UcallM® m⁶A site identification Kit

SELECT (single-base elongation-and ligation-based qPCR amplification method) is a qPCR amplification technology based on single-base elongation and ligation, developed by the research team of Professor Jia Guifang at Peking University. This method enables single-base-resolution m⁶A detection in low-abundance transcripts within just three hours. Without the need for antibody enrichment, it allows targeted quantification of m⁶A modification at specific sites, comparative analysis of modification abundance differences between samples, and identification of whether a target site harbors m⁶A modification. UcallM has entered into a technology transfer (patent license) agreement with Peking University for the SELECT-m⁶A modification quantitative detection technology, obtaining worldwide rights for the commercialization of this technology. The company now offers a series of SELECT detection kits, filling the gap in routine detection methods for site-specific m⁶A modification. These kits assist researchers in identifying the target genes of m⁶A-related proteins and further exploring the regulatory mechanisms underlying m⁶A modification. Kit Specifications

Key Advantages 1.qPCR-based readout delivering single-base-resolution information 2.No IP or radioisotope labeling; easy-to-operate workflow 3.High sensitivity: compatible with ≥ 1 μg total RNA input Applications 1.Inter-sample comparison of m⁶A modification abundance at defined RNA sites 2.Determination whether a given RNA locus carries m⁶A modification 3.Absolute quantification of m⁶A modification level at target positions Technical Principle

Technical Comparison

Customer Publications 1.Adv Sci: CRISPR/dCas13(Rx)-Mediated Dynamic RNA m⁶A Editing System Enhances Drought Resistance in Cotton (DOI:10.1002/advs.202401118) This study developed a programmable RNA m⁶A editing toolkit (TME and TDE) based on CRISPR/dCas13(Rx). By fusing methyltransferase GhMTA or demethylase GhALKBH10, dynamic modification of specific m⁶A sites on endogenous plant transcripts GhGHECA1 and GhDi19 was achieved.

Figure 1-14. SELECT reagent validation of m⁶A modification efficiency in the 3'UTR region of GhGHECA1 transcript and the 5'UTR region of GhDi19 transcript. 2.Acta Pharmacol Sin: METTL14-mediated m⁶A Methylation of pri-miR-5099 Drives Cardiomyocyte Pyroptosis in Myocardial Infarction: Molecular Mechanism (DOI: 10.1038/s41401-025-01485-y) This study reveals the molecular mechanism by which METTL14-mediated m⁶A methylation promotes cardiomyocyte pyroptosis via regulating pri-miR-5099 processing. The SELECT reagent was used for specific detection of m⁶A methylation sites on pri-miR-5099. FTO demethylation treatment and EDTA control experiments were performed to compare the qPCR cycle threshold differences between the two groups of samples, confirming the existence of specific m⁶A modification sites in the pri-miR-5099 sequence.

Figure 1-15. Validation of specific m⁶A modification sites in pri-miR-5099 sequence using the epi biotech SELECT Kit (Epi-SELECT™ m⁶A Site Identification Kit with FTO-assisted step).

Figure 1-16. Detection of pri-miR-5099 m⁶A methylation level by SELECT reagent in myocardial tissue of METTL14 knockdown mice.