How Phosphorylation and ATPase Activity Regulate Anion Flux though the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)

Dissolved Oxygen-Sensing Chip Integrating an Open Container Connected with a Position-Raised Channel for Estimation of Cellular Mitochondrial Activity

“…Therefore, the respiratory activity can be defined as ( I ss‑DMEM – I ss‑cell‑test )/( I ss‑DMEM – I ss‑cell‑DMEM ), where I ss‑DMEM , I ss‑cell‑DMEM , and I ss‑cell‑test are the I ss obtained in blank DMEM, cell-culturing DMEM, and cell-culturing HBS containing different testing drugs, respectively. The calculation of respiratory activity is modified from Bionas analyzing systems. − …”

“…However, when culturing adherent cells in a small closed microchannel to form a cell-based sensing platform, it is worth noting whether the fluidic shear force detaches the adhered cells. In addition to adequate fluidic manipulation, enough cultivation time and surface modification of substrate can facilitate cells to resist the fluidic shear force. − For example, the commercial Cytosensor Microphysiometer (Molecular Devices Corp.) and Bionas analyzing systems (Bionas GmbH), − using closed microchannels, suggest users culture cells overnight or for 1 day before performing fluidic flow. In addition, a channel-closed chip needs more fluid-controlled equipment, such as switch valves and pumps, and precise manipulation for drug injection and medium replacement during cell testing and culturing.…”

NM23 proteins: innocent bystanders or local energy boosters for CFTR?

“…10,35 How such a system operates in an intact cell is not agreed with some recent data even suggesting that NBDs may be permissive for CFTR phosphorylation. 7 We will return to the N-terminus and the C terminus later when we (respectively) consider t-SNARES of the syntaxin family and protein kinases such as CK2 and AMPK along with linkers from the DTRL motif at the end of CFTR to the cytoskeleton such as ezrin. Interestingly, the origins of the capture and insertion of the R domain in CFTR are unknown as no significant sequence homology with other proteins has been found to date.…”

“…CFTR is driven by one ATP-binding site acting as a non-hydrolyzing 'degenerate' ATP holding 'bridgelike' domain with the other site permitting free hydrolysis that enables domain shifts to facilitate pore access. The relationship between ATP binding and channel gating is a very complex process as reviewed recently by Zwick et al 7 However, these models take no account of the binding of CFTR-associated proteins that drive a cAMP or calciumdependent CFTR activation 12,18 or to the possibility that CFTR might also become a (protease) split molecule that could recombine its N-and C-terminal fragments 28 in the membrane to create an array of different CFTR halves that add to the diversity of CFTR molecules in the membrane. It is accepted that hydrolysis of clamped ATP drives conformational changes in the translocator 'blades' structure, fueling the transport of biological substrates across the cellular membranes.…”

“…This minireview provides a summary of the current knowledge of the functions of two isoforms from group I in airway epithelia, highlighting the role NDPKs might play in provision of energy for processes related to the protein whose mutation causes cystic fibrosis (CF). 7 In the airway, ciliary clearance of inhaled contaminantsdependent upon transport of chloride and other anions into the lumen of the airways, accompanied by water and mucus movement. In CF, a disease mostly caused by just one triplet nucleotide deletion in the CF gene (the cystic fibrosis transmembrane conductance regulator, CFTR), lack of normal fluid, and mucus transport results in an abnormal airway surface liquid layer that accumulates thick mucus with frequent lung infections from a host of unusual microorganisms.…”