Walter Knight Email & Phone Number

Boston, Ma, Us

Lawrence Township, Nj, Us

Pleasanton, California, Us

Worked on a small team to develop novel approaches to mammalian gene editing by combining state-of-the-art techniques with Inscripta's existing MADzyme technology. • Developed and integrated new editing workflows within a matter of months• Brought new editing approaches into the group from ideation to execution• Required deep understanding of salient gene editing literature• Worked on a small team in a fast-paced environment

Pleasanton, California, Us

Worked within a large team developing a novel product relevant to the mammalian genome engineering space. • Developed and optimized high-throughput mammalian editing protocols• Tested and optimized multiple editing workflows• Conducted experimentation and analysis under tight deadlines• Presented results and drove/informed decision making to stakeholders within program on a frequent basis

Aurora, Co, Us

The focus of my postdoctoral fellowship has been to develop protocols for use of human stem cell derived cardiomyocytes (hiPSC-CMs) to model cardiovascular disease in the petri dish, and use these approaches to identify novel disease mechanisms and treatment strategies. Specific projects: • Developed a combination of methods to improve maturity in human stem cell derived cardiomyocytes (hiPSC-CMs) producing adult-like cardiac cells (findings published in January 2021). • Using CRISPR-Cas9 mutation strategies, created an hiPSC-CM based model of the cardiac disease hypertrophic cardiomyopathy (HCM). Now, focused on phenotypically characterizing HCM in human cardiac tissue and hiPSC-CMs. • Using gene edited hiPSC-CMs, developing high throughput screening approaches to uncover novel treatment strategies for HCM.• Research supported by AHA Postdoctoral Fellowship from 2019-2020.• Research supported by CCTSI Co-Pilot Award in 2019-2020.

Rochester, New York, Us

I lead and developed a project characterizing the role of the protein phosphodiesterase 1C (PDE1C) in heart failure. We found that by degrading the small molecule cAMP, PDE1C regulates protective signaling mediated by cardiac adenosine A2 receptors. In heart failure, increased expression of PDE1C blocks this protective signaling, leading to cardiomyocyte cell death, cardiac hypertrophy, and fibrosis. Conversely, pharmacologically inhibiting or genetically deleting PDE1C is highly protective in heart failure. Although this work was conducted primarily in mouse models, PDE1C is highly expressed in human heart, and is indeed upregulated in human heart failure, making a potentially attractive therapeutic target. In conducting this project, I gained expertise in project planning, grant and scientific writing, and collaborated with a number of peers both in my lab and in other labs and institutions.

Washington, Dc, Us

I used mass spectrometry-based approaches (specifically MALDI-TOF) to innovate approaches for detecting the inflammatory marker C-reactive protein, CRP. CRP is thought to be a potentially important biomarker for the health of marine environments, consequently developing approaches to allow for its rapid quantification from samples would be useful.

Doctor Of Philosophy - Phd, Molecular Pharmacology

Bachelor Of Arts - Ba, Chemistry & Biochemistry (Double Major)

Bachelor Of Arts - Ba, Chemistry And Biology/Biochemistry (Double Major)