Biotechnology at CCSF

Yuhui Huang

I moved to SF about ten years ago. After graduating from Balboa High School, I went to UC Davis where I decided to do a double major in psychology and neurobiology, physiology and behavior because both majors discuss many topics in neuroscience, all inter-connected.

I joined CCSF’s Biotech Program to get more hands-on lab experience and instruction in working well with cells. Cells are very vulnerable, and they get contaminated so easily! I ended up applying for a CIRM internship.

At my internship, I am studying Huntington's Disease, which can make our brain cells slowly degenerate or die. Huntington’s is caused by a mutated gene segment with too many CAG fragments. Currently, I am working on two projects. One is studying the relationship between the length of CAG repeats and the neurons' risk of death, and the onset of Huntington's Disease. The other is testing a set of designed CAG fragment-inhibiting genes by inserting them into cells with too many CAG fragments. Therefore, we can prevent the protein from getting misfolded by the long CAG fragment and prevent cell degeneration.

The most important thing from this internship is to get real experience working in an actual lab. Being immersed in the environment I learn a lot from other researchers, and I have built relationships with them which will probably help me in the future.

Although my internship will be ending soon, I plan to continue work at the lab that hosted my internship for a short time longer to finish up my projects. Then I would like to start applying to graduate school, hopefully a great Ph.D. program in neuroscience.

Yuhui Huang-Simulating Huntington’s Disease in vitro-2022.pdf

CIRM Intern: Yuhui Huang

Stem Cell Internship Lab: Finkbeiner Lab, Gladstone Institutes

Project Title: Simulating Huntington’s Disease in vitro:

Survival of iPSC-derived Cortical Neuron with Overexpansion of CAG Trinucleotide Repeats in Htt Gene

Abstract: Huntington’s disease (HD) is a neurodegenerative disease caused by the expansion of the Cytosine, Adenine, Guanine (CAG) trinucleotide repeat in HTT gene. The CAG repeat causes the Htt protein to misfold and aggregate leading to numerous cellular pathologies and cell death. We have investigated several pluripotent stem cell (PSC) models of HD including an isogenic series with CAG expansions as well as induced pluripotent stem cells (iPSCs) from patients with HD. To examine if PSCs displayed phenotypes related to HD, we differentiated them into cortical neurons and evaluated degenerative phenotypes such as the risk of death. To do this, we tracked the survival of CAG expanded and control neurons over time and then used Cox Mixed Effect Models (Cox ME) to determine their survival. We found that PSCs that harbored CAG repeat expansions displayed a relatively higher cumulative risk of death than unaffected control neurons. We have also made cortical neurons from HD patients with different age-onset and are evaluating if they also display death rates that are correlated to their disease trajectory.

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Yuhui Huang

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