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pro vyhledávání: '"James O. Jackson"'
Thanks, but No Tanks Now that the Berlin Wall is open, the U.S. Army plays war a little differently.
Autor:
HEIDELBERG, JAMES O. JACKSON
Publikováno v:
TIME Magazine. 2/5/1990, Vol. 135 Issue 6, p21. 3p.
Publikováno v:
Applied Microbiology and Biotechnology. 93:2563-2570
Bacterial spores are the most resistant form of life and have been a major threat to public health and food safety. Nonthermal atmospheric gas discharge plasma is a novel sterilization method that leaves no chemical residue. In our study, a helium ra
Publikováno v:
Journal of Clinical Investigation. 120:369-378
Inherited mutations in voltage-gated sodium channels (VGSCs; or Nav) cause many disorders of excitability, including epilepsy, chronic pain, myotonia, and cardiac arrhythmias. Understanding the functional consequences of the disease-causing mutations
Alternative splicing of NaV1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T
Publikováno v:
Channels. 3:261-269
Alternative splicing is known to alter pharmacological sensitivities, kinetics, channel distribution under pathological conditions, and developmental regulation of VGSCs. Mutations that alter channel properties in Na(V)1.7 have been genetically impli
Autor:
James O. Jackson, Theodore R. Cummins, Sulayman D. Dib-Hajj, Patrick L. Sheets, Stephen G. Waxman
Publikováno v:
The Journal of Physiology. 581:1019-1031
Mutations in the TTX-sensitive voltage-gated sodium channel subtype Nav1.7 have been implicated in the painful inherited neuropathy, hereditary erythromelalgia. Hereditary erythromelalgia can be difficult to treat and, although sodium channels are ta
Autor:
Xixuan Karen Du, James Fossetta, Daniel Lundell, Loretta A. Bober, R. Kyle Palmer, James O. Jackson, Odette de Bouteiller, Xuedong Fan, Gregory Deno, Christophe Caux, Anne Soudé-Bermejo, Charles A. Lunn
Publikováno v:
Molecular Pharmacology. 63:342-350
Extensive characterization of adenosine receptors expressed by human monocyte-derived dendritic cells (MDDCs) was performed with quantitative polymerase chain reaction, radioligand binding, and calcium signaling. Transcript for the A3 adenosine recep
Publikováno v:
The Journal of biological chemistry. 286(31)
The voltage sensors of domains II and IV of sodium channels are important determinants of activation and inactivation, respectively. Animal toxins that alter electrophysiological excitability of muscles and neurons often modify sodium channel activat
Publikováno v:
Molecular pharmacology. 78(6)
The voltage-gated sodium channel Nav1.7 plays a crucial role in pain, and drugs that inhibit hNav1.7 may have tremendous therapeutic potential. ProTx-II and huwentoxin-IV (HWTX-IV), cystine knot peptides from tarantula venoms, preferentially block hN
Publikováno v:
Biophysical Journal. 96(3)
Voltage-gated sodium (Nav1.1-9) channels are dynamic transmembrane proteins that, in response to changes in the potential across the lipophilic cell membrane, undergo specific conformational (gating) modifications, between ion-conducting (open) and n
Publikováno v:
The Journal of physiology. 586(17)
Single-point missense mutations in the peripheral neuronal voltage-gated sodium channel Nav1.7 are implicated in the painful inherited neuropathy paroxysmal extreme pain disorder (PEPD). The Nav1.7 PEPD mutations are located in regions of the channel