Job Description:

Two Postdoctoral Associate positions in the laboratory of Dr. Hyunglok Chung in the Department of Neurology at Houston Methodist Research Institute & Weill Cornell Medicine are available.
Chung lab is seeking two postdocs: A) focus on determining how lipids in glia contribute to neurodegeneration, particularly via neuroinflammation. B) help diagnose of rare disease patients and identify the therapeutic options using a fly model. Successful applicants will have a Ph.D. in Genetics, Developmental Biology, Neuroscience, or related fields, and previous experiences using Drosophila melanogaster is highly preferred but not required. The candidate is expected to drive and take ownership of their research project, design and perform biological experiments rigorously, work collaboratively with members within and outside the lab, be highly organized and communicative, and maintain a high work ethic.

U.S. News & World Report has named Houston Methodist Hospital the Best Hospital in Texas for 11years in a row, and No. 15 nationwide. Houston Methodist Research Institute (HMRI) is a non-profit academic research institute affiliated with Weill Cornell Medical College and provides unique translational research opportunities. HMRI is located in the Texas Medical Center, adjacent to Rice University, Baylor College of Medicine, and MD Anderson Cancer Center, providing ample opportunities to interact with researchers in these neighboring institutions.

Houston Methodist & Weill Cornell Medicine will support a relocation fee, visa & Health insurance. The salary of this yearly renewable position will be established according to NIH guidelines ($54,840-$66,000).

Applicants should directly e-mail Dr. Chung at hchung2@houstonmethodist.org, a single PDF file that includes their CV and the names/contact information of three references. Please refer to the representative publications for details.

1. Chung et al. #. (2022) Glial derived Sphingosine 1-phosphate activates the immune system and promotes neuronal dysfunction: implications for multiple sclerosis. (minor revision, Cell metabolism) #Corresponding author.
http://dx.doi.org/10.2139/ssrn.4121836
2. Chung et al. (2022) De novo variants in EMC1 lead to neurodevelopmental delay and cerebellar degeneration and affect glial function in Drosophila. Human Molecular Genetics. PMID: 35234901
3. Chung et al. (2020) De novo variants in CDK19 are associated with a new syndrome with intellectual disability and epileptic encephalopathy. American Journal of Human Genetics: 106:717-725. PMID: 32330417
4. Chung et al. (2020) Loss- or gain-of-function mutations in ACOX1 cause axonal loss via different mechanisms. Neuron: 106:589-606. PMID: 32169171
5. Ansar & Chung et al. (2019) Biallelic variants in IQSEC1 cause intellectual disability, developmental delay, and short stature. American Journal of Human Genetics: 105:907-920. PMID: 31607425
6. Ansar & Chung et al. (2018) Bi-allelic loss-of-function variants in DNMBP cause infantile cataracts. American Journal of Human Genetics: 103:568-578. PMID: 30290152
7. Ansar & Chung et al. (2018) Visual impairment and progressive phthisis bulbi caused by recessive pathogenic variant in MARK3. Human Molecular Genetics: 27:2703-2711. PMID: 29771303
8. Chung et al. (2016) Drosophila Schip1 links Expanded and Tao-1 to regulate Hippo signaling. Developmental Cell: 36(5):p.511-24. PMID: 2695454