Publications by authors named "Anke Fabian"

Unraveling the mechanisms involved in chemotactic navigation of immune cells is of particular interest for the development of new immunoregulatory therapies. It is generally agreed upon that members of the classical transient receptor potential channel family (TRPC) are involved in chemotaxis. However, the regulatory role of TRPC channels in chemoattractant receptor-mediated signaling has not yet been clarified in detail.

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Cell motility is central to tissue homeostasis in health and disease, and there is hardly any cell in the body that is not motile at a given point in its life cycle. Important physiological processes intimately related to the ability of the respective cells to migrate include embryogenesis, immune defense, angiogenesis, and wound healing. On the other side, migration is associated with life-threatening pathologies such as tumor metastases and atherosclerosis.

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Cell migration is crucial for many important physiological and pathophysiological processes ranging from embryogenesis to tumor metastasis. It requires the coordination of mechanical forces generated in different regions of the migrating cell. It has been proposed that stretch-activated, Ca(2+)-permeable channels are involved in mechanosignaling during cell migration.

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Potassium channels play a key role in establishing the cell membrane potential and are expressed ubiquitously. Today, more than 70 mammalian K(+) channel genes are known. The diversity of K(+) channels is further increased by the fact that different K(+) channel family members may assemble to form heterotetramers.

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Movement toward the source of a chemoattractant gradient is a basic cellular property in health and disease. Enhanced migration during metastasis involves deregulated growth factor signaling. Growth factor stimulation and cell migration converge both on the important second messenger Ca(2+).

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Cell motility is a prerequisite for the creation of new life, and it is required for maintaining the integrity of an organism. Under pathological conditions, "too much" motility may cause premature death. Studies over the past few years have revealed that ion channels are essential for cell motility.

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Tumor cell migration is crucial for the formation of tumor metastases and the progression of tumor disease. Fibroblast growth factor-2 (FGF-2) is one of the cytokines involved in the autocrine stimulation of tumor development. FGF-2 also stimulates transcription of Ca(2+)-sensitive K(+) channels (IK1 or K(Ca)3.

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Migration and morphology of human melanoma cells (MV3) depend on extracellular pH (pHe) and the activity of the Na+/H+ exchanger NHE1. To distinguish effects of NHE1 activity per se from effects of pHe we compared an NHE1-deficient mutant with rescued and wild-type cells. Time lapse video microscopy was used to investigate migratory and morphological effects caused by pHe and NHE1 activity, and a membrane-bound fluorescein conjugate was employed for ratiometric pH measurements at the outer leaflet of the cell membrane.

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Cell migration is a process that plays an important role throughout the entire life span. It starts early on during embryogenesis and contributes to shaping our body. Migrating cells are involved in maintaining the integrity of our body, for instance, by defending it against invading pathogens.

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