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Gene model reviewed during 5.42
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.45
10, 5.5, 4.5, 2.4 (northern blot)
None of the polypeptides share 100% sequence identity.
1174 (aa)
The voltage-dependent potassium channel is a heterotetramer of potassium channel proteins (By similarity). Interaction with CASK.
When in complex with CASK, the efficiency of Thr-787 phosphorylation is increased.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\eag using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signals
View Dmel\eag in GBrowse 21-49
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Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: eag CG10952
Mutants are hypersensitive to paraquat.
eag channels are voltage-dependent, outwardly rectifying and highly selective for K+ over Na+ ions. In contrast to results published in FBrf0064383, the eag channel electrophysiological properties in Xenopus oocytes reveal (i) no evidence for Ca2+ permeation, (ii) a transient component of outward current reflecting channel inactivation, and (iii) non-superimposable Cole-Moore shift similar in magnitude to that reported for rat-EAG. eag currents run down more rapidly than do mouse-EAG currents in excised macropatches. Rundown is reversible by inserting the patch into the interior the oocyte, indicating that a cytosolic factor regulates channel activity or stability.
There are parallels in the physiological and behavioural phenotypes caused by eag mutations and Rat\CamKII-I. Interactions of eag and Rat\CamKII-I have been investigated at the behavioural, physiological, genetical and biochemical level.
Ion channel mutants alter synaptic activity at the embryonic neuromuscular junction (NMJ). GluRIIA expression in the postsynaptic membrane is reduced by changes in presynaptic electrical activity. The size of the synaptic domain depends on the level of neural activity during embryonic synaptogenesis.
NOTE: Aspects of these conclusions subsequently challenged, see FBrf0090763.
eag expression in Xenopus oocytes generates channels that have properties of both voltage- and ligand-gated channels. The ability to mediate potassium outward and calcium inward currents is dependent on voltage and cAMP, these properties are likely to be important in the modulation of synaptic efficiency in both the central and peripheral nervous system.
In eag,Sh hyperexcitable double mutants nerve/muscle synaptic ultrastructure is dramatically altered. Two types of synaptic vesicle are depleted and a third is altered in appearance, and there are changes in number and appearance of synaptic densities, and multivesicular bodies.
The eag locus provides a subunit common to different K+ channels. The role of the eag subunit for modulating channels, as opposed to that of Sh subunits required for gating, selectivity and conductance of the channel, suggests a combinatorial genetic framework for generating diversified K+ channels.
Effects of potassium channel blocking drugs on the presynaptic action potential repolarization after electrotonic stimulation was studied. At least four K+ currents contribute to repolarization of the nerve terminal.
The product of the eag locus is involved in the function of one or more type of voltage-gated potassium channel.
The eag polypeptide is more closely related to polypeptides of cyclic nucleotide gated cation channels than to those of voltage gated K+ channels.
eag encodes a subunit common to different K+ channels, this supports the idea that combinatorial assembly of different polypeptides contributes to the diversity of K+ channels.
Sequence and voltage clamp analysis demonstrate that the eag locus encodes a subunit common to different K+ channels. Combinatorial assembly of polypeptides from different genes may contribute to potassium channel diversity.
eag mutations interact synergistically with Shaker mutations, i.e., double mutants are severely abnormal both behaviorally and physiologically (Ganetzky and Wu, 1983).