Severe acute Respiratory Syndrome Coronavirus (SARS-CoV) Research








UcallM® RNA Immunoprecipitation Kit is built upon RIP (RNA Immunoprecipitation) technology for studying RNA-protein interactions inside cells. Target RNA-protein complexes are immunocaptured by protein-specific antibodies; bound RNA is purified and subjected to downstream RIP-qPCR, RIP-Chip or RIP-seq. RIP-seq enables transcriptome-wide identification of RNA targets bound by given RNA-binding proteins and permits multi-sample differential analysis. ## Experimental Workflow  ## Customer Publications 1.Nat Commun. Up-regulation and subcellular-localization control of YTHDF2 govern CD8⁺ T-cell polyfunctionality in anti-tumor immunity (DOI:10.1038/s41467-024-53997-6).  Fig. 1-17. In this study, the UcallM RNA immunoprecipitation kit was used to capture YTHDF2 and its interacting RNA molecules, followed by RIP-seq to identify YTHDF2 RNA targets at the transcriptome-wide level. 2.Cell Discov. Mycobacterium tuberculosis inhibits METTL14-mediated Nox2 mRNA m⁶A modification via EsxB to dampen anti-TB immune responses (DOI:10.1038/s41421-024-00653-4).  Fig. 1-18. In this study, the UcallM RNA immunoprecipitation kit was used to perform RIP-seq and RIP-qPCR to validate the binding of METTL14 to Nox2 mRNA, to investigate the interaction between IGF2BP1 and m⁶A-modified RNA, and to analyze the effect of EsxB on RNA–protein interactions.
View ProductN4-acetylcytidine (ac4C) is an evolutionarily-conserved RNA chemical modification, originally identified in tRNA and 18S rRNA; recent studies reveal abundant ac4C also exists in mRNA, where it regulates translation efficiency, RNA stability and alternative splicing. UcallM® ac4C Immunoprecipitation Kit adopts optimized antibody-magnetic-bead direct-coupling chemistry for efficient enrichment of ac4C-modified RNA fragments with minimized non-specific background. Enriched fragments can be analyzed by acRIP-qPCR or built into sequencing libraries to draw transcriptome-wide ac4C modification landscapes. ## Key Advantages 1.High-specificity enrichment with markedly reduced off-target background 2.Seamless compatibility with downstream library-prep workflows for acRIP-seq profiling 3.Multiple peer-reviewed publications generated with this kit ## Experimental Workflow  ## Empirical NGS Data  Figure 1-19. Metagene plot of ac4C distribution.  Figure 1-20. Circos plot of Peak distribution across chromosomes.  Figure 1-21. Pie chart of Peak distribution on RNA structural regions.  Figure 1-22. Volcano plot. ## Customer Publications 1.Eur Heart J. NAT10-dependent mRNA ac4C modification controls vascular remodeling (DOI:10.1093/eurheartj/ehae707). acRIP-seq and acRIP-qPCR identified ITGB1 and Col1a1 as NAT10-regulated ac4C targets.  Figure 1-23. In this study, ac4C-modified RNA fragments were enriched using Epimark acRIP Kit. acRIP-seq was then performed to identify ac4C target genes regulated by NAT10. acRIP-qPCR analysis confirmed that NAT10 knockdown markedly reduced the ac4C modification levels of ITGB1 and Col1a2 mRNA. 2.Cell Res. NAT10-mediated lysine 2-hydroxyisobutyrylation promotes cancer metastasis through ac4C mRNA modification (DOI:10.1038/s41422-023-00793-4). acRIP-seq compared ac4C profiles between NAT10-overexpressing and control cells; acRIP-qPCR validated NOTCH3-mRNA ac4C changes.  Figure 1-24. In this study, Epimark acRIP Kit was used for immunoprecipitation of ac4C-containing fragments. ac4C modification profiles between NAT10-overexpressing cells and control cells were compared by acRIP-seq to identify ac4C target sites regulated by NAT10. acRIP-qPCR was applied to verify changes in ac4C modification levels on NOTCH3 mRNA under different experimental conditions. 3.Nat Commun. NAT10-dependent N4-acetylcytidine modification governs PAN-RNA stability, KSHV reactivation and IFI16-mediated inflammatory-signal activation (DOI:10.1038/s41467-023-42135-3).  Figure 1-25. In this study, after immunoprecipitation of ac4C fragments with mark acRIP Kit, acRIP-seq was carried out.
