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largest decrease » largest decreases (Expand Search), larger decrease (Expand Search)
marked decrease » marked increase (Expand Search)
c largest » _ largest (Expand Search), c large (Expand Search)
n marked » _ marked (Expand Search), _ market (Expand Search), _ marker (Expand Search)
a marked » a marker (Expand Search), _ marked (Expand Search), a market (Expand Search)
c marked » _ marked (Expand Search), _ market (Expand Search), _ marker (Expand Search)
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Deletion of Hhp2 markedly increased Sre1 activity.
Published 2020“…<p>Deletion of <i>hhp2</i><sup>+</sup> gene markedly increased Sre1 activity in the presence/absence of CLZ (2 μg/ml to 8 μg/ml) (A), TER (2 μg/ml to 8 μg/ml) (B) or CoCl<sub>2</sub> (0.08 mM to 0.32 mM) (C). …”
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Altered expression of genes related to Ca<sup>2+</sup> cycling or myocardial contraction.
Published 2025Subjects: -
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Persistence of β-cell responsiveness for over two years in autoantibody-positive children with marked metabolic impairment at screening
Published 2022“…</p> <p><strong>Results:</strong> Longitudinal analyses revealed annualized AUC C-peptide increases in non-progressors vs. decreases in progressors (p≤0.026 for DPT-1 and TNPTP). …”
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Deletion of microglial NKCC1 markedly impacts on baseline cell morphology and alters transformation to reactive microglia.
Published 2022“…(<b>B)</b> We generated a novel microglia-specific conditional NKCC1 KO transgenic mouse line by crossing NKCC1<sup>fl/fl</sup> (exon 8 of the <i>Slc12a2</i> gene was flanked with lox P sites) and Cx3CR1-Cre<sup>ERT2</sup> mice. (<b>C)</b> NKCC1 mRNA levels in isolated NKCC1 KO microglia was markedly reduced in comparison to WT cells. …”
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The activation of MARK2 is correlated with the phosphorylation of eIF2α, and the signaling pathway is independent of the previously known kinases.
Published 2021“…<p>(<b>A</b>) Deletion of the MARK2 gene decreases the phosphorylation of eIF2α-<sup>51</sup>S in human HAP1 cells. …”
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Changes during germination in % of amino acids with marked preferences at a particular position.
Published 2024Subjects: -
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