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

Calcium homeostasis modulator 1

CALHM1, calcium homeostasis modulator 1
This gene encodes a calcium channel that plays a role in processing of amyloid-beta precursor protein. A polymorphism at this locus has been reported to be associated with susceptibility to late-onset Alzheimer's disease in some populations, but the pathogenicity of this polymorphism is unclear.[provided by RefSeq, Mar 2010] (from NCBI)
Top mentioned proteins: AGE, APP, Tec, CAN, HAD
Papers on CALHM1
miR-9 Mediates CALHM1-Activated ATP-P2X7R Signal in Painful Diabetic Neuropathy Rats.
Hu et al., Hengyang, China. In Mol Neurobiol, Feb 2016
UNASSIGNED: In this study, we planned to illuminate the mechanisms of the expression and function of CALHM1 in painful diabetic neuropathy (PDN).
Genetic association of CALHM1 rs2986017 polymorphism with risk of Alzheimer's disease: a meta-analysis.
Wang et al., Wuhan, China. In Neurol Sci, Jan 2016
UNASSIGNED: Recent studies investigating the association of Calcium homeostasis modulator 1 (CALHM1) p.P86L polymorphism (rs2986017) with Alzheimer's disease (AD) are controversial.
CALHM1 and its polymorphism P86L differentially control Ca(2+) homeostasis, mitogen-activated protein kinase signaling, and cell vulnerability upon exposure to amyloid β.
Cano-Abad et al., Madrid, Spain. In Aging Cell, Dec 2015
The mutated form of the Ca(2+) channel CALHM1 (Ca(2+) homeostasis modulator 1), P86L-CALHM1, has been correlated with early onset of Alzheimer's disease (AD).
Calcium homeostasis modulator (CALHM) ion channels.
Foskett et al., Philadelphia, United States. In Pflugers Arch, Dec 2015
UNASSIGNED: Calcium homeostasis modulator 1 (CALHM1), formerly known as FAM26C, was recently identified as a physiologically important plasma membrane ion channel.
Candidate genes for Alzheimer's disease are associated with individual differences in plasma levels of beta amyloid peptides in adults with Down syndrome.
Lee et al., New York City, United States. In Neurobiol Aging, Oct 2015
Broadly classified, variants in these genes may influence amyloid precursor protein processing (CALHM1, IDE), vesicular trafficking (SORCS1), and response to oxidative stress (SOD1).
Mice Lacking Pannexin 1 Release ATP and Respond Normally to All Taste Qualities.
Kinnamon et al., Aurora, United States. In Chem Senses, Sep 2015
Several ATP release channels are expressed in taste cells including CALHM1, Pannexin 1, Connexin 30, and Connexin 43, but whether all are involved in ATP release is not clear.
Benzothiazepine CGP37157 and its 2'-isopropyl analogue modulate Ca²⁺ entry through CALHM1.
Cano-Abad et al., Madrid, Spain. In Neuropharmacology, Aug 2015
CALHM1 is a Ca(2+) channel discovered in 2008, which plays a key role in the neuronal electrical activity, among other functions.
CALHM1 ion channel elicits amyloid-β clearance by insulin-degrading enzyme in cell lines and in vivo in the mouse brain.
Marambaud et al., New York City, United States. In J Cell Sci, Aug 2015
CALHM1, a cell-surface Ca(2+) channel expressed in brain neurons, has anti-amyloidogenic properties in cell cultures.
Mechanisms linking connexin mutations to human diseases.
Laird et al., London, Canada. In Cell Tissue Res, Jun 2015
Connexins share similar topology but no sequence homology with mammalian pannexins and CALHM1 (calcium homeostasis modulator 1), which are also large-pore transmembrane channels.
ATP signaling in brain: release, excitotoxicity and potential therapeutic targets.
Matute et al., Leioa, Spain. In Cell Mol Neurobiol, 2015
Finally, the participation of calcium homeostasis modulator 1 is also suggested, another non-selective ion channel that can release ATP, and that could play a role in ischemic events, together with P2X7 and Panx1 during excitotoxicity by ATP.
Hunting for connexin hemichannels.
Leybaert et al., Valparaíso, Chile. In Febs Lett, 2014
Defining functions of hemichannels and their involvement in any biological event requires ruling out possible participation of other channels that share biophysical and regulatory properties, for example pannexins, CALHM1 and P2X receptors.
How do taste cells lacking synapses mediate neurotransmission? CALHM1, a voltage-gated ATP channel.
Foskett et al., Kyoto, Japan. In Bioessays, 2013
CALHM1 was recently demonstrated to be a voltage-gated ATP-permeable ion channel and to serve as a bona fide conduit for ATP release from sweet-, umami-, and bitter-sensing type II taste cells.
CALHM1 ion channel mediates purinergic neurotransmission of sweet, bitter and umami tastes.
Foskett et al., Philadelphia, United States. In Nature, 2013
Here we show that calcium homeostasis modulator 1 (CALHM1), a voltage-gated ion channel, is indispensable for taste-stimuli-evoked ATP release from sweet-, bitter- and umami-sensing taste bud cells.
No association between CALHM1 polymorphism and Alzheimer's disease risk in a Hungarian population.
Janka et al., Szeged, Hungary. In Psychiatr Genet, 2011
An association between the CALHM1 polymorphism and the risk for Alzheimer's disease, was not detected.
CALHM1 P86L polymorphism modulates CSF Aβ levels in cognitively healthy individuals at risk for Alzheimer's disease.
Marambaud et al., New York City, United States. In Mol Med, 2011
Data show a significant association of CALHM1 P86L with elevated CSF Abeta42 and Abeta40 in the normal cohort at risk for Alzheimer's disease.
Calcium homoeostasis modulator 1 (CALHM1) reduces the calcium content of the endoplasmic reticulum (ER) and triggers ER stress.
García-Sancho et al., Valladolid, Spain. In Biochem J, 2011
CALHM1 increases Ca(2+) leak from the ER and, more importantly, reduces the endoplasmic reticulum Ca(2+) uptake by decreasing both the transport capacity and the Ca(2+) affