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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Sodium channel, voltage-gated, type VIII, alpha

Omi, HtrA2, Seal, Scn8a, Nav1.6
This gene encodes a serine protease. The protein has been localized in the endoplasmic reticulum and interacts with an alternatively spliced form of mitogen-activated protein kinase 14. The protein has also been localized to the mitochondria with release to the cytosol following apoptotic stimulus. The protein is thought to induce apoptosis by binding the apoptosis inhibitory protein baculoviral IAP repeat-containing 4. Nuclear localization of this protein has also been observed. Alternate splicing of this gene results in two transcript variants encoding different isoforms. Additional transcript variants have been described, but their full-length sequences have not been determined. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PrP, CAN, Smac, XIAP, V1a
Papers using Omi antibodies
Modulation of mitochondrial function and morphology by interaction of Omi/HtrA2 with the mitochondrial fusion factor OPA1
Plun-Favreau Hélène et al., In Cell Death and Differentiation, 2009
... Generation and characterization of HtrA2 transgenic mice was supported by ...
Papers on Omi
Glucose Delays the Insulin-induced Increase in Thyroid Hormone-mediated Signaling in Adipose of Prolong-Fasted Elephant Seal Pups.
Ortiz et al., Berkeley, United States. In Am J Physiol Regul Integr Comp Physiol, Feb 2016
However, in elephant seal pups, prolonged fasting does not suppress TH levels, and is associated with up-regulation of adipose TH-mediated cellular mechanisms and adipose-specific insulin resistance.
Knockdown of Litopenaeus vannamei HtrA2, an up-regulated gene in response to WSSV infection, leading to delayed shrimp mortality.
Rattanarojpong et al., Bangkok, Thailand. In J Biotechnol, Jan 2016
UNASSIGNED: HtrA2 is an apoptosis-activating gene that enhances the apoptotic process by preventing the formation of the IAP-caspase complex, thereby freeing caspase to trigger the apoptosis pathway.
Intra- and intersubunit changes accompanying thermal activation of the HtrA2(Omi) protease homotrimer.
Lipinska et al., Gdańsk, Poland. In Biochim Biophys Acta, Jan 2016
UNASSIGNED: HtrA2(Omi) protease is involved in the maintenance of mitochondrial homeostasis and stimulation of apoptosis as well as in development of cancer and neurodegenerative disorders.
Upregulation of the sodium channel NaVβ4 subunit and its contributions to mechanical hypersensitivity and neuronal hyperexcitability in a rat model of radicular pain induced by local DRG inflammation.
Zhang et al., Indianapolis, United States. In Pain, Jan 2016
The sodium channel isoform NaV1.6 contributes to pain behaviors and spontaneous activity in this model.
An update on transcriptional and post-translational regulation of brain voltage-gated sodium channels.
Beltran-Alvarez et al., Kingston upon Hull, United Kingdom. In Amino Acids, Nov 2015
and SCN8A (NaV1.6), by transcription factors, by alternative splicing, and by post-translational modifications.
Selective blocking effects of 4,9-anhydrotetrodotoxin, purified from a crude mixture of tetrodotoxin analogues, on NaV1.6 channels and its chemical aspects.
Yotsu-Yamashita et al., Saga, Japan. In Mar Drugs, Feb 2015
Recently, it has been reported that 4,9-anhydroTTX selectively blocks the activity of NaV1.6 channels with a blocking efficacy 40-160 times higher than that for other TTX-sensitive NaV1.x channel isoforms.
Recurrent and Non-Recurrent Mutations of SCN8A in Epileptic Encephalopathy.
Meisler et al., Ann Arbor, United States. In Front Neurol, 2014
Mutations of the voltage-gated sodium channel SCN8A have been identified in approximately 1% of nearly 1,500 children with early-infantile epileptic encephalopathies (EIEE) who have been tested by DNA sequencing.
Cloning and Transcriptional Activity of the Mouse Omi/HtrA2 Gene Promoter.
Liu et al., Beijing, China. In Int J Mol Sci, 2014
HtrA serine peptidase 2 (HtrA2), also named Omi, is a pro-apoptotic protein that exhibits dramatic changes in expression levels in a variety of disorders, including ischemia/reperfusion injury, cancer, and neurodegeneration.
