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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.
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
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human lncrna expression microarray v3.0 (8 × 60 k) - by Bioz Stars, 2026-10
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human lncrna expression microarray v3.0  (Arraystar inc)
90
Arraystar inc human lncrna expression microarray v3.0
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, 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/product/human+lncrna+expression+microarray+v3%2E0/human+lncrna+microarray+v3+0/10__1097_slash_hjh__0000000000003140-10-34-33
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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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human lncrna/mrna expression microarray v3.0  (Arraystar inc)
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Arraystar inc human lncrna/mrna expression microarray v3.0
TaqMan qRT-PCR validation of lncRNA <t>microarray</t> analysis. Fold-change in comparison of ACCversusNAC, *P < 0.05.
Human Lncrna/Mrna Expression Microarray V3.0, 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/product/human+lncrna+expression+microarray+v3%2E0/human+lncrna+microarray+v3+0/pmc06904435-103-5-4
Average 90 stars, based on 1 article reviews
human lncrna/mrna expression microarray v3.0 - by Bioz Stars, 2026-10
90/100 stars
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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