Lu Lab_Columbia
@LuLaboratory
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Chromatin & Cancer Biologists at Columbia university
New York, NY
Joined October 2017
RT @sproul_lab: Want to work with us on DNA methylation and rare genetic disease? Fully funded PhD project with deadline 16th May:. https://….
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Excited to share this review on chromatin-metabolism crosstalk, lead by our star student Varun Sahu. Here, Varun summarizes the molecular principles governing metabolite-chromatin interaction & highlights emerging technologies that could advance the field. There’re lots to learn!.
In this review for our focus issue on patterns in molecular biology, @LuLaboratory explores how metabolites and metabolic enzymes regulate chromatin and histone modification patterns, highlighting the crosstalk between the metabolome and the epigenome.
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Check out this important work - congrats to KJ, Victoria and the team!.
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RT @WhetstineLab: Please Repost-.Excited to be recruiting @CeiFccc @FoxChaseCancer #epigenetic #faculty to continue building our energetic,….
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Lastly, shoutout to two other papers that characterize the interaction between DNMT3A and H2AK119Ub nucleosome. by Jikui Song and Greg Wang groups. by @mdrwilson group.
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Congrats again to @KristjanGretars @Xagbomson Susan Gloor, Dan Weinberg, @KJArmache @GCloner @epicypher and everyone involved! Thanks to the reviewers and editor @ScienceAdvances for improving our manuscript.
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Here we go - our preprint on the interplay between DNMT3A and polycomb H2AK119Ub mark is published. We believe these findings offer a potential mechanism driving DNA hypermethylation in cancer. Pls see tweetorial for more details.
Excited to share our new preprint on the interaction between DNMT3A1 and H2AK119Ub. This work is the fruit of a collaboration between @LuLaboratory, @KJArmache Lab and @epicypher and co led with @Xagbomson
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RT @RothbartLab: What's new and what's next in cancer epigenetics research? Join us for the 2024 VAI Epigenetics Symposium. Our allstar spe….
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Please see tweetorial above for more details! As always, we welcome your feedback and suggestions.
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It also implies that perturbing the interaction between DNMT3A-H2AK119Ub could be a potential strategy to prevent or reverse DNA hypermethylation in cancer.
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Our results suggest that polycomb CGI methylation state reflects the balance between DNMT3A and TET activity. In cancers, either insufficient TET activity, or increased DNMT3A binding, can lead to CGI hypermethylation.
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Please see tweetorial below for the latest from the lab led by @KristjanGretars. In collaboration with @GCloner @KJArmache @Xagbomson, this work reveals molecular details of DNMT3A targeting to polycomb CGIs and its implication for cancer-associated DNA hypermethylation.
Excited to share our new preprint on the interaction between DNMT3A1 and H2AK119Ub. This work is the fruit of a collaboration between @LuLaboratory, @KJArmache Lab and @epicypher and co led with @Xagbomson
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RT @WhetstineLab: Free Hybrid World Class Symposium- Featuring Academic and Pharma/Biotech Leaders!.Register asap. >400 registered and coun….
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We thank the editor and reviewers for suggestions of improving our work. And as always, appreciate your feedback!.
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We propose cancer metabolic alterations may serve as biomarkers for applying HDAC inhibitors and perhaps other chromatin drugs.
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Isotope tracing analysis with @Warburg_Ye lab indeed shows reduced flux of amino acid uptake/breakdown and nucleotide synthesis following HDAC inhibition, which are more detrimental to metabolically demanding NRF2-active cancer cells.
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ie. global increases in histone acetyl "titrate" BRD4 binding from highly expressed genes, causing their downregulation. These include many metabolic genes (eg. glutamine transporter/catabolic enzymes).
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