Oxidative stress-induced signaling pathways implicated in the pathogenesis of Parkinson's disease.
Papavassiliou et al., Athens, Greece. In Neuromolecular Med, 2014
The E3 ubiquitin ligase Parkin, the protease presenilin-associated rhomboid-like serine protease, the tyrosine kinase c-Abl, the protein kinase MARK2, the protease HtrA2, and the tumor necrosis factor receptor-associated protein 1 (TRAP1) provide different steps of control in protection against oxidative stress.
Targeted resequencing in epileptic encephalopathies identifies de novo mutations in CHD2 and SYNGAP1.
Mefford et al., Seattle, United States. In Nat Genet, 2013
We also expand the phenotypic spectra explained by SCN1A, SCN2A and SCN8A mutations.
Sodium channel SCN8A (Nav1.6): properties and de novo mutations in epileptic encephalopathy and intellectual disability.
Meisler et al., Ann Arbor, United States. In Front Genet, 2012
The sodium channel Nav1.6, encoded by the gene SCN8A, is one of the major voltage-gated channels in human brain.
Interaction of voltage-gated sodium channel Nav1.6 (SCN8A) with microtubule-associated protein Map1b.
Meisler et al., Ann Arbor, United States. In J Biol Chem, 2012
Mutation of the Map1b binding site of Na(v)1.6 prevented generation of sodium current in transfected cells. The data indicate that Map1b facilitates trafficking of Na(v)1.6 to the neuronal cell surface
Mutation analysis of LRRK2, SCNA, UCHL1, HtrA2 and GIGYF2 genes in Chinese patients with autosomal dorminant Parkinson's disease.
Tang et al., Changsha, China. In Neurosci Lett, 2012
Our result indicated that SCNA, LRRK2, UCHL1, HtrA2 and GIGYF2 genes' mutations might not be a main reason for Chinese Autosomal dorminant Parkinson's disease
De novo pathogenic SCN8A mutation identified by whole-genome sequencing of a family quartet affected by infantile epileptic encephalopathy and SUDEP.
Hammer et al., Tucson, United States. In Am J Hum Genet, 2012
Discovered a de novo heterozygous missense mutation (c.5302A>G [p.Asn1768Asp]) in the voltage-gated sodium-channel gene SCN8A in the proband.
Matrix metalloproteinase-3 is activated by HtrA2/Omi in dopaminergic cells: relevance to Parkinson's disease.
Hwang et al., Seoul, South Korea. In Neurochem Int, 2012
HtrA2/Omi, which normally exists in the mitochondria, can cause Matrix metalloproteinase-3 activation in the cytosol under a cell stress condition, which can ultimately lead to demise of dopaminergic neuronal cells
Reduced Retinal Function in the Absence of Na(v)1.6.
Côté et al., Halifax, Canada. In Plos One, 2011
Loss of Scn8a is associated with reduced Retinal Function.
Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons.
Ihle et al., Memphis, United States. In Nature, 2008
Hax1, is required to suppress apoptosis in lymphocytes and neurons; suppression requires the interaction of Hax1 with the mitochondrial proteases Parl and HtrA2
Allosteric activation of DegS, a stress sensor PDZ protease.
Sauer et al., Cambridge, United States. In Cell, 2007
Residues involved in the DegS allosteric switch are conserved in the DegP/HtrA and HtrA2/Omi families, suggesting that many PDZ proteases use a common mechanism of allosteric activation.
The mitochondrial protease HtrA2 is regulated by Parkinson's disease-associated kinase PINK1.
Downward et al., London, United Kingdom. In Nat Cell Biol, 2007
In mice, targeted deletion of the serine protease HtrA2 (also known as Omi) causes mitochondrial dysfunction leading to a neurodegenerative disorder with parkinsonian features.
Expanding insights of mitochondrial dysfunction in Parkinson's disease.
Wood et al., London, United Kingdom. In Nat Rev Neurosci, 2006
The alpha-synuclein-centric theory of protein aggregation with the adjunct of parkin-driven proteasome deregulation has, in recent years, been complemented by the discovery and increasing knowledge of the functions of DJ1, PINK1 and OMI/HTRA2, which are all associated with the mitochondria and have been implicated in cellular protection against oxidative damage.
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