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N1-methyladenosine (m¹A) is an important post-transcriptional modification of RNA, referring to methylation at the N1 position of the adenine base in RNA. Accumulating studies reveal that m¹A not only affects local RNA structure, protein-RNA interactions and translation of 5'UTR, but also exists in tRNA, rRNA, mRNA and mitochondrial transcripts. It plays a critical role in maintaining the correct structure and biological functions of these ncRNAs. The UcallM® m¹A Immunoprecipitation Kit adopts an optimized antibody-magnetic bead directional coupling strategy to efficiently capture m¹A-modified fragments and effectively reduce non-specific binding. After enriching m¹A-modified fragments in samples via immunoprecipitation, the fragments can be used as templates for quantitative detection of m¹A modification levels by m¹A meRIP-qPCR. In addition, libraries can be constructed for transcriptome sequencing to draw the genome-wide m¹A modification landscape. ## Experimental Workflow  ## Key Advantages 1.High-specific enrichment, m¹A antibody validated by multiple published articles 2.Optimized elution system & workflow, markedly reducing non-specific binding 3.Optimized magnetic bead-antibody coupling efficiency to ensure data reproducibility ## Application 1.Tumor pathogenesis: e.g. dissecting pro-tumor pathways regulated by m¹A in cancers 2.Metabolic and immune regulation: study m¹A in T cell immune response, mitochondrial function and metabolic reprogramming 3.Stem cell fate regulation: investigate how dynamic m¹A modification modulates translation efficiency in stem cells ## Customer Publications PNAS: RNA modification regulates tumor cell glycolysis via ATP5D (DOI:10.1073/pnas.2119038119) This study verified via sequencing and functional assays that ATP5D is one of the core subunits of ATP synthase, participating in tumor cell glycolysis regulated by m¹A demethylase ALKBH3. The m¹A-modified exon of ATP5D increases binding to the YTHDF1/eRF1 complex to fine-tune its translational elongation, thereby promoting ribosome complex to release mRNA.  Figure 1-26. The study identified m¹A modification sites on ATP5D mRNA by m¹A-seq; m¹A-RIP-qPCR, SELECT-PCR and primer extension assays were used to verify m¹A modification at the A71 site of ATP5D mRNA.
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N7-methylguanosine (m⁷G) is a key structural component of the 5' cap structure of eukaryotic mRNA, and also one of the most abundant modifications on tRNA. m⁷G plays core roles in regulating RNA stability, nucleocytoplasmic transport and translation initiation. Abnormal m⁷G modification is closely associated with tumorigenesis, viral infection and other disease processes. The UcallM® m⁷G Immunoprecipitation Kit achieves high-density immobilization of m⁷G antibody via optimized antibody-magnetic bead directional coupling strategy. Combined with fragmented RNA enrichment and gradient elution system, it effectively reduces non-specific binding and ensures efficient capture of m⁷G-modified fragments. After enriching m⁷G-modified fragments in samples by immunoprecipitation, RT-qPCR can be performed using enriched fragments as templates to quantitatively analyze m⁷A modification levels. Libraries can also be constructed for transcriptome sequencing to generate m⁷G modification profiles. ## Experimental Workflow  ## Key Advantages 1.Low sample input, compatible with trace samples 2.High-specificity m⁷G antibody to effectively improve capture efficiency 3.Genome-wide coverage of m⁷G modification sites ## Application 1.Profiling transcriptome-wide m⁷G modification landscape 2.Investigate the mechanism by which m⁷G modification affects tumorigenesis and drug resistance via regulating tRNA, mRNA and ncRNA 3.Integrate translatome analysis to uncover RNA translation and dynamic regulatory mechanisms ## Application Case J Exp Clin Cancer Res: The P300/SP1 complex promotes progression of castration-resistant prostate cancer by regulating METTL1-mediated internal m⁷G modification of CDK14 mRNA (DOI:10.1186/s13046-023-02777-z)  Figure 1-27. m⁷G meRIP combined with qPCR validated METTL1-mediated regulation of internal m⁷G modification on CDK14 mRNA.
