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Kcnh8  -  potassium channel, voltage gated eag...

Rattus norvegicus

Synonyms: ELK channel 3, ELK3, Elk1, Elk3, Ether-a-go-go-like potassium channel 3, ...
 
 
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High impact information on Kcnh8

  • We show here that cAMP can activate the transcription factor Elk-1 and induce neuronal differentiation of PC12 cells via its activation of the MAP kinase cascade [1].
  • Here we investigated the role of nuclear and cytosolic Ca(2+) signals in epidermal growth factor (EGF)-induced transactivation of the ternary complex factor Elk-1 using a GAL4-Elk-1 construct [2].
  • Elk-1 phosphorylation and nuclear localization following EGF stimulation were also unaffected by suppressing nuclear Ca(2+) signals [2].
  • Suppression of nuclear but not cytosolic Ca(2+) signals inhibited EGF-induced transactivation of Elk-1 [2].
  • Overexpression of sElk-1 but not Elk-1 increases neurite extension, an effect critically linked to its phosphorylation [3].
 

Biological context of Kcnh8

  • In the present study the role of mGluRs in the regulation of ERK1/2 pathways leading to CREB and Elk-1 phosphorylation by amphetamine was investigated using immunohistochemistry and Western blot in the rat dorsal striatum [4].
  • Elk-1 translated in dendrites was transported to the nucleus, and cell death depended upon transcription, supporting the dendritic imprinting hypothesis and highlighting the importance of the dendritic environment on protein function [5].
  • Here we use a focal transfection procedure, 'phototransfection', to introduce Elk1 mRNA into specific regions of live, intact primary rat neurons [5].
  • Instead, sElk, but not a mutant that cannot be phosphorylated, inhibits transactivation driven by Elk-1 [3].
  • This is blocked by mutating a normally cryptic nuclear export signal in Elk-1 [3].
 

Anatomical context of Kcnh8

  • Multiple nuclear transcription factors including E-26-like protein 1 (Elk-1) have been found in neuronal dendrites, yet the functional significance of such localization has not yet been explained [5].
  • To determine the relative contribution of nuclear and cytosolic Ca(2+) signals during EGF-mediated Elk-1 transactivation, Ca(2+) signals in either compartment were selectively impaired by targeted expression of the Ca(2+)-binding protein parvalbumin to either the nucleus or cytosol [2].
  • Interestingly, overexpression of Cav-WT in Cos-7 cells significantly enhanced insulin-stimulated phosphorylation of Elk-1 (a mitogen-activated protein kinase-dependent pathway) while overexpression of Cav-Mut was without effect [6].
  • We examined the activities of ERK, JNK/SAPK, and p38 MAPK along with their nuclear targets (Elk-1 and c-Jun) in rat visual cortex after light stimulation [7].
  • Its target c-Jun was selectively phosphorylated in CA1, CA3 and the dentate gyrus and c-Fos, the transcription of which is under the positive control of c-Jun N-terminal kinase target Elk1, was selectively up-regulated in CA1 and CA3 [8].
 

Associations of Kcnh8 with chemical compounds

  • Expression of the D125A mutant AT(1A) receptor in COS7 cells endowed the receptor with moderate constitutive activity, as indicated by its enhanced basal Elk1 promoter activity and inositol phosphate response to partial agonists [9].
  • Angiotensin II-induced stimulation of the Elk1 promoter showed parallel impairment with inositol phosphate signal generation in receptors containing mutations in this region of the AT(1A) receptor [9].
  • In contrast to serum, however, ouabain failed to activate the Elk-1, serum response factor, CREB and activator protein-1 transcription factors identified within the c-Fos promoter [10].
  • Induction of Elk-1 mRNA was significantly reduced dose-dependently up to 100 nM of estrogen [11].
  • Group I metabotropic glutamate receptors control phosphorylation of CREB, Elk-1 and ERK via a CaMKII-dependent pathway in rat striatum [12].
 

