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One of the contributing factors to cancer cell adaptation is a hypoxic environment [54].

Furthermore, selection driven by antibody evasion or host cell adaptation is rarely detected by population-based analysis [ 38, 48, 49].

The association of KV1.3 with vascular smooth muscle cell adaptation is intriguing because this channel is already linked to the proliferation of lymphocytes, oligodendrocytes, and cancer cells.

Therefore, regulation of cell signaling during cell adaptation is mainly at the level of signaling inputs at the extracellular space, and minor highly specific rearrangements within the intracellular network.

These data are of crucial importance since cell adaptation is a dynamic process; we need to use available technologies such as fused fluorescent proteins and biosensors dedicated to following RhoGTPase activities in order to decipher cell adaptation in conditions of microgravity.

To examine Ao38 cell adaptation and growth in serum-free medium, Ao38 cell adaptation was initially examined in several commercial serum-free media formulations.

Beta cell mass adaptation is an important mechanism to maintain normoglycaemia in obese insulin-resistant individuals, in whom beta cell mass is almost doubled compared with lean individuals [ 31].

In β-cells this adaptation is essential for survival under conditions of ER stress.

This is probably less true for the morphology of yeast cells, where adaptation is guided by the shape and performances of the colony as a whole, but not of individuals.

A key mediator of hypoxic cell survival and adaptation is the hypoxia-inducible factor-1 (HIF-1) pathway (Semenza, 2000).

The cell growth in the adaptation is shown in Additional file 1: Figure S1A.