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   Home  »  Epigenetic Resources  »  Epigenetic Research Papers 5/15/23 - 5/19/23 
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Epigenetic Research Papers 5/15/23 - 5/19/23


Li S et. al. (May 2023). Paternal combined botanicals contribute to the prevention of estrogen receptor-negative mammary cancer in transgenic mice. J Nutr.
In this study, the researchers aimed to investigate the potential preventive effects of combined paternal consumption of broccoli sprouts (BSp) and green tea polyphenols (GTPs) on estrogen receptor-negative (ER(-)) mammary cancer in transgenic mice. They examined tumor growth, epigenetic changes, and gene expression profiles in offspring, revealing promising transgenerational influences and epigenetic regulation as mechanisms for cancer prevention.
(Products Used: EpiQuik Nuclear Extraction Kit)

Huang XW et. al. (May 2023). Autophagy benefits the in vitro and in vivo clearance of Talaromyces marneffei. Microb Pathog. :106146.
This study investigated the role of autophagy in host defense against Talaromyces marneffei, a fungal infection associated with high mortality. The researchers found that autophagy promoted by rapamycin or EBSS inhibited the viability of the fungus in macrophages and that autophagy activation reduced fungal burden and lung inflammation in a mouse model, suggesting autophagy as a potential therapeutic target for treating talaromycosis.
(Products Used: EpiQuik Whole Cell Extraction Kit)

Sapehia D et. al. (April 2023). High dietary folate and low vitamin B12 in the parental diet disturbed the epigenetics of imprinted genes MEST and PHLDA2 in mice placenta.  J Nutr Biochem. :109354.
This study investigated the impact of dietary combinations of folic acid and low vitamin B12 on the epigenetics of imprinted genes in the placenta of mice. The results showed that the imprinted genes MEST and PHLDA2 were significantly affected by vitamin B12 deficiency and high folate conditions, leading to changes in gene expression and histone modifications, suggesting that imbalanced parental diet can disrupt the epigenetic regulation of these genes.
(Products Used: MethylFlash Global DNA Methylation (5-mC) ELISA Easy Kit (Colorimetric))

Li Y et. al. (August 2023). TRAF3-EWSR1 signaling axis acts as a checkpoint on germinal center responses. J Exp Med. 220(8)
This study reveals that the TRAF3-EWSR1 signaling axis acts as a checkpoint in regulating germinal center (GC) responses, which are crucial for humoral immunity and vaccine effectiveness. The axis inhibits the upregulation of Bcl6, a key regulator of GC formation and immunoglobulin G (IgG) production, providing insights into the molecular mechanism controlling persistent GC generation and suggesting it as a potential therapeutic target for modulating GC responses and enhancing humoral immunity in infectious diseases.
(Products Used: EpiQuik Plant ChIP Kit)

Xu Z et. al. (April 2023). NaWRKY3 is a master transcriptional regulator of the defense network against brown spot disease in wild tobacco. J Exp Bot.
This study identifies NaWRKY3 as a key transcription factor that plays a crucial role in the defense response against tobacco brown spot disease caused by Alternaria alternata in Nicotiana attenuata. NaWRKY3 regulates multiple defense genes involved in jasmonic acid and ethylene biosynthesis, phytoalexin production, and resistance against A. alternata, highlighting its role as a master regulator in coordinating various defense mechanisms in response to the pathogen.
(Products Used: EpiQuik Plant ChIP Kit)

Guo Z et. al. (May 2023).  Carbon Dots from Lycium barbarum Attenuate Radiation-Induced Bone Injury by Inhibiting Senescence via METTL3/Clip3 in an m(6)A-Dependent Manner.  ACS Appl Mater Interfaces. 15(17):20726-20741.
This study demonstrates the efficacy of Lycium barbarum-derived carbon dots in alleviating radiation-induced bone injury by inhibiting senescence via METTL3/Clip3-mediated N6-methyladenosine (m6A) modification. The carbon dots promote bone healing, prevent osteoradionecrosis, and offer a promising approach for managing radiation-induced bone injury.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

