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Alexander Greben

@alexandergreben.bsky.social

Postdoc in Canzio Lab at UCSF. Studying chromatin in the brain and stochasticity in gene expression.

Alexander Greben @alexandergreben.bsky.social · 04/11/2025

Thanks to @xiaoliwu.bsky.social, @lisatraunmueller.bsky.social, and other collaborators and lab members for making this possible!

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Alexander Greben @alexandergreben.bsky.social · 04/11/2025

We hope that our work will be a step toward a fuller understanding of interconnections between chromatin regulators and shed light on a disorder lacking mechanistic insight. We are also very interested in the possible interplay between ZMYND11 and KMT2A in regulating oncogenesis.

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Alexander Greben @alexandergreben.bsky.social · 04/11/2025

Many chromatin regulators have been linked to NDD and ASD, an expanding family of “chromatinopathies” with overlapping symptoms and convergence in gene misregulation. To understand the network-scale behaviour of these systems, we need to unravel the dense interconnections between regulatory nodes.

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Alexander Greben @alexandergreben.bsky.social · 04/11/2025

We link ZMYND11 function to KMT2A, a histone methyltransferase and transcriptional activator which is itself the cause of a neurodevelopmental disorder. We find that ZMYND11 binds and inhibits KMT2A, repressing non-neuronal developmental programs and safeguarding neuronal gene expression.

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Alexander Greben @alexandergreben.bsky.social · 04/11/2025

Very pleased to share this work from my time as a graduate student with the Greenberg lab. We investigate the molecular function of ZMYND11, a tumor suppressor and chromatin reader which is also a cause of syndromic intellectual disability. Preprint available now: www.biorxiv.org/content/10.1...

biorxiv.org

ZMYND11 Restrains KMT2A to Enable a Neuronal Developmental Program

Mutations in the chromatin reader and tumor suppressor ZMYND11 are the cause of ZMYND11-related syndromic intellectual disability (ZRSID), a disorder characterized by symptoms such as language and mot...

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