Naked Gold, 30 nm
- Known as:
- Naked Gold, 30 nanometer
- Catalog number:
- G-NG-30G-500ml
- Product Quantity:
- 500 ml
- Category:
- -
- Supplier:
- Imgen
- Gene target:
- Naked Gold 30
Related genes to: Naked Gold, 30 nm
- Gene:
- NKD2 NIH gene
- Name:
- NKD inhibitor of WNT signaling pathway 2
- Previous symbol:
- -
- Synonyms:
- Naked2
- Chromosome:
- 5p15.33
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-19
- Date modifiied:
- 2019-01-25
Related products to: Naked Gold, 30 nm
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- The aleurone layer, located on the outermost region of the endosperm, is rich in lipids, proteins, and minerals and can substantially enhance grain nutritional value with increased thickness. ADP-glucose pyrophosphorylase is a critical rate-limiting enzyme in starch biosynthesis, with Shrunken2 (Sh2) and Brittle2 (Bt2) encoding its large and small subunits, respectively. Nevertheless, the influence of these genes on maize (Zea mays) aleurone layer development remains poorly understood. We conducted genetic analysis, map-based cloning, and allelic validation using the Huajian1F (HJ1F) paternal line containing multialeurone layers and identified that Sh2 regulates aleurone layer thickness in HJ1F. Additional studies demonstrated that the bt2 mutant (MT) displayed the phenotype of aleurone layer thickening. Both sh2 and bt2 MTs exhibited a substantial increase in the contents of grain oil, total protein, and mineral elements. RNA sequencing analysis indicated that differentially expressed genes were enriched in fatty acid and amino acid metabolic pathways during aleurone layer formation. ZmDof3 (DNA-binding one zinc finger protein 3) and NKD2 (NAKED ENDOSPERM2), which participate in aleurone layer thickening in maize, showed significant differential expression during the aleurone layer development of sh2 and bt2 MTs. Yeast 1-hybrid assays, β-galactosidase activity assays, and the luciferase reporter system confirmed that ZmDof3 and NKD2 regulate the expression of Sh2 and Bt2. This study has established that Sh2 and Bt2 control starch biosynthesis and play a pivotal role in maize aleurone layer development. - Source: PubMed
Du YimoYang BomingLu YipengZhao LiZhang TengfeiLiu JiePei YuanrongCai DarunZhang HuairenZhang ZhiliangLi HuiyongWang LifengZhang LongChen HuabangLiu Juan - Interactions between genetic variants and environmental factors influence malignancy risk, including for colorectal cancer (CRC). Prevalent CRC susceptibility loci reside predominantly in noncoding regulatory DNA where they may interact with dietary influences to dysregulate expression of specific genes predisposing to neoplasia. The impacts of CRC protective and risk dietary metabolites, butyrate and deoxycholic acid, were thus studied on the transcription-directing activity of 3703 regulatory CRC-associated variants via massively parallel reporter assays (MPRA) in human colonic cells. 1595 variant-dietary metabolite interactions were identified, pointing to dysregulation of MED13L, NKD2, and several modulators of Wnt/β-catenin signaling in potential CRC gene-environment interactions (GxE). Opposing impacts of butyrate and deoxycholic acid were also uncovered, indicating dietary influences may converge on common CRC risk loci and nominating FOSL1 and SP1 as mediators of these opposing responses. Coupling MPRA to relevant environmental factors offers an approach to extend insight into GxE in common human cancers. - Source: PubMed
Publication date: 2025/09/08
Fabo Tania NMeyers Robin MPadhi EvinKellman Laura NZhao YangKundu SoumyaReynolds David LChen ZiweiYang XueKo LisaElfaki IbtihalMontgomery Stephen BKhavari Paul A - Chronic kidney disease (CKD) is closely associated with cardiovascular disease (CVD). This includes aortic valve stenosis (AS), one of the most common valve diseases among adults. CKD leads to the retention of uremic toxins such as indoxyl sulfate (IS), which is known to induce inflammatory and pro-calcific processes. We hypothesize that IS specifically induces AS formation. - Source: PubMed