An X et. al. (April 2023). ZBTB7C m6A modification incurred by METTL3 aberration promotes osteosarcoma progression Transl Res.
This study demonstrates that aberrant N6-methyladenosine (m6A) modification mediated by METTL3 promotes osteosarcoma progression. The upregulation of METTL3 and subsequent increase in m6A modification contribute to the oncogenic effects by targeting the ZBTB7C oncogenic protein, suggesting that targeting the METTL3/ZBTB7C axis could be a potential therapeutic strategy for osteosarcoma.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Fu Y et. al. (April 2023). LncRNA GAS5 regulated by FTO-mediated m6A demethylation promotes autophagic cell death in NSCLC by targeting UPF1/BRD4 axis Mol Cell Biochem.
This study reveals that long non-coding RNA GAS5, regulated by FTO-mediated m6A demethylation, promotes autophagic cell death in non-small cell lung cancer (NSCLC) by targeting the UPF1/BRD4 axis. GAS5 downregulation in NSCLC is associated with poor prognosis, and its inhibition by FTO reduces m6A methylation, leading to autophagic cell death and suppression of NSCLC tumor growth through interactions with UPF1 and regulation of BRD4 mRNA stability.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Piell KM et. al. (May 2023). Disruption of the mouse liver epitranscriptome by long-term aroclor 1260 exposure Environ Toxicol Pharmacol. 100:104138.
This study investigates the effects of chronic exposure to Aroclor 1260, a mixture of polychlorinated biphenyls (PCBs), on the liver epitranscriptome in mice. The findings reveal that long-term exposure to Aroclor 1260, in combination with a low-fat diet, leads to alterations in hepatic RNA modifications associated with non-alcoholic fatty liver disease (NAFLD) and identifies specific pathways affected by diet and PCB exposure.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Li S et. al. (April 2023). A germline variant in the BET1L 3'-UTR confers colorectal cancer susceptibility by reducing miRNA binding and m6A modification Cancer Res.
This study identifies a genetic variant (rs11245997) in the BET1L gene's 3'-UTR that is associated with increased susceptibility to colorectal cancer. The variant disrupts miR-140-3p binding, leading to reduced N6-methyladenosine (m6A) modification and increased expression of BET1L, promoting tumor growth and poor patient prognosis.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Chen YH et. al. (May 2023).  m6A-dependent mevalonate kinase in juvenile hormone synthesis pathway regulates the diapause process of bivoltine silkworm (Bombyx mori) Mol Biol Rep.
This study investigates the role of N6-adenosine methylation (m6A) in regulating the diapause process of bivoltine silkworms (Bombyx mori). The findings show that m6A methylation, particularly in the mevalonate kinase (MK) gene involved in hormone synthesis, influences diapause regulation, as demonstrated by the knockdown of MK resulting in a shift from non-diapause to diapause egg production.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Zhu K et. al. (May 2023).  RNA N6-methyladenosine reader IGF2BP3 interacts with MYCN and facilitates neuroblastoma cell proliferation Cell Death Discov. 9(1):151.
This study focuses on the role of insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) in neuroblastoma and its interaction with N-myc. The findings demonstrate that IGF2BP3 promotes NB cell proliferation by regulating N-myc RNA stability through N6-methyladenosine (m6A) modification, revealing a positive feedback loop between IGF2BP3 and N-myc that facilitates NB progression.
(Products Used: EpiQuik m6A RNA Methylation Quantification Kit (Colorimetric))

Geng S et. al. (May 2023). METTL3-Mediated m6A Modification of TRIF and MyD88 mRNAs Suppresses Innate Immunity in Teleost Fish, Miichthys miiuy J Immunol.
This study investigates the role of methyltransferase METTL3 and N6-methyladenosine (m6A) modification in regulating innate immunity in Miichthys miiuy, a teleost fish species. The findings reveal that METTL3-mediated m6A modification of TRIF and MyD88 mRNAs suppresses innate immunity by inhibiting the TLR pathway, providing insights into the molecular mechanism by which RNA methylation controls immune response to pathogens in teleost fish.
(Products Used: EpiQuik CUT&RUN m6A RNA Enrichment (MeRIP) Kit)


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Suggested Reads:

Enhancer Activation and H3K27ac in Cell-State Plasticity
m6A RNA Methylation in Cancer Immunity and Therapeutic Resistance
cfDNA Methylation in Liquid Biopsy Research: Where Global 5-mC, 5-hmC, Enrichment, and RRBS Readouts Fit
Understanding Open Chromatin Bias in CUT&RUN and CUT&Tag
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