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human lncrna expression microarray v3.0 (8 × 60 k)  (Arraystar inc)

 
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    Arraystar inc human lncrna expression microarray v3.0 (8 × 60 k)
    Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the <t>lncRNA</t> NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.
    Human Lncrna Expression Microarray V3.0 (8 × 60 K), supplied by Arraystar inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human lncrna expression microarray v3.0 (8 × 60 k)/product/Arraystar inc
    Average 90 stars, based on 1 article reviews
    human lncrna expression microarray v3.0 (8 × 60 k) - by Bioz Stars, 2026-04
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    1) Product Images from "LncRNA NIPA1-SO confers atherosclerotic protection by suppressing the transmembrane protein NIPA1"

    Article Title: LncRNA NIPA1-SO confers atherosclerotic protection by suppressing the transmembrane protein NIPA1

    Journal: Journal of Advanced Research

    doi: 10.1016/j.jare.2023.01.017

    Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the lncRNA NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.
    Figure Legend Snippet: Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the lncRNA NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.

    Techniques Used: Expressing, Phospho-proteomics



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    Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the <t>lncRNA</t> NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.
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    Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the lncRNA NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.

    Journal: Journal of Advanced Research

    Article Title: LncRNA NIPA1-SO confers atherosclerotic protection by suppressing the transmembrane protein NIPA1

    doi: 10.1016/j.jare.2023.01.017

    Figure Lengend Snippet: Schematic diagram of the signalling pathways regulated by NIPA1-SO . Our study has uncovered an athero-protective role of the lncRNA NIPA1-SO , which, by interacting with a single transcription factor, is capable of inhibiting monocyte adhesion and foam cell formation, two fundamental processes in atherosclerosis. The transcription factor FUBP1 negatively regulates NIPA1 expression; this inhibitory effect is increased by the interaction of NIPA1-SO with FUBP1, resulting in lower transcription of NIPA1. A reduction in NIPA1 protein results in increased BMPR2 protein due to a reduction in NIPA1-mediated BMPR2 endocytosis and degradation, leading to higher levels of Smad1/5/8 phosphorylation (pSmad1/5/8), which, through complexation with Smad4, inhibit transcription of the adhesion molecules VCAM1 and ICAM1, reducing monocyte adhesion to endothelial cells. Further, the pSmad1/5/8:Smad4 complex promotes ABCA1 and ABCG1 transcription, both of which promote cholesterol efflux via high-density lipoprotein (HDL) particles, thereby inhibiting foam cell formation.

    Article Snippet: Labeled cRNAs were hybridized with Human LncRNA Expression Microarray v3.0 (8 × 60 K, Arraystar) and scanned using Agilent Scanner G2505C.

    Techniques: Expressing, Phospho-proteomics

    TaqMan qRT-PCR validation of lncRNA microarray analysis. Fold-change in comparison of ACCversusNAC, *P < 0.05.

    Journal: Surgery

    Article Title: Adrenocortical tumors have a distinct, long, non-coding RNA expression profile and LINC00271 is downregulated in malignancy *

    doi: 10.1016/j.surg.2019.04.067

    Figure Lengend Snippet: TaqMan qRT-PCR validation of lncRNA microarray analysis. Fold-change in comparison of ACCversusNAC, *P < 0.05.

    Article Snippet: LncRNA expression profile using ArrayStar Human LncRNA/mRNA Expression Microarray V3.0 was analyzed in samples from 11 ACA, 9 ACC, and 5 NAC.

    Techniques: Quantitative RT-PCR, Biomarker Discovery, Microarray, Comparison