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<!DOCTYPE html>
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<title>Research · Brent Y. Chick</title>
<meta name="description" content="Research themes: chromatin remodeling, T cell fate, in vitro T cell engineering, and signaling dynamics.">
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<h1 class="name"><a href="index.html">Brent Y. Chick</a></h1>
<p class="tagline">PhD Candidate · Salk Institute · La Jolla, CA</p>
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<a href="mailto:bchick@salk.edu">Email</a>
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<a href="https://scholar.google.com/citations?user=QQkDZcAAAAAJ&hl=en" target="_blank" rel="noopener">Scholar</a>
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<p class="lead">
I work on how cells use chromatin to encode, stabilize, and rewire identity, and how to leverage those mechanisms
to understand and engineer cell behavior. My approach pairs wet-lab genomics and bioengineering with computational analysis.
</p>
<h2><span class="num">01</span>Chromatin remodeling and T cell fate</h2>
<p>
My PhD work focuses on the BAF (mSWI/SNF) chromatin remodeling complex in T cells.
In a 2023 <a href="https://doi.org/10.1016/j.immuni.2023.05.005" target="_blank" rel="noopener"><em>Immunity</em></a>
paper (co-first author), we showed that canonical BAF activity shapes the enhancer landscape that licenses
CD8⁺ T cell effector and memory fates. Loss of BAF function blocks the chromatin priming required for memory commitment,
implicating BAF as a key regulator of T cell durability with direct relevance to next-generation cell therapies.
</p>
<h2><span class="num">02</span>Dynamic signaling and chromatin</h2>
<p>
The final chapter of my PhD is focused on how chromatin decodes dynamic signaling. Most chromatin profiling treats signaling as a static input,
but cells in vivo encounter signals that vary in amplitude, duration, and timing. To get at this, I pair optogenetic
control of signaling pathways with a simplified 96-well CUT&RUN protocol I built, mapping how time-varying inputs translate
into changes in chromatin state and gene regulation.
</p>
<h2><span class="num">03</span>In vitro T cell engineering from stem cells</h2>
<p>
Earlier in the <a href="https://crookslab.mednet.ucla.edu/" target="_blank" rel="noopener">Crooks lab at UCLA</a>,
I contributed to the development of the artificial thymic organoid (ATO) system, a stromal cell-based platform for
generating mature T cells from human hematopoietic stem cells <em>in vitro</em>. The
<a href="https://www.nature.com/articles/nmeth.4237" target="_blank" rel="noopener">original methodology</a>
(<em>Nature Methods</em>, 2017) and extensions in
<a href="https://doi.org/10.1016/j.stem.2018.12.011" target="_blank" rel="noopener"><em>Cell Stem Cell</em></a>
(2019) and <a href="https://doi.org/10.1016/j.celrep.2020.108320" target="_blank" rel="noopener"><em>Cell Reports</em></a>
(2020) gave the field a tractable system to dissect human T cell development and to generate engineered T cells from iPSCs.
</p>
<h2><span class="num">04</span>Bioengineering and signaling dynamics</h2>
<p>
My MA work at UCSB with <a href="https://labs.mcdb.ucsb.edu/wilson/max/" target="_blank" rel="noopener">Max Wilson</a>
used optogenetic tools to perturb signaling pathways with quantitative control over timing and amplitude.
The bioengineering perspective of that lab still shapes how I think about chromatin and cell-state transitions:
dynamics, feedback, and hysteresis, rather than static localization.
</p>
<h2><span class="num">05</span>What I'm thinking about next</h2>
<p>
Where I want to push next is the intersection of chromatin biology and modern ML,
with an eye toward therapeutic applications of chromatin engineering. More on this to come.
</p>
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<span>© 2026 Brent Y. Chick</span>
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<a href="mailto:bchick@salk.edu">bchick@salk.edu</a>
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