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N6-methyladenosine (N6-methyladenosine, m⁶A) is the most abundant RNA modification in eukaryotic mRNA, regulating more than 80% of RNA metabolism processes. It functions as a molecular switch in key biological events such as stem cell differentiation, tumorigenesis and neurodegenerative diseases. The UcallM® m⁶A Immunoprecipitation Library Kit adopts optimized antibody-magnetic bead directional coupling strategy to realize high-density immobilization of m⁶A antibody. Combined with gradient elution system and double-strand specific purification technology, it can effectively reduce non-specific adsorption and ensure efficient capture of m⁶A modified fragments. After enriching m⁶A modified RNA fragments via meRIP, RT-qPCR can be applied for quantitative analysis of m⁶A modification levels. Libraries can also be built for sequencing to generate m⁶A modification profiles. ## Experimental Workflow  ## Product Highlights 1.Ultra-low starting input, compatible with trace samples 2.High-specificity m⁶A antibody to effectively improve capture efficiency 3.Optimized system, conditions and workflow for simple operation 4.Applicable to multiple cell and tissue types, multiple customer publications released ## Application Scenarios 1.Acquire information of m⁶A modification levels 2.Combine with library sequencing to draw transcriptome-wide m⁶A modification landscape 3.Study abnormal m⁶A modification in tumors, immune disorders and other diseases 4.m⁶A modification modulates physiological/pathological processes including stem cell differentiation and cellular stress response by regulating RNA stability, splicing and translation efficiency NGS Empirical Data  Figure 1-28. Metagene plot of Peak distribution on RNA structures  Figure 1-29. Pie chart of Peak distribution on RNA structures  Figure 1-30. Chromosome coverage map of Peaks from two groups  Figure 1-31. Circos plot of Peak distribution across chromosomes ## Customer Publications 1.Circulation: Mechanism study of AVCAPIR promoting aortic valve calcification via regulating m⁶A modification (DOI:10.1161/CIRCULATIONAHA.123.065213)  Figure 1-32. The authors performed meRIP-seq analysis and found that AVCAPIR inhibits FTO-mediated demethylation of CD36 mRNA, enhances its m⁶A level and RNA stability, and activates the CD36/PCSK9 pathway to drive aortic valve calcification. Multiple validations were performed via meRIP-qPCR. 2.Nat Commun: YTHDF2 promotes anti-tumor immunity by regulating CD8 T cell polyfunctionality through m⁶A modification (DOI:10.1038/s41467-024-53997-6) This study used multi-omics methods including meRIP-seq, ATAC-seq and Ribo-seq to reveal that YTHDF2 (m⁶A reader protein) drives CD8 T cell polyfunctionality (such as cytokine secretion and metabolic adaptability) by regulating target RNA stability, mitochondrial metabolism and chromatin accessibility via m⁶A modification, thereby enhancing anti-tumor immunity.  Figure 1-33. meRIP-seq analysis revealed that YTHDF2 directly binds and regulates m⁶A modification of key effector genes (e.g. Stat5a, Rasgrp1), promoting their translation efficiency and T cell persistence.
