mitoBK is functionally expressed in murine and human breast cancer cells and potentially contributes to metabolic reprogramming.

Alterations in the function of K channels such as the voltage- and Ca-activated K channel of large conductance (BK) reportedly promote breast cancer (BC) development and progression. Underlying molecular mechanisms remain, however, elusive. Here, we provide electrophysiological evidence for a BK splice variant localized to the inner mitochondrial membrane of murine and human BC cells (mitoBK).

IK channels control breast cancer metabolism including AMPK-driven autophagy.

Ca-activated K channels of intermediate conductance (IK) are frequently overexpressed in breast cancer (BC) cells, while IK channel depletion reduces BC cell proliferation and tumorigenesis. This raises the question, of whether and mechanistically how IK activity interferes with the metabolic activity and energy consumption rates, which are fundamental for rapidly growing cells. Using BC cells obtained from MMTV-PyMT tumor-bearing mice, we show that both, glycolysis and mitochondrial ATP-production are reduced in cells derived from IK-deficient breast tumors.

Modulating endothelial adhesion and migration impacts stem cell therapies efficacy.

Background: Limited knowledge of stem cell therapies` mechanisms of action hampers their sustainable implementation into the clinic. Specifically, the interactions of transplanted stem cells with the host vasculature and its implications for their therapeutic efficacy are not elucidated. We tested whether adhesion receptors and chemokine receptors on stem cells can be functionally modulated, and consequently if such modulation may substantially affect therapeutically relevant stem cell interactions with the host endothelium.

Subunits of BK channels promote breast cancer development and modulate responses to endocrine treatment in preclinical models.

Background And Purpose: Pore-forming α subunits of the voltage- and Ca -activated K channel with large conductance (BKα) promote malignant phenotypes of breast tumour cells. Auxiliary subunits such as the leucine-rich repeat containing 26 (LRRC26) protein, also termed BKγ1, may be required to permit activation of BK currents at a depolarized resting membrane potential that frequently occur in non-excitable tumour cells.

Experimental Approach: Anti-tumour effects of BKα loss were investigated in breast tumour-bearing MMTV-PyMT transgenic BKα knockout (KO) mice, primary MMTV-PyMT cell cultures, and in a syngeneic transplantation model of breast cancer derived from these cells.

K3.1 Channels Confer Radioresistance to Breast Cancer Cells.

K3.1 K channels reportedly contribute to the proliferation of breast tumor cells and may serve pro-tumor functions in the microenvironment. The putative interaction of K3.

Cancer-Associated Intermediate Conductance Ca-Activated K⁺ Channel K3.1.

Several tumor entities have been reported to overexpress K3.1 potassium channels due to epigenetic, transcriptional, or post-translational modifications. By modulating membrane potential, cell volume, or Ca signaling, K3.

Thumb amputations from team roping.

Background: Thumb injuries during team roping have elements of both avulsion and crush, resulting in a poor prognosis for replantation success.

Purpose: To review 19 cases of thumb amputation from team roping at our institution since 1983.

Study Design: Retrospective cohort study.