Düsing PhilipGöbel IsabelAckerschott AnsgarReese LaurineGiavalisco PatrickDethloff FrederikNiepmann Sven ThomasStei MartaBeiert ThomasZimmer SebastianKurts ChristianNickenig GeorgJansen FelixZietzer Andreas - The activation of the human interferon-inducible protein X (IFIX) isoform is associated with maintaining a stable cytoskeleton and inhibiting epithelial-mesenchymal transition (EMT). However, the mechanisms and pathways underlying IFIX-mediated oncogenesis are not well understood. In this study, we investigated the effects of IFIX overexpression and knockdown in CAL-27 and SCC-25 oral squamous cell carcinoma (OSCC) cells. We observed significant variations in the expression of E-cadherin, N-cadherin, vimentin and Snail, as well as changes in wingless/integrated (Wnt) signalling. Our results indicated a strong correlation between IFIX and EMT, as evidenced by quantitative reverse-transcription PCR and Western blotting, which revealed that Wnt3a and Wnt4 pathway components were regulated in IFIX-overexpressing or knockdown cells, with naked cuticle 2 (NKD2) showing the strongest positive correlation. Both IFIX overexpression and knockdown modulated NKD2 expression. NKD2 silencing mimicked the phenotypic effects of IFIX knockdown, inhibiting E-cadherin expression and increasing N-cadherin, Snail and vimentin expression. Additionally, silencing NKD2 restored the anticarcinogenic phenotype associated with IFIX overexpression, affecting cell proliferation, invasion and migration. These findings provide mechanistic insights into the antioncogenic effects of IFIX in OSCC, involving the inhibition of Wnt signalling through NKD2, which leads to cancer-inhibiting phenotypic effects, including restricted EMT. - Source: PubMed
Wang ShanFan HaixiaBai Jie - In this work, we sought to apprehend quercetin binding affinity and its interaction behavior in complex with human serum albumin (HSA) and calf thymus DNA (ctDNA) through multi spectroscopy and molecular dynamics and also evaluated its effects on colorectal cancer. The binding constants of ctDNA-quercetin and HSA-quercetin complexes at 298 K, which were calculated to be (2.67 ± 0.04) × 10 M and (4.77 ± 0.05) × 10 M respectively, denoted the strong binding of quercetin with ctDNA and HSA. The K and K values decrease with increasing temperature, indicating that the quenching of HSA and ctDNA in the presence of quercetin is caused by the combined dynamic and static effects. The obtained thermodynamic parameters for the ctDNA-quercetin interaction represented the existence of electrostatic forces (ΔH < 0 and ΔS > 0), and the thermodynamic parameters of HSA-quercetin complex disclose the dominance of hydrogen bonds and van der Waals interactions (ΔH < 0 and ΔS < 0). Moreover, the interactions were exothermic, as evidenced by the negative ΔH value for both interactions. According to molecular docking and MD simulation data, quercetin was capable of placing into the site 1 of HSA and forming stable interaction plus this ligand tended to unwind DNA's strands as an intercalator ligand, which was confirmed by experimental results. The fluorescence competition studies between the two intercalator probes of ethidium bromide (EB) and acridine orange (AO), as well as the effect of ionic strength, proposed the strong tendency of quercetin to exist between the two strands of ctDNA as a sign of its intercalative property. Consequently, quercetin can be assumed as an efficient intercalator ligand carried by HSA with an anticancer property. We also conducted cell viability experiments on HT-29 and SW620 cell lines to validate the anticancer ability of quercetin, and observed its decreasing impact on the cell viability of these two cell lines. Additionally, the outcomes of Real-time qPCR proved its capability to reduce the CXCR4 expression and increase the NKD2 expression in Wnt signaling pathway. Therefore, these facts confirm the inhibiting ability of quercetin towards colorectal cancer growth via the prevention of Wnt pathway and approve its functionality as a potential anticancer agent for this cancer. - Source: PubMed
Publication date: 2024/12/20
Samandar FarzanehMohsenpour AidaRastin FarangisDoustmohammadi-Salmani SaraSaberi Mohammad RezaChamani Jamshidkhan