Chen Yuan Kam

Assistant Professor

email: chenyuankam@mednet.ucla.edu
phone: 310-267-0133
office: CHS 43-118
lab website

Research Interests

Our research is centered on blood vessels with a focus on understanding remodeling of the vascular network in physiological and pathological settings. Leveraging a live imaging approach that utilizes multiphoton microscopy, we aim to deepen our understanding of the cellular mechanisms that dictate the developmental, regenerative and pathological states of the mammalian vasculature. Utilizing the mouse skin as a model, our longitudinal imaging platform allows us to track the same vascular endothelial cells (ECs) over hours, days, weeks, or months to understand the behaviors of these cells within their native tissue environment.

Selected Publications

Kam CY, Singh ID, Gonzalez DG, Matte-Martone C, Sola P, Solanas G, Bonjoch J, Marsh EM, Hirschi KK*, Greco V*. Mechanisms of skin vascular maturation and maintenance captured by longitudinal imaging of live mice. Cell. 2023 May 10; 186(11):2345-2360. *Co-corresponding authors.

Kam CY, Greco V. Lymph vessels find a hairy niche. EMBO Journal. 2019 Oct 1;38(19):e103219. (Commentary).

Kam CY, Dubash AD, Sheikh F, Lampe PD, Green KJ. Desmoplakin maintains gap junctions by inhibiting Ras/MAPK and lysosomal degradation of connexin-43. Journal of Cell Biology. 2018 Sep 3;217(9):3219-3235.

Jones JC, Kam CY, Harmon RM, Woychek AW, Hopkinson SB, Green KJ. Intermediate Filaments and the Plasma Membrane. Cold Spring Harbor Perspectives in Biology. 2016, doi: 10.1101/cshperspecta025866

Dubash AD*, Kam CY*, Aguado BA, Patel DM, Delmar M, Shea LD, Green KJ. Plakophilin-2 loss promotes TGF-β1/p38 MAPK-dependent fibrotic gene expression in cardiomyocytes. Journal of Cell Biology. 2016 Feb 15;212(4):425-38. *These authors contributed equally to this work.

Boyden LM, Kam CY, Hernández-Martín A, Zhou J, Craiglow BG, Sidbury R, Mathes EF, Maguiness SM, Crumrine DA, Williams ML, Hu R, Lifton RP, Elias PM, Green KJ, Choate KA. Dominant de novo DSP mutations cause erythrokeratodermia-cardiomyopathy syndrome. Human Molecular Genetics. 2016 Jan 15;25(2):348-57.