478,436 research outputs found
LIN28B (lin-28 homolog B (C. elegans))
Full text linkReview on LIN28B (lin-28 homolog B (C. elegans)), with data on DNA, on the protein encoded, and where the gene is implicated
A single E-box in the <i>Cel-lin-3</i> CRM is not sufficient for <i>lin-3</i> expression in the anchor cell of <i>C</i>. <i>elegans</i>.
No full text(A) New cis-regulatory lin-3 alleles with deleted E-boxL and NHR or NHR and E-boxR. (B) Quantification of vulval induction in these new mutants. Note the complete absence of any induction in the recovered lin-3 alleles (n>30). Scorings of lin-3(1417) animals are the same as those reported in Fig 5 and are used here to indicate that this mutation leads to vulval hypo-induction rather than no induction at all. (C-D) smFISH in lin-3(mf72) (C) and N2 (D) animals. Green spots correspond to lin-3 transcripts and red spots to lag-2 that is used as an anchor cell marker. Blue is DAPI staining of nuclei. Note the absence of lin-3 expression in the anchor cell in the lin-3(mf72) mutant animal. Absence of lin-3 signal in the anchor cell was also confirmed for the other lin-3 alleles.</p
Branching fraction and CP asymmetry of the decays B+→K0Sπ+ and B+→K0SK+
Full text linkAn analysis of B+ → K0
Sπ+ and B+ → K0
S K+ decays is performed with the LHCb experiment. The pp
collision data used correspond to integrated luminosities of 1 fb−1 and 2 fb−1 collected at centre-ofmass
energies of
√
s = 7 TeV and
√
s = 8 TeV, respectively. The ratio of branching fractions and the
direct CP asymmetries are measured to be B(B+ → K0
S K+
)/B(B+ → K0
Sπ+
) = 0.064 ± 0.009 (stat.) ±
0.004 (syst.), ACP(B+ → K0
Sπ+
) = −0.022 ± 0.025 (stat.) ± 0.010 (syst.) and ACP(B+ → K0
S K+
) =
−0.21 ± 0.14 (stat.) ± 0.01 (syst.). The data sample taken at
√
s = 7 TeV is used to search for
B+
c
→ K0
S K+ decays and results in the upper limit ( fc · B(B+
c
→ K0
S K+
))/( fu · B(B+ → K0
Sπ+
)) <
5.8 × 10−2 at 90% confidence level, where fc and fu denote the hadronisation fractions of a ¯b
quark
into a B+
c or a B+ meson, respectively
"Third Generation"-Type Functional Tris(2-pyridyl)borate Ligands and their Transition-Metal Complexes
No full textPhenyltris(2-pyridyl)borates (Tpyb) are a promising class of tripodal “scorpionate”-type ligands with potential utility in the development of transition metal complexes with interesting optical, electronic or magnetic properties, and as building blocks to metallosupramolecular polymers. We report here a new class of “third generation”-type Tpyb ligands that contain different functional groups attached to the boron-bound aryl moiety. The synthesis, characterization and metal ion complexation behavior of ligands with iodo and trimethylsilyl groups is discussed. The electrochemical and absorption characteristics of the corresponding low-spin Fe(II) and Ru(II) complexes are compared. We demonstrate the further elaboration of the iodo derivatives with alkynes via Sonogashira-Hagihara coupling, a process that proceeds with high yield for the Fe(II) and Ru(II) complexes, but not for the free ligand. The borylation of the silyl-substituted Ru(II) complex with BBr3 was also investigated. In addition to the expected borylation product, Ru(Tpyb-Bpin)2, the replacement of one (major product) or two phenyl groups is observed, suggesting that electrophilic borylation occurs at both the C(Ph)-Si and the C(Ph)-B aromatic carbons. The successful attachment of a range of different functional groups at the periphery of the Tpyb metal complexes is expected to provide opportunities to access new polymeric materials via C-C coupling or click-type reactions.Peer reviewe
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
LIN-39 does not regulate TRN fate markers in AVM.
