IndraLab

Statements


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"MicroR-140-5p suppresses tumor cell migration and invasion by targeting ADAM10 mediated Notch1 signaling pathway in hypopharyngeal squamous cell carcinoma."

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"While also expressed in immune cells, TSPAN14 has an intestinal epithelial role as a positive regulator of ligand induced ADAM10 mediated Notch1 activation."

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"Taken together, our study demonstrates that miR-140-5p suppresses tumor migration and invasion by inhibiting ADAM10 mediated Notch1 signaling pathway and suggests that miR-140-5p could have potential therapeutic applications in HSCC."

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"In human patients with non small cell lung cancer, ADAM10 overexpression activated the Notch1 signaling pathway, leading to increased cell migration and invasion [XREF_BIBR]."

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"Most recently, two groups using ADAM10 -/- MEFs concluded that ADAM10 mediates ligand dependent Notch1 cleavage, whereas other proteases regulate ligand independent cleavage."

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"In cultured microvascular endothelial cells, Piezo1 channel activation by either shear stress or a chemical agonist Yoda1 activated a disintegrin and metalloproteinase domain containing protein 10 (ADAM10), a Ca 2+ -regulated transmembrane sheddase that mediates S2 Notch1 cleavage."

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"Adam10, which cleaves the Notch ligands at the S2 site and produces the NICD to activate Notch signalling [15], had the same expression trend with Notch1 and Notch2."

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"Inhibition of ADAM10 abrogates NOTCH1 signaling in human T-ALL."

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"Therefore, IMD could inhibit ADAM10 protein expression via its CRLR and RAMP receptor and the PI3K and Akt signaling pathway, thereby inhibiting the activation of Notch1."

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"It was also shown that NOTCH1 can be activated by ADAM10 (A Disintegrin and metalloproteinase domain containing protein 10), a sheddase with alpha-secretase activity, and promoted migration and invasion of the A549 lung adenocarcinoma cells [XREF_BIBR]."

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"After activation, Notch can be cleaved to its intracellular domain (NICD) by ADAM10, TACE and gamma-secretase, allowing the NICD to become capable of target gene activation [XREF_BIBR]."

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"These results indicate that knockdown of ADAM10 by siRNA in TNBC cells inhibits cell proliferation by regulating Notch1, HES1 and c-Myc, and induces cell-cycle arrest by regulating Cyclin D3 and p21 Waf1 and Cip1."

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"Hence, we focused on the role of ADAM10 mediated Notch1 signaling shedding and activation in HSCC.To date, the dysregulated Notch1 signaling pathway has been observed to mediate tumor migration and in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"ADAM10 mediated Notch1 cleavage and shedding in T-cells controls T-cell development [XREF_BIBR], and also contributes to oncogenic Notch signaling by shedding Notch1 mutants in T-cell acute lymphoblastic leukemia (T-ALL) [XREF_BIBR]."

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"For instance, miR-140-5p suppresses tumor cell migration and invasion by targeting ADAM10 mediated Notch1 signaling pathway in hypopharyngeal squamous cell carcinoma [XREF_BIBR]."

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"Similarly, expression of exogenous Adam10 or Adam17 in mouse embryonic fibroblasts (MEFs) derived from Adam10 and Adam17 knockout animals, effectively increased activation of NOTCH1 signaling upon expression of activated forms of NOTCH1 in these cells (XREF_FIG)."

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"As shown in XREF_FIG, overexpression of ADAM10 elicited stronger fluorescent signals of Notch1 IC and Notch3 IC in the nucleus, reflecting increased nuclear translocation of these molecules, whereas Notch1 IC and Notch3 IC signals were evenly distributed in the vector transduced cells."

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"However, further studies are needed to unequivocally establish if ADAM10 mediates the cleavage of both NOTCH1 and NOTCH3 during early retinal neurogenesis."

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"Interestingly, a recent report suggested that Notch1 signaling pathway activated by ADAM10 shedding played non small cell lung cancer in the migration and invasion of non small cell lung cancer (Guo e[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"It was also shown that NOTCH1 can be activated by ADAM10 (A Disintegrin and metalloproteinase domain-containing protein 10), a sheddase with α -secretase activity, and promoted migration and invasion of the A549 lung adenocarcinoma cells [ xref ]."