Velia M. Fowler

MYH9-related disease mutations cause abnormal red blood cell morphology through increased myosin-actin binding at the membrane.

Age-related changes in eye lens biomechanics, morphology, refractive index and transparency.

Megakaryocyte migration defects due to nonmuscle myosin IIA mutations underlie thrombocytopenia in MYH9-related disease.

The Tudor-domain protein TDRD7, mutated in congenital cataract, controls the heat shock protein HSPB1 (HSP27) and lens fiber cell morphology.

Non-uniform distribution of myosin-mediated forces governs red blood cell membrane curvature through tension modulation.

Tropomyosin 3.1 Association With Actin Stress Fibers is Required for Lens Epithelial to Mesenchymal Transition.

Tropomodulins.

Nanoscale dynamics of actin filaments in the red blood cell membrane skeleton.

Erythroid differentiation in mouse erythroleukemia cells depends on Tmod3-mediated regulation of actin filament assembly into the erythroblast membrane skeleton.

Proteomic and functional analyses of the periodic membrane skeleton in neurons.

An interview with Velia M. Fowler, Department of Biological Sciences, University of Delaware, DE, USA.

Nonmuscle Myosin IIA Regulates the Precise Alignment of Hexagonal Eye Lens Epithelial Cells During Fiber Cell Formation and Differentiation.

Recessive TMOD1 mutation causes childhood cardiomyopathy.