human spi1 transcript variant 1  (OriGene)

Journal: Nature Communications

Article Title: A common 19 bp APOE enhancer deletion is protective against Alzheimer’s disease in African Americans

doi: 10.1038/s41467-026-68808-3

Figure Lengend Snippet: a Alignment of phased long-read alleles. b gnomAD minor allele frequency of the 19 bp SNP. c Relative frequency of the deletion in 1000 Genomes Project populations ordered by relative abundance. * = African Ancestry in Southwest US. d Number of alleles with the deletion in APOE-ε4 homozygous individuals from the 1000 Genomes Project populations. e UCSC genome browser track showing the location of the deletion allele relative to APOE and transcription factor binding sites on the GRCh37 build. f Presence of the deletion and strong (red) and modest (orange) predicted SPI1 binding sites along with sequence conservation in the mouse genome.

Article Snippet: Briefly, the SPI1 expression plasmid containing the human SPI1 transcript variant 1 driven by a CMV promoter was obtained from Origene (RC217488).

Techniques: Binding Assay, Sequencing

Journal: Nature Communications

Article Title: A common 19 bp APOE enhancer deletion is protective against Alzheimer’s disease in African Americans

doi: 10.1038/s41467-026-68808-3

Figure Lengend Snippet: a Schematic of the luciferase experimental design and constructs. The APOE 3′UTR ( APOE 3′UTR only) plus ~400 bp of downstream DNA containing the 19 bp deletion region and SPI1 binding site were cloned into a psiCheck2.2 dual luciferase reporter construct. b Renilla:Firefly luciferase expression data in HMC3 cells after delivery of APOE SPI1 WT sequence ( p = 0.0016 relative to the APOE 3′UTR only) or delivery of the 19 bp deletion [ p = 0.8252; one-way ANOVA, n = 12 samples/group (3 biological replicates, 4 technical replicates), ± SD]. c –e HMC3 gene expression following SPI1 overexpression. c Effect of SPI1 overexpression on c APOE expression ( p = 0.3831, F = 1.789, unpaired two-tailed t-test, n = 12 control and 12 SPI1 biological replicates derived from the average of 4 technical replicates/sample, ± SEM), d APOC1 expression ( p = <0.0001, F = 2.987, unpaired two-tailed t-test, n = 11 control and 12 SPI1 biological replicates derived from the average of 4 technical replicates/sample, ± SEM), and e lncRNA ENSG00000280087 expression ( p = 0.0170, F = 5.414, unpaired two-tailed t-test, n = 12 control and 10 SPI1 biological replicates derived from the average of 4 technical replicates/sample, ± SEM). f – h HMC3 gene expression following Aβ 1:42 treatment. f Effect of Aβ 1:42 treatment on APOE expression ( p = 0.2098, F = 1.243, unpaired two-tailed t-test, n = 12 control and 12 Aβ biological replicates derived from the average of 4 technical replicates/sample, ± SEM), g APOC1 expression ( p = 0.0015, F = 4.657, unpaired two-tailed t-test, n = 11 control and 12 Aβ biological replicates derived from the average of 4 technical replicates/sample, ± SEM) and h, lncRNA ENSG00000280087 expression ( p = 0.0255, F = 2.502, unpaired two-tailed t-test, n = 12 control and 12 Aβ biological replicates derived from the average of 4 technical replicates/sample, ± SEM) in HMC3 cells.

Article Snippet: Briefly, the SPI1 expression plasmid containing the human SPI1 transcript variant 1 driven by a CMV promoter was obtained from Origene (RC217488).

Techniques: Luciferase, Construct, Binding Assay, Clone Assay, Expressing, Sequencing, Gene Expression, Over Expression, Two Tailed Test, Control, Derivative Assay