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However, establishing the cellular, molecular, or genetic pathways leading to disease requires microscopic, metabolic and/or functional information.
We show R2D2 functions in the ovary, specifically in the somatic tissues giving rise to the stalk and other follicle cells critical for establishing the cellular architecture of the oocyte.
Dissecting the relative contributions of direct and indirect endothelial cell activation to this response, establishing the cellular source of TNFα, and determining possible involvement of other cytokine(s) will require further investigation.
Whether DNA methylation is fundamental in establishing the cellular programs defining the main characteristics of these cells should be the focus of future studies.
The results reported here are in agreement with a model in which DNA methylation plays a pivotal role in establishing the cellular program of liver cancer cell subpopulations.
To clarify the role of specific Notch receptors in establishing the cellular identities in the lung epithelium, we generated an allelic series for Notch1, Notch2 and Notch3 to eliminate Notch signaling from the lung epithelium while retaining Rbpj-mediated repression.
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To establish the cellular mechanism for the architectural changes, vertebrae were analyzed by histomorphometry 1, 3, and 14 days following irradiation.
Here, we extended our investigation to establish the cellular compatibility of gelatin-grafted PDLLA with respect to mechanical properties of biological tissues.
Having established the cellular expression pattern of Sez-6 in the rat retina, we carried out morphological, immunohistochemical and electrophysiological analyses of Sez-6 knockout mouse retina.
To establish the cellular source of the cytokines released in the co-cultures of M and MSC, the production of TNF-α and IL-10 was also analyzed by intracellular staining and flow cytometry.
Having established the cellular model, we then investigated the regulation of procentriole stability by testing the sensitivity of centriole biogenesis in RPE-1 cells to nocodazole after the depletion of potential factors.
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