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teer decrease » greater decrease (Expand Search)
e decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
a decrease » _ decrease (Expand Search), _ decreased (Expand Search), _ decreases (Expand Search)
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14081
Ensemble inference of <i>E. coli</i> GRN from error-free and the complete set of 's.
Published 2014“…<p>The plot shows the network distances of the lower and upper bounds from as a function of the number of 's for the 50 most informative 's, i.e. the top 50 highest number of testable edges. …”
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14082
NRF2 deficiency increases obesity susceptibility in a mouse menopausal model
Published 2020“…In conclusion, the combination of <i>Nrf2</i> deletion and a decline in estrogen level induced a significant increase in bodyweight, which may be associated with their altered glucose and LDL metabolism and decreased 5-HT levels. …”
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14083
Image_4_E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer.pdf
Published 2019“…<p>E-cadherin is a transmembrane glycoprotein responsible for cell-to-cell adhesion, and its loss has been associated with metastasis development. …”
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14084
Image_2_E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer.pdf
Published 2019“…<p>E-cadherin is a transmembrane glycoprotein responsible for cell-to-cell adhesion, and its loss has been associated with metastasis development. …”
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14085
Image_1_E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer.pdf
Published 2019“…<p>E-cadherin is a transmembrane glycoprotein responsible for cell-to-cell adhesion, and its loss has been associated with metastasis development. …”
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14086
Image_3_E-Cadherin Downregulation is Mediated by Promoter Methylation in Canine Prostate Cancer.pdf
Published 2019“…<p>E-cadherin is a transmembrane glycoprotein responsible for cell-to-cell adhesion, and its loss has been associated with metastasis development. …”
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14087
TGFβ downregulates the SUMO E3 ligase PIAS1 in cells undergoing EMT.
Published 2010“…<p>A) E-cadherin immunofluorescence images of NMuMG cells, left untreated (− TGFβ), or incubated with TGFβ (+ TGFβ), the TGFβ-receptor type I kinase (TβRI) inhibitor SB431542 (+ KI), alone or together for 48 h. …”
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14088
Engraftment of hE in NOD<i><sup>scid/β2m−/−</sup></i>.
Published 2013“…<p>(A) Long term kinetics of engraftment of NOD<i><sup>scid β2m−/−</sup></i> mice with hE. …”
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14089
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14090
Normal Fibroblasts Induce E-Cadherin Loss and Increase Lymph Node Metastasis in Gastric Cancer
Published 2014“…<div><p>Background</p><p>A tumor is considered a heterogeneous complex in a three-dimensional environment that is flush with pathophysiological and biomechanical signals. …”
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14091
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14092
Blocking eNOS uncoupling mitigates TNFα-induced endothelial dysfunction and inflammatory response.
Published 2015“…<p><b>A,</b> TNFα decreases VE-cadherin and eNOS expression in VEC over 48 hours (arrows), rescued by BH<sub>4</sub> or peg-SOD. …”
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14093
Pre-symptomatic VKA mice exhibit reduced E-cadherin expression prior to inflammation onset.
Published 2019“…<b>(D)</b> Immunoblot analysis of adherens junction proteins from isolated IECs reveals decreased levels of E-cadherin, but not p120<sup>ctn</sup> or β-catenin, in 12-week old VKA mice compared to NonTg siblings.…”
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14094
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14095
Characterization of Nt5e activity on <i>S. sanguinis</i> 133-79 whole cells.
Published 2012“…<p>Nt5e activity was measured by the release of inorganic phosphate (Pi) from adenine nucleotides. …”
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14096
Survival and Development of Atherosclerotic Lesions in Apo E KO mice with AngII-induced atherosclerosis.
Published 2013“…<p>A. Survival graph of Angiotensin II-induced atherosclerosis in Apo E KO mice with saline injection, AngII-infused, and AngII with sRAGE-treated groups. …”
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14097
Lactoferrin inhibits SARS pseudovirus infection of HEK293E/ACE2-Myc cells.
Published 2013“…<p>(<b>A–D</b>) Fluorescence microscopy illustrates that the number of SARS pseudovirus-infected GFP-expressing HEK293E/ACE2-Myc cells decreases in the presence of LF. …”
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14098
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14099
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14100