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Wang J et. al. (March 2024). Natural variation in BnaA9.NF-YA7 contributes to drought tolerance in Brassica napus L Nat Commun. 15(1):2082.
The study identifies a transcription factor, BnaA9.NF-YA7, in Brassica napus that negatively regulates drought tolerance. This factor is affected by specific SNPs, leading to downregulation of its expression and subsequent activation of inhibitory factors of ABA-induced stomatal closure. These findings provide insights into the molecular mechanisms of drought tolerance in B. napus and suggest a potential target for breeding drought-tolerant cultivars.
Products Used: EpiQuik Plant ChIP Kit
Muhammad A et. al. (March 2024). Sex-specific epigenetics drive low GPER expression in gastrointestinal smooth muscles in type 2 diabetic mice Sci Rep. 14(1):5633.
This study examines how epigenetic modifications, particularly low G-protein coupled estrogen receptor (GPER) expression, contribute to gastrointestinal (GI) symptoms in type 2 diabetes mellitus (T2D), with a focus on sex-specific differences. The findings suggest that T2D alters GPER expression through DNA methylation and histone modifications, influencing GI motility in a sex-specific manner, which may have implications for understanding and managing GI symptoms in diabetic patients.
Products Used: EpiQuik Dnmt3A Assay Kit, EpiQuik Dnmt3B Assay Kit
Xu X et. al. (March 2024). N6-methyladenosine demethyltransferase FTO mediated m6A modification of estrogen receptor alpha in non-small cell lung cancer tumorigenesis Oncogene.
In this study, researchers investigated the role of the N6-methyladenosine (m6A) demethyltransferase FTO in non-small cell lung cancer (NSCLC) tumorigenesis. They found that FTO expression was reduced in NSCLC samples and correlated with poor prognosis, and that FTO inhibited tumor cell growth and metastasis in vitro and in vivo by targeting estrogen receptor alpha (ESR1) mRNA for m6A modification, which affected its stability and facilitated tumor growth. This study suggests a potential therapeutic strategy targeting the FTO-YTHDF1-IGF2BP3-ESR1 axis in NSCLC.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Tong KY et. al. (March 2024). Novel PLCZ1 mutation caused polyspermy during in vitro fertilization Asian J Androl.
The article investgates a novel missense mutation (c.1154C>T, p.R385Q) in the phospholipase C zeta 1 (PLCZ1) gene associated with polyspermy during in vitro fertilization (IVF). They found that multiple PLCZ1-mutated sperm induced pronuclear (PN) formation, suggesting that the mutated PLCZ1 caused Ca2+ oscillations that exceeded the threshold for PN formation. Assisted oocyte activation (AOA) after intracytoplasmic sperm injection (ICSI) enabled normal fertilization, highlighting the potential therapeutic value of AOA for patients with sperm-derived polyspermy.
Products Used: PLCZ1 Polyclonal Antibody
Pianka ST et. al. (March 2024). D-2-HG Inhibits IDH1mut Glioma Growth via FTO Inhibition and Resultant m6A Hypermethylation Cancer Res Commun.
This study investigates how D-2-hydroxyglutarate (D-2-HG), produced in IDH1mut gliomas, inhibits tumor growth by targeting the m6A epitranscriptomic regulator FTO. The research shows that D-2-HG reduces glioma cell proliferation by inhibiting FTO, leading to m6A hypermethylation of specific mRNA transcripts, including ATF5, which contributes to increased apoptosis. These findings suggest that targeting the D-2-HG-FTO-m6A axis could be a potential therapeutic strategy for IDH1wt gliomas.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Ge L et. al. (March 2024). The RNA m6A reader IGF2BP3 regulates NFAT1/IRF1 axis-mediated anti-tumor activity in gastric cancer Ge L et. al. (March 2024).
