ArticleMolecular biology reports2026
Development of an isoform-discriminating RT-qPCR assay for transcript-level profiling of human ASAH2 in colorectal cancer cell models.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
backgroundN-Acylsphingosine Amidohydrolase 2 (ASAH2) encodes neutral ceramidase (nCDase), one of several ceramidases involved in sphingolipid metabolism. nCDase hydrolyzes ceramide into sphingosine and contributes to the regulation of the ceramide-sphingosine-1-phosphate signaling axis. Compared with acid and alkaline ceramidases, nCDase remains less well characterized, and the expression and functional relevance of alternatively spliced ASAH2 isoforms are poorly understood. Dysregulated ASAH2 expression has been implicated in colorectal cancer (CRC), suggesting that transcript-level analysis may provide useful information regarding ASAH2 regulation in tumor-related contexts. Human ASAH2 exists as two alternatively spliced isoforms that differ within the catalytic domain, but their accurate quantification is complicated by the highly homologous paralog ASAH2B. METHODS AND
resultsWe developed an RT-qPCR-based method that combines a universal primer set for total ASAH2 with an isoform 1-specific primer set, enabling differential quantification of ASAH2 isoforms without detectable amplification of the homologous ASAH2B paralog. Absolute quantification was performed using standard curves generated from sequence-verified amplicons. Both assays demonstrated linear amplification over a range of 10²-10⁷ copies, with high correlation coefficients (r² = 0.999 for both assays). Melting curve analysis and agarose gel electrophoresis confirmed single, specific amplification products. Application of this assay to human CRC cell lines revealed that isoform 2, estimated by subtracting the isoform 1 copy number from the total ASAH2 copy number, was the predominant ASAH2 transcript across all tested cell lines.
conclusionsThis assay provides a practical approach for transcript-level profiling of ASAH2 isoforms in colorectal cancer cell models and may support future studies of ASAH2 isoform regulation in tumor-related laboratory investigations.
Indexed as
Identifiers
42611369What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.