top of page

Selected Publications


FEBS J​. 2022 Apr;289(8):2301-2317.

We examine how impaired germline gene repression by chromatin regulators may lead to impaired brain development & function in certain neurodevelopmental disorders (NDDs). We also discuss how to test hypotheses to determine the contribution of ectopic germline transcripts to chromatin-NDDs.


Genome Res. 2021 Jan 7;31(2):186-197. 

We found that loss of Kdm1a in mouse neurons lead to premature activation of neuronal activity-dependent enhancers & genes. A basic research step towards understanding the associated human KDM1A / LSD1 neurodevelopmental syndrome.

Cell Rep. 2020 Aug 11;32(6):108002.

August 10, 2020

We devised metabolic labeling of nascent RNAs and sequencing in the neural ensemble. Using this approach, we found a role of RAI1, Smith-Magenis Syndrome gene, in neuronal-activity dependent transcription and synaptic plasticity. Great collaboration with Dr. Michael Sutton lab at Michigan Neuroscience Institute. 

Communications Biology 2020 Jun 1;3(1):278.

June 01, 2020

We found mutually suppressive roles of H3K4me writer KMT2A and eraser KDM5C. This work provides proof of the principle of modulating single methyl histone enzymes to ameliorate neurodevelopmental disorders. Great collaboration with Tronson Lab!

Front Mol Neurosci 11:104

April 04, 2018

Christina's first first-author research article. We describe a patient mutation in KDM5C which has altered gene regulatory function in neurons.

Neuroscience 370:170-180

May 29, 2017

Bobby's first first-author research paper published.

Cell Rep. 14(5):1000-9.

February 09, 2016

Characterization of Kdm5c-Knockout mice. These mice will be valuable for future therapeutic development of intellectual disability and autism spectrum disorders. 

Nat Commun. ;6:6002. doi: 10.1038/ncomms7002.

January 22, 2015

The first paper from the lab! We developped a new RNA-seq method which allows us to profile full-length transcripts. 

Nat Struct Mol Biol. 18(7):769-76. doi: 10.1038/nsmb.2062.

June 22, 2011

We found that ADD domain of ATRX, which is enriched with ATRX-syndrome mutations, is a reading module for heterochromatin histone methylation status, low H3K4me and hight H3K9me3.

Cell. 128(6):1077-88. Epub 2007 Feb 22.

February 22, 2007

We discovered the first family of enzymes which can remove H3K4me3. One of the family members, JARID1C/KDM5C was known to be mutated in X-linked intellectual disability. We linked hitone methylation dynamics and human cognitive development for the first time. 

Please reload

Visit here for full publication list

bottom of page