Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033036 (APC)
 10,214 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This work aims to contribute to a better understanding of the ionic strength effect on microcystin and natural organic matter (NOM) surrogate adsorption by analyzing the importance of adsorbate molecular size, and surface concentration. Adsorption kinetics and/or isotherms were performed on PAC Norit SA-UF for four microcystin variants (MC-LR, MC-LY, MC-LW, MC-LF), and three NOM surrogates (salicylic acid (SA), tannic acid (TA), Aldrich humic acid (AHA)) at different solution ionic strengths. Results showed that the ionic strength effect depends upon the adsorbate surface concentration, cation charge (mono or divalent), and adsorbate molecular size. Potassium seemed not to affect the MC-LR adsorption, while calcium enhanced MC-LR kinetics and adsorption capacity. K+ and, particularly, Ca2+ improved the adsorption kinetics of the other microcystin variants. For identical surface concentration and ionic strength, the impact of K+ and Ca2+ on NOM surrogates depended on the adsorbate molecular size: K+ effect was only observed for AHA, whereas Ca2+ caused no effect on SA adsorption, slightly enhanced TA adsorption, and greatly enhanced AHA adsorption. MC-LR isotherms with two salt concentrations (KCl or CaCl2) indicated that, for the studied range of equilibrium surface concentration (5.3-18.7 mg/g), an enhanced adsorption regime prevails, and no transition regime was observed.
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PMID:The ionic strength effect on microcystin and natural organic matter surrogate adsorption onto PAC. 1661 83

Hepatoblastoma (HB), a leading primary hepatic malignancy in children, originates from primitive hepatic stem cells. This study aimed to uncover the genetic variants that are responsible for HB oncogenesis. One family, which includes the healthy parents, and two brothers affected by HB, was recruited. Whole-genome sequencing (WGS) of germline DNA from all the family members identified two maternal variants, located within APC gene and X-linked WAS gene, which were harbored by the two brothers. The mutation of APC (rs137854573, c.C1606T, p.R536X) could result in HB carcinogenesis by activating Wnt signaling. The WAS variant (c.G3T, p.M1-P5del) could promote HB cell proliferation and inhibit T-cell-based immunity by activating PLK1 signaling and inactivating TCR signaling. Further analysis reflected that WAS deficiency might affect the antitumor activity of natural killer and dendritic cells. In summary, the obtained results imply that an APC mutant together with an X-linked WAS mutant, could lead to HB tumorigenesis by activating Wnt and PLK1 signaling, inhibiting TCR signaling, and reducing the antitumor activity of natural killer and dendritic cells.
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PMID:Whole-Genome Sequencing Identifies a Novel Variation of WAS Gene Coordinating With Heterozygous Germline Mutation of APC to Enhance Hepatoblastoma Oncogenesis. 3061 85