAP-1 mRNA expression. Our results demonstrate that STAP-1 contributes to the BCR-ABL/STAT5 and BCR-ABL/Ca2+/NFAT signals to induce proliferation and STAP-1 mRNA expression in CML cells, respectively
Core Outcome Set-STAndardised Protocol Items: The COS-STAP Statement
No full textBackground: Several hundred core outcome set (COS) projects have been systematically identified to date which, if adopted, ensure that researchers measure and report those outcomes that are most likely to be relevant to users of their research. The uptake of a COS by COS users will depend in part on the transparency and robustness of the methods used in the COS development study, which would be increased by the use of a standardised protocol. This article describes the development of the COS-STAP (Core Outcome Set-STAndardised Protocol Items) Statement for the content of a COS development study protocol. Methods: The COS-STAP Statement was developed following the Enhancing the Quality and Transparency Of Health Research (EQUATOR) Network's methodological framework for guideline development. This included an initial item generation stage, a two-round Delphi survey involving more than 150 participants representing three stakeholder groups (COS developers, journal editors and patient and public involvement researchers interested in COS development), followed by a consensus meeting with eight voting participants. Results: The COS-STAP Statement consists of a checklist of 13 items considered essential documentation in a protocol, outlining the scope of the COS, stakeholder involvement, COS development plans and consensus processes. Conclusions: Journal editors and peer reviewers can use the guidance to assess the completeness of a COS development study protocol submitted for publication. By providing guidance for key content, the COS-STAP Statement will enhance the drafting of high-quality protocols and determine how the COS development study will be carried out
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