No full text(A) AVM was posteriorly displaced in lin-39(n1760) mutants, but the expression of TRN fate marker uIs115[mec-17p::TagRFP] was not affected in lin-39 mutants. (B) The displaced AVM also expressed the TRN fate marker zdIs5[mec-4p::GFP] in lin-39 mutants. Scale Bars = 100 μm. (TIF)</p
Differential roles of the microRNA let-7 in C. elegans tissue development
Full text linkThe organs and tissues of the human body comprise of an astonishing variety of cells as different in morphology and function as muscle cells and neurons. Amazingly, despite their different protein contents, they largely contain the identical genomic information. In order to understand the processes that enable this differentiation, we need to determine the underlying regulatory mechanisms. A very recent discovery in this context was the posttranscriptional regulation of gene expression by microRNAs (miRNAs). miRNAs are small RNA molecules that mediate translational repression and degradation of mRNA transcripts through partial complementarity to their 3’ untranslated region (UTR) . Among the first miRNAs to be identified, let-7 stands out for its high conservation in sequence and developmental functions in development throughout the animal kingdom. During my PhD, I studied the role of let-7 in Caenorhabditis elegans in the context of two distinct processes of tissue development, namely differentiation of the epidermis (called hypodermis), and morphogenesis of the vulva. The functions of the let-7 miRNA in formation of the adult cuticle have been extensively studied and are well understood. let-7 controls differentiation of specific, mitotically active epidermal cells by inducing cell cycle exit, fusion, and switch to an adult specific transcriptional program upon repression of targets such as lin-41, daf-12, hbl-1 and let-60/ras. I set out to identify novel interactors of let-7 in a genome-wide RNAi screen for suppression of the lethal let-7 bursting phenotype. Candidates were then verified using fluorescence-based reporter systems for onset of hypodermis differentiation and intensity of repression of a known target. Thereby, I was able to validate a whole set of novel members of the let-7 network, comprising genes downstream in the pathway as well as potential regulators of let-7 activity. Notably, both groups of repressors contain factors required for cell cycle progression and mitosis, which indicates an active crosstalk between let-7 and the cell-cycle machinery. In a second project, I explored the molecular basis for the prominent let-7 vulval bursting phenotype. Despite the absence of overproliferation or any other obvious phenotype in vulval morphogenesis, I was able to show that let-7 activity is required in the vulva, and that its major function in this context is repression of a single target, namely lin-41. Disruption of let-7 binding to lin-41 through modification of the let-7 complementary sites by CRISPR/Cas9 mediated genome editing suffices to trigger the bursting phenotype, proving that repression of a single target is the key function of the miRNA in this context. In summary, my work shows that while both differentiation of hypodermis as well as vulval integrity are mediated through repression of lin-41, the downstream effect of this regulation seem to differ, suggesting that let-7 can be wired to control distinct processes depending on the cellular context. With respect to the latest findings both in C. elegans as well as in mammals, it will be interesting to determine if this depends on differential molecular functions of LIN-41 in the two tissues
The stem cell E3-ligase Lin-41 promotes liver cancer progression through inhibition of microRNA-mediated gene silencing
No full textLin-41 is a stem cell-specific E3 ligase and a known target of the tumour suppressor microRNA (miRNA) let-7. Lin-41 was recently reported to mediate ubiquitylation and degradation of the miRNA pathway protein Ago2. We demonstrate that Lin-41 is over-expressed in hepatocellular carcinoma (HCC). Lin-41 over-expression correlates with high a-fetoprotein level, high tumour grade and high tumour stage and predicts early tumour recurrence. Lin-41 is a strong predictor of poor long-term survival for patients with HCC. Lin-41 knock-down by RNA interference in HCC cell lines Huh7 and Hep3B suppressed proliferation in vitro and reduced in vivo tumour growth in NOD/SCID mice. On the other hand, over-expression of Lin-41 in the HCC cell line SK-Hep1 enhanced tumourigenicity. Over-expression and knock-down of Lin-41 led to inverse changes in the levels of Ago1 and Ago2 proteins. Over-expression of Ago1 and Ago2 reduced in vivo tumour growth. Lin-41 over-expression suppressed let-7 activity in HCC cell lines and expression of Lin-41 enhanced the expression of let-7-regulated oncogenes c-Myc, Lin-28B, HMGA2 and type 1 insulin-like growth factor receptor (IGF1R). Expression of Lin-28B and c-Myc enhanced the expression of Lin-41. Chromatin immunoprecipitation and reporter assays revealed direct association of c-Myc with the Lin-41 promoter, resulting in transcriptional transactivation. Our results indicate that Lin-41 plays an important role in the growth of HCC by regulating RISC complex proteins Ago1 and Ago2 to inhibit miRNA-mediated gene silencing and promote the expression of oncogenic proteins. Lin-41 is also a strong prognostic factor for patients with HCC. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd
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