Regulatory relationships of Kcnh8

 

Other interactions of Kcnh8

 

Analytical, diagnostic and therapeutic context of Kcnh8

References

  1. cAMP activates MAP kinase and Elk-1 through a B-Raf- and Rap1-dependent pathway. Vossler, M.R., Yao, H., York, R.D., Pan, M.G., Rim, C.S., Stork, P.J. Cell (1997) [Pubmed]
  2. Epidermal growth factor-mediated activation of the ETS domain transcription factor Elk-1 requires nuclear calcium. Pusl, T., Wu, J.J., Zimmerman, T.L., Zhang, L., Ehrlich, B.E., Berchtold, M.W., Hoek, J.B., Karpen, S.J., Nathanson, M.H., Bennett, A.M. J. Biol. Chem. (2002) [Pubmed]
  3. Opposing roles of Elk-1 and its brain-specific isoform, short Elk-1, in nerve growth factor-induced PC12 differentiation. Vanhoutte, P., Nissen, J.L., Brugg, B., Gaspera, B.D., Besson, M.J., Hipskind, R.A., Caboche, J. J. Biol. Chem. (2001) [Pubmed]
  4. Amphetamine increases phosphorylation of extracellular signal-regulated kinase and transcription factors in the rat striatum via group I metabotropic glutamate receptors. Choe, E.S., Chung, K.T., Mao, L., Wang, J.Q. Neuropsychopharmacology (2002) [Pubmed]
  5. Region-directed phototransfection reveals the functional significance of a dendritically synthesized transcription factor. Barrett, L.E., Sul, J.Y., Takano, H., Van Bockstaele, E.J., Haydon, P.G., Eberwine, J.H. Nat. Methods (2006) [Pubmed]
  6. Caveolin-1 interacts with the insulin receptor and can differentially modulate insulin signaling in transfected Cos-7 cells and rat adipose cells. Nystrom, F.H., Chen, H., Cong, L.N., Li, Y., Quon, M.J. Mol. Endocrinol. (1999) [Pubmed]
  7. Rapid phosphorylation of Elk-1 transcription factor and activation of MAP kinase signal transduction pathways in response to visual stimulation. Kaminska, B., Kaczmarek, L., Zangenehpour, S., Chaudhuri, A. Mol. Cell. Neurosci. (1999) [Pubmed]
  8. N-methyl-d-aspartate-triggered neuronal death in organotypic hippocampal cultures is endocytic, autophagic and mediated by the c-Jun N-terminal kinase pathway. Borsello, T., Croquelois, K., Hornung, J.P., Clarke, P.G. Eur. J. Neurosci. (2003) [Pubmed]
  9. The role of a conserved region of the second intracellular loop in AT1 angiotensin receptor activation and signaling. Gáborik, Z., Jagadeesh, G., Zhang, M., Spät, A., Catt, K.J., Hunyady, L. Endocrinology (2003) [Pubmed]
  10. c-Fos expression in ouabain-treated vascular smooth muscle cells from rat aorta: evidence for an intracellular-sodium-mediated, calcium-independent mechanism. Taurin, S., Dulin, N.O., Pchejetski, D., Grygorczyk, R., Tremblay, J., Hamet, P., Orlov, S.N. J. Physiol. (Lond.) (2002) [Pubmed]
  11. Inhibition of MEK1,2/ERK mitogenic pathway by estrogen with antiproliferative properties in rat aortic smooth muscle cells. Hwang, K.C., Lee, K.H., Jang, Y. J. Steroid Biochem. Mol. Biol. (2002) [Pubmed]
  12. Group I metabotropic glutamate receptors control phosphorylation of CREB, Elk-1 and ERK via a CaMKII-dependent pathway in rat striatum. Choe, E.S., Wang, J.Q. Neurosci. Lett. (2001) [Pubmed]
  13. Effects of calcium modulation on percutaneous absorption of a model drug. Singla, R., Choe, E.S., Lee, C.H. Pharm. Res. (2002) [Pubmed]
 
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