Cardiac α1-adrenoceptor stimulation elicits a positive inotropic effect because of myofilament Ca2+ sensitization with a small increase in Ca2+ transients predominantly mediated by α1B-adrenoceptors via the intracellular alkalinization and potential myosin light chain 2 phosphorylation. However, the α1-adrenoceptor– mediated inotropy exhibits a wide range of species-dependent variation. In addi...

During apoptosis, Bak and Bax are activated by BH3-only proteins binding to the α2-α5 hydrophobic groove; Bax is also activated via a rear pocket. Here we report that antibodies can directly activate Bak and mitochondrial Bax by binding to the α1-α2 loop. A monoclonal antibody (clone 7D10) binds close to α1 in non-activated Bak to induce conformational change, oligomerization, and cytochrome c ...

and Applied Analysis 3 Corresponding to a function hp α1, . . . , αq; β1, . . . , βs; z defined by hp ( α1, . . . , αq; β1, . . . , βs; z ) z−pqFs ( α1, . . . , αq; β1, . . . , βs; z ) , 1.11 we now consider a linear operator Hp ( α1, . . . , αq; β1, . . . , βs ) : Σ ( p ) −→ Σp, 1.12 defined by means of the Hadamard product or convolution as follows: Hp ( α1, . . . , αq; β1, . . . , βs ) f z :...

Hereditary hyperekplexia, or startle disease, is a neuromotor disorder caused mainly by mutations that either prevent the surface expression of, or modify the function of, the human heteromeric α1 β glycine receptor (GlyR) chloride channel. There is as yet no explanation as to why hyperekplexia mutations that modify channel function are almost exclusively located in the α1 to the exclusion of β...

The current study examined the role of Na/K-ATPase α1-subunit in animals subjected to 5/6th partial nephrectomy (PNx) using Na/K-ATPase α1-heterozygous (α1(+/-)) mice and their wild-type (WT) littermates. After PNx, both WT and α1(+/-) animals displayed diastolic dimension increases, increased blood pressure, and increased cardiac hypertrophy. However, in the α1(+/-) animals we detected signifi...

α1-Adrenoceptors (ARs; 1A, 1B, and 1D) have been determined to perform different prominent functions in the physiological responses of the sympathetic nervous system. A high-throughput screening assay (HTS) was set up to detect α1-AR subtype-selective agonists by a dual-luciferase reporter assay in HEK293 cells. Using the HTS assay, two novel compounds, CHE3 and CHK3, were discovered as α1-ARs ...

The Z mutation (E342K) of α1-antitrypsin (α1-AT), carried by 4% of Northern Europeans, predisposes to early onset of emphysema due to decreased functional α1-AT in the lung and to liver cirrhosis due to accumulation of polymers in hepatocytes. However, it remains unclear why the Z mutation causes intracellular polymerization of nascent Z α1-AT and why 15% of the expressed Z α1-AT is secreted in...

After peripheral nerve injury, nociceptive afferents acquire an abnormal excitability to adrenergic agents, possibly due to an enhanced expression of α1-adrenoceptors (α1-ARs) on these nerve fibres. To investigate this in the present study, changes in α1-AR expression on nerve fibres in the skin and sciatic nerve trunk were assessed using immunohistochemistry in an animal model of neuropathic p...

Integrin proteins are very important adhesion receptors that mediate cell-cell and cell-extracellular matrix interactions. They play essential roles in cell signaling and the regulation of cellular shape, motility, and the cell cycle. Here, the transmembrane and cytoplasmic (TMC) domains of integrin α1 and β1 were over-expressed and purified in detergent micelles. The structure and backbone rel...

Let α1 be a formula from N5 logic, and let α2 be the formula that is obtained from α1 by replacing conjunction, disjunction and implication by respectively a t-norm ⊗, a t-conorm ⊕ and an implicator →. Noting that V − 2 (w, a) ∈ {0, 1} and V + 2 (w, a) ∈ {0, 1} for all a ∈ At and w ∈ {h, t}, it follows easily from the definitions (17)–(23) that V1(w,α1) = 1 iff V2(w,α2) = [1, 1], V1(w,α1) = 1 i...