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Banson Kwamina Ewur Asare Daniel Kwasi Dery Fidelis Doodaa Boakye Kwadwo Boniface Akudugu Asamoah Moses Awotwe Lourees Esi 《Systemic Practice and Action Research》2020,33(2):237-264
Systemic Practice and Action Research - Fall armyworm (FAW) infestation in African countries presents significant threats to maize production. Such infestation has major economic implications in... 相似文献
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Voltage-gated ion channels are responsible for generating electrical impulses in nerves and other excitable cells. The fourth transmembrane helix (S4) in voltage-gated channels is the primary voltage-sensing unit that mediates the response to a changing membrane electric field. The molecular mechanism of voltage sensing, particularly with respect to the magnitude of the transmembrane movement of S4, remains controversial. To determine the extent of this transmembrane movement, we use fluorescent resonance energy transfer between the S4 domain and a reference point in the lipid bilayer. The lipophilic ion dipicrylamine distributes on either side of the lipid bilayer depending on the membrane potential, and is used here as a resonance-energy-transfer acceptor from donor molecules attached to several positions in the Shaker K+ channel. A voltage-driven transmembrane movement of the donor should produce a transient fluorescence change because the acceptor also translocates as a function of voltage. In Shaker K+ channels no such transient fluorescence is observed, indicating that the S4 segment does not translocate across the lipid bilayer. Based on these observations, we propose a molecular model of voltage gating that can account for the observed 13e gating charge with limited transmembrane S4 movement. 相似文献
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Kolachala V Asamoah V Wang L Obertone TS Ziegler TR Merlin D Sitaraman SV 《Cellular and molecular life sciences : CMLS》2005,62(22):2647-2657
Adenosine is an endogenous signaling molecule upregulated during inflammatory conditions. Acting through the A2b receptor
(A2bR), the predominant adenosine receptor in human colonic epithelia, adenosine has been directly implicated in immune and
inflammatory responses in the intestine. Little is known about expression and regulation of A2bR during inflammation. Tumor
necrosis factor alpha (TNF-α) is highly upregulated during chronic and acute inflammatory diseases. This study examined the
expression of A2bR during colitis and studied effects of TNF-α on A2bR expression, signaling and function. Results demonstrated
that A2bR expression increases during active colitis. TNF-α pretreatment of intestinal epithelial cells increased A2bR messenger
RNA and protein expression. TNF-α significantly increased adenosine-induced membrane recruitment of A2bR and cyclic adenosine
monophosphate downstream signaling. Further, TNF-α potentiated adenosine-induced shortcircuit current and fibronectin secretion.
In conclusion, we demonstrated that TNF-α is an important regulator of A2bR, and during inflammation, upregulation of TNF-α
may potentiate adenosine-mediated responses.
Received 21 July 2005; received after revision 22 August 2005; accepted 19 September 2005
†These authors contributed equally to this work. 相似文献
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Ballif BC Hornor SA Jenkins E Madan-Khetarpal S Surti U Jackson KE Asamoah A Brock PL Gowans GC Conway RL Graham JM Medne L Zackai EH Shaikh TH Geoghegan J Selzer RR Eis PS Bejjani BA Shaffer LG 《Nature genetics》2007,39(9):1071-1073
We have identified a recurrent de novo pericentromeric deletion in 16p11.2-p12.2 in four individuals with developmental disabilities by microarray-based comparative genomic hybridization analysis. The identification of common clinical features in these four individuals along with the characterization of complex segmental duplications flanking the deletion regions suggests that nonallelic homologous recombination mediated these rearrangements and that deletions in 16p11.2-p12.2 constitute a previously undescribed syndrome. 相似文献
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