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Why write a popular article?
Published in John Measey, How to Publish in Biological Sciences, 2023
What's the hook? Your popular article will not be the same as your paper. You should plan to have a single fact or message that you want the public to walk away with after reading your article. This is likely to be the same as the main result in your paper.
Schinzel−Giedion Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Three putative bipartite NLS motifs are thought to assist the signal-dependent nuclear transport of SETBP1 across the nuclear pore. The AT-hook motifs increase the DNA-binding capacity of SETBP1 and thus enhance its potential in transcriptional regulation.
What causes Rett Syndrome
Published in Rosa Angela Fabio, Tindara Caprì, Gabriella Martino, Understanding Rett Syndrome, 2019
Rosa Angela Fabio, Tindara Caprì, Gabriella Martino
Earlier truncation mutation, which also abolishes an AT-hook motif (R270X), MeCP2, binds to DNA without being able to induce modification of the chromatin structure. This kind of R270X mutation provokes a more severe disease phenotype in humans and in animal models in comparison with G273X or R306C (Baker et al., 2013).
Novel chromobox 2 inhibitory peptide decreases tumor progression
Published in Expert Opinion on Therapeutic Targets, 2023
Lindsay W. Brubaker, Donald S. Backos, Vu T. Nguyen, Philip Reigan, Tomomi M Yamamoto, Elizabeth R. Woodruff, Ritsuko Iwanaga, Michael F. Wempe, Vijay Kumar, Christianne Persenaire, Zachary L. Watson, Benjamin G. Bitler
To further assess the specificity of peptide 77, we examined the extra precision Glide score (XPGlide score) in the in silico models of CBX2 and CBX4 with or without the A/T-hook DNA binding domain. The lower the XPGlide score indicates enhanced binding. The following XPGlide scores were calculated for CBX4 without A/T-hook: −12.668, CBX4 with A/T-hook: −12.308, CBX2 without A/T-hook: −14.811, and CBX2 with A/T-hook: −16.709. The CBX2 and CBX4 with or without the A/T-hook DNA binding domain docked with peptide 77 demonstrated improved binding to both CBX2 over CBX4 and CBX2 with the A/T-hook DNA binding domain over CBX2 without the A/T-hook DNA binding domain (Figure 4a-d, arrows indicate binding pocket and docking). Both XPGlide score and docking simulations indicate that peptide 77 engages preferentially to CBX2 containing an A/T-hook domain.
Targeting the intrinsically disordered architectural High Mobility Group A (HMGA) oncoproteins in breast cancer: learning from the past to design future strategies
Published in Expert Opinion on Therapeutic Targets, 2020
Silvia Pegoraro, Gloria Ros, Michela Sgubin, Sara Petrosino, Alberto Zambelli, Riccardo Sgarra, Guidalberto Manfioletti
HMGA genes are paralogues, and the resulting proteins have approximately 50% identity, sharing similar domains and molecular functions, allowing the regulation of a common set of genes [13,14]. Nevertheless, each member of the HMGA family has unique regulatory and structural features. First, the expression of HMGA1 and HMGA2 is regulated mainly at different levels. Indeed, while HMGA1 expression is principally controlled by TFs acting at the promoter/enhancer level, HMGA2 expression regulation occurs mainly at the post-transcriptional level [reviewed within [15,16]]. HMGA2 expression is in fact strictly regulated by miRNA, in particular let-7, and disruption or loss of the 3ʹUTR of HMGA2 causes its overexpression [17]. Second, although all the HMGA proteins have highly conserved AT-hooks, they display strong differences in terms of amino acid sequence and AT-hook spacing, and these features support the ability of each factor to bind to different nucleotide stretches [18] and proteins [reviewed within [19]]. Indeed, HMGA1a and HMGA1b are structurally different from HMGA2, in particular at the N-terminal and at the C-terminal acidic tail. Moreover, the HMGA2 protein includes a short peptide of 12 amino acid residues after the third AT-hook [5] that is not present in HMGA1a/HMGA1b. In addition, HMGA1 and HMGA2 proteins are heavily post-translationally modified, showing a very distinct pattern of post-translational modifications (PTMs) [20,21] that supports a different modulation of their functions.
Distinctive alteration in the expression of autophagy genes in Drosophila models of amyloidopathy and tauopathy
Published in Upsala Journal of Medical Sciences, 2020
Mehrnaz Haghi, Raheleh Masoudi, Seyed Morteza Najibi
As mentioned earlier, Hook is a mediator to facilitate interaction between motor proteins and their cargo as a pre-autophagy protein (37). In the AD brain, reduction in Hook3 expression and increase in Hook2 mRNA levels have been observed. Interestingly, when Hook3 is knocked down, there is an increase in Aβ production (38). While there are three forms of Hook in humans, only one form of Hook has been reported in Drosophila. Here, we assessed the effect of Aβ42 and Tau R406W on the expression levels of dHook (Drosophila Hook) using transgenic flies. As can be seen in Figure 2 and from Bayesian contrast estimations in Table 2, although there was no significant change in the levels of dHook expression in 5-day-old flies expressing Tau R406W, a prominent increase was observed in the levels of this gene in 25-day-old flies. It seems that Tau R406W exerts its effect on the Hook expression at a later time point of the life cycle of this fly. Regarding Aβ42-expressing flies, there was a significant decrease in the levels of Hook expression in both 5- and 25-day-old flies. For more details see Figure 4; and also Supplementary Table S4.