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Gu T et. al. (June 2024). METTL3-mediated pre-miR-665/DLX3 m6A methylation facilitates the committed differentiation of stem cells from apical papilla Exp Mol Med.
This study explored the role of METTL3 in the differentiation of stem cells from the apical papilla (SCAPs) into odonto/osteoblastic lineages. METTL3 influences m6A modification levels, impacting SCAP differentiation. It was found that METTL3-mediated m6A methylation accelerates pre-miR-665 degradation with the help of YTHDF2, and that miR-665 targets DLX3, which is also directly regulated by METTL3 via YTHDF1. METTL3+/- mice showed root dysplasia and increased bone loss. The METTL3/pre-miR-665/DLX3 pathway may be a new target for SCAP-based tooth root and maxillofacial bone tissue regeneration.
Products Used: EpiQuik Quantitative PCR Fast Kit, EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Wen D et. al. (May 2024). N6-methyladenosine-modified SENP1, identified by IGF2BP3, is a novel molecular marker in acute myeloid leukemia and aggravates progression by activating AKT signal via de-SUMOylating HDAC2 Mol Cancer. 23(1):116.
This study found that SENP1 is upregulated in high-risk acute myeloid leukemia (AML) patients and linked to poor prognosis. SENP1 promotes AML cell proliferation and survival by activating the AKT/mTOR pathway through desumoylation of HDAC2, which enhances EGFR transcription. IGF2BP3, also upregulated in high-risk AML, binds to SENP1's 3'-UTR in an m6A-dependent manner, increasing SENP1 expression and further activating AKT signaling. This research identifies the IGF2BP3/SENP1/HDAC2-AKT axis as a crucial mechanism in AML progression.
Products Used: EpiQuik Nuclear Extraction Kit, EpiQuik HDAC2 Assay Kit (Colorimetric)
Chao M et. al. (May 2024). Profling of m6A methylation in porcine intramuscular adipocytes and unravelling PHKG1 repress porcine intramuscular lipid deposition in an m6A-dependent manner Int J Biol Macromol. :132728.
The article explored m6A methylation's role in porcine intramuscular fat (IMF) deposition. Researchers found that reducing m6A levels via METTL3 knockdown decreased PHKG1 expression, promoting adipogenic differentiation. Bamei pigs showed higher IMF content but lower m6A and PHKG1 expression than Large White pigs. These results highlight the importance of m6A modification and PHKG1 in regulating IMF content and meat quality.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Park SH et. al. (June 2024). The m6A writer RBM15 drives the growth of triple-negative breast cancer cells through the stimulation of serine and glycine metabolism Exp Mol Med.
This study examined the role of m6A writer RBM15 in triple-negative breast cancer (TNBC) cells. Elevated RBM15 levels were linked to poor clinical outcomes in basal-like breast cancer patients. Gene expression profiling showed that RBM15 correlates with serine and glycine metabolic genes. RBM15 directly binds to RNA targets, influencing m6A levels and promoting cancer cell growth through altered serine and glycine metabolism. These findings suggest RBM15 as a potential therapeutic target in breast cancer.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Zhao L et. al. (May 2024). Transcription factor OsWRKY11 induces rice heading at low concentrations but inhibits rice heading at high concentrations J Integr Plant Biol.
The article investigates the role of the transcription factor OsWRKY11 in regulating the heading date of rice. Using CRISPR-Cas9 screening, it was found that both oswrky11 mutants and OsWRKY11-overexpressing plants exhibited delayed heading compared to wild-type plants. OsWRKY11 promotes flowering by inducing OsMADS14 and OsMADS15. However, high OsWRKY11 levels form a complex with Hd1 and DTH8, suppressing Ehd1 and delaying heading. Mild drought increases OsWRKY11, promoting heading, while severe drought further upregulates OsWRKY11, causing delays. This study reveals OsWRKY11's dual role in rice heading regulation.
Products Used: EpiQuik Plant ChIP Kit
Riccardi F et. al. (June 2024). Age-dependent regulation of ELP1 exon 20 splicing in Familial Dysautonomia by RNA Polymerase II kinetics and chromatin structure PLoS One. 19(6):e0298965.
This study investigates how RNA Polymerase II (RNAPII) kinetics and chromatin structure affect ELP1 exon 20 splicing in Familial Dysautonomia (FD). Results show that slower RNAPII elongation and repressive chromatin marks promote exon skipping, while more relaxed chromatin favors exon inclusion. In a mouse model, aging correlated with reduced RNAPII density, increased repressive chromatin marks, and decreased inclusion of ELP1 exon 20. Demethylation of H3K27 in cell experiments increased RNAPII elongation and promoted exon inclusion. These findings suggest a model where age-related changes in chromatin modify RNAPII elongation rates, affecting ELP1 splicing in FD.
Products Used: EpiQuik Tissue Chromatin Immunoprecipitation (ChIP) Kit
Akhter MZ et. al. (May 2024). FAK regulates tension transmission to the nucleus and endothelial transcriptome independent of kinase activity Cell Rep. 43(6):114297.
This study reveals that focal adhesion kinase (FAK) regulates tension transmission to the nucleus and the endothelial transcriptome in endothelial cells (ECs), independent of its kinase activity. FAK depletion leads to RhoA-Rho-kinase pathway hyperactivation, increasing EC tension and activating DNMT3a. DNMT3a then methylates the KLF2 promoter, impairing KLF2 and its target S1PR1 synthesis, resulting in a leaky EC transcriptome. Restoring FAK activity or inhibiting RhoA-emerin-DNMT3a in damaged lung ECs restores the restrictive EC transcriptome, suggesting a crucial role for FAK in maintaining lung endothelial homeostasis.
Products Used: EpiQuik DNA Methyltransferase (DNMT) Activity/Inhibition Assay Kit
Pan B et. al. (June 2024). Activation of AMPK inhibits cervical cancer growth by hyperacetylation of H3K9 through PCAF Cell Commun Signal. 22(1):306.
This article explores how AMP-activated protein kinase (AMPK) activation inhibits cervical cancer growth through the PCAF-dependent hyperacetylation of H3K9. Metformin, an AMPK activator, was found to inhibit cervical cancer proliferation both in vitro and in vivo by inducing H3K9 acetylation and promoting chromatin remodeling. This leads to increased binding of H3K9ac to the promoters of tumor suppressor genes, enhancing their transcriptional activation. Importantly, the absence of PCAF prevents AMPK activation from inducing H3K9 acetylation. These findings highlight the role of PCAF in AMPK-mediated inhibition of cervical cancer growth and suggest potential clinical applications of metformin.
Products Used: EpiQuik Total Histone Extraction Kit