The article examines the role of the RNA m6A reader protein IGF2BP3 in regulating the NFAT1/IRF1 axis and its anti-tumor activity in gastric cancer (GC). IGF2BP3 is upregulated in GC tissues and associated with poor prognosis, promoting GC progression by enhancing NFAT1 expression and inhibiting IRF1 expression, thus suppressing the interferon signaling pathway. Targeting IGF2BP3 may offer a potential therapeutic strategy for GC treatment.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Muhammad A et. al. (March 2024). Sex-specific epigenetics drive low GPER expression in gastrointestinal smooth muscles in type 2 diabetic mice Muhammad A et. al. (March 2024).
The study explores the role of sex-specific epigenetic modifications in driving low GPER expression in gastrointestinal smooth muscles in type 2 diabetic (T2D) mice. T2D leads to decreased GPER expression, which is associated with promoter hypermethylation and reduced histone modifications, particularly in female mice, suggesting a female hormone-mediated mechanism. Targeting GPER expression through epigenetic modifications may offer a potential therapeutic avenue for gastrointestinal complications in T2D.
Products Used: EpiQuik Nuclear Extraction Kit
Han X et. al. (March 2024). Arginine methylation of ALKBH5 by PRMT6 promotes breast tumorigenesis via LDHA-mediated glycolysis Front Med.
The article investigates the role of arginine methylation of ALKBH5 by PRMT6 in promoting breast tumorigenesis. The findings suggest that PRMT6-mediated arginine methylation of ALKBH5 enhances LDHA-mediated glycolysis, highlighting a potential therapeutic target for breast cancer treatment.
Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric)
Rea M et. al. (March 2024). A dynamic model of inorganic arsenic-induced carcinogenesis reveals an epigenetic mechanism for epithelial-mesenchymal plasticity Environ Pollut. :123586.
This study presents a dynamic in vitro model of inorganic arsenic (iAs)-induced carcinogenesis that extends to 28 weeks of iAs exposure, revealing intermediate, stable cellular states during epithelial-to-mesenchymal transition (EMT). The model highlights the importance of considering all aspects of EMT and the mesenchymal-to-epithelial transition (MET), and suggests potential for developing targeted therapeutics by understanding the epigenetic systems controlling these transitions.
Products Used: Protease Inhibitor Cocktail
Nakazawa Y et. al. (March 2024). Delivery of a BET protein degrader via a CEACAM6-targeted antibody-drug conjugate inhibits tumour growth in pancreatic cancer models Nat Commun. 15(1):2192.
This study explores a novel therapeutic approach for pancreatic ductal adenocarcinoma (PDAC) using a bromodomain and extra-terminal (BET) protein degrader delivered via a CEACAM6-targeted antibody-drug conjugate (ADC). The ADC, named 84-EBET, demonstrates potent tumor-killing effects on PDAC organoids and bystander efficacy on CEACAM6-negative PDAC cells and cancer-associated fibroblasts, leading to marked tumor regression in PDAC patient-derived xenografts in mouse models without significant toxicity.
Products Used: EpiQuik Nuclear Extraction Kit II (Nucleic Acid-Free)
Lin Z et. al. (March 2024). MiR-200c reprograms fibroblasts to recapitulate the phenotype of CAFs in breast cancer progression Cell Stress. 8:1-20.
This study reveals a subgroup of cancer-associated fibroblasts (CAFs) in breast cancer with high miR-200c expression, driving mesenchymal-to-epithelial transition (MET) and promoting breast cancer aggressiveness. MiR-200c induction in fibroblasts mimics CAF-like features, stimulating pro-tumorigenic inflammation and glycolysis via NFκB-HIF signaling, and inducing a senescent phenotype, ultimately fostering carcinoma cell resistance to apoptosis, proliferation, and immunosuppression. Conversely, inhibiting miR-200c in fibroblasts restrains tumor growth, highlighting the potential of targeting this pathway as an anti-cancer strategy.
Products Used: FitAmp General Tissue Section DNA Isolation Kit