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UcallM® HisMod CUT&Tag Library Fast Kit is developed based on CUT&Tag technology for high-sensitivity, low-background and cost-effective histone modification research. The kit adopts optimized reagents and system. In a single incubation step, NanoTn5-M/R (nanobody-Tn5 transposase fusion protein) is coupled with secondary nanobody, eliminating separate incubation and pAG-Tn5 ligation. Adapter sequences are inserted concurrently with in-situ targeted DNA cleavage. CUT&Tag technology breaks the reliance of ChIP-seq on sonication and immunoprecipitation. It features low sample input, low background noise and simple operation. No traditional ligation for adapter addition is required, with simple operation and shorter experimental cycle. It is widely applied in tumor epigenetic heterogeneity, drug target screening and super-enhancer research. # Experimental Workflow  # Product Highlights 1.Low cell input, high signal-to-noise ratio and good reproducibility 2.Shorter experimental period and simpler operation compared with ChIP-seq 3.Proprietary primary antibody binding enhancer & DNA fragment release enhancer for high library specificity # Application 1.Studies on histone modification and gene regulation, uncovering chromatin state and gene expression mechanisms 2.Explore disease-related epigenetic changes and support drug screening 3.Super-enhancer analysis, identify regulatory elements and link target genes 4.Multi-omics validation, construct multi-dimensional gene regulatory networks # Empirical Data  Figure 1-34. CUT&Tag Library Quality Control.  Figure 1-35. IGV Genome Browser Tracks Top: published reference data; Bottom: UcallM® HisMod CUT&Tag Library Fast Kit  Figure 1-36. TSS Signal Enrichment Plot Left: UcallM® HisMod CUT&Tag Library Fast Kit; Right: published reference data  Figure 1-37. Super-Enhancer (SE) Identification # Customer Publications 1.eLife: Super-enhancer driven ZFP36L1 promotes PD-L1-mediated immune escape in gastric cancer via HDAC3 mRNA degradation (DOI:10.7554/eLife.96445)  Figure 1-38. SE identification results by CUT&Tag  Figure 1-39. The study used H3K27ac CUT&Tag profiling to reveal super-enhancer (SE) heterogeneity in infiltrative and expanding gastric cancer. ZFP36L1-SE was significantly enriched in infiltrative GC. SE inhibitor (JQ1/THZ1) validated its function driving ZFP36L1 transcription. 2.Adv Sci: Mechanism of histone lactylation modification in glioblastoma drug resistance (DOI:10.1002/advs.202309290)  Figure 1-40. CUT&Tag analysis revealed that H3K9la is widely enriched in gene promoter regions (LUC7L2) in TMZ-resistant cells.
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Assure safe centrifugation and storage of reagents, restriction enzymes and other biochemical reagents and samples by using the screw cap micro tubes. Their robust design and material selection are well suited for biologics. Screw cap micro tube caps offer a durable design incorporating an O-ring (e.g. with an insert TPE O-ring molded directly into the cap) that helps prevent leaks under demanding conditions and 2D bar code can help with samples tracking and identification. Feature - Manufactured from ultra-pure polypropylene (USP Class VI) which was specifically selected for high clarity and biologic applications. - Produced in ISO 13485:2016 and ISO 9001:2015. - The bottom 2D code facilitates sample identification - Unique dual-forming technology, multiple-point sealed safety latch design - The soft gasket and tube cap are integrally molded, eliminating the risk of the sealing gasket falling off and achieving excellent sealing performance - Sterile, Non-DNase/RNase, Pyrogen-free - Non-silicone coated - Withstand a centrifugal force of up to 20,000 x g - Provide leak-proof sealing at -80℃ - Offer 10 colour options for screw cap The color of the cap can be customized. Custom requests are welcome. Please inquire.
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U-Blot® GAPDH Rabbit mAb
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PCR reaction vessels adopt ultra-pure medical-grade polypropylene used in the finest quality molding process to ensure the highest quality tubes, strips, caps, and microplates for PCR.
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PCR reaction vessels adopt ultra-pure medical-grade polypropylene used in the finest quality molding process to ensure the highest quality tubes, strips, caps, and microplates for PCR.
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PCR reaction vessels adopt ultra-pure medical-grade polypropylene used in the finest quality molding process to ensure the highest quality tubes, strips, caps, and microplates for PCR.
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PCR reaction vessels adopt ultra-pure medical-grade polypropylene used in the finest quality molding process to ensure the highest quality tubes, strips, caps, and microplates for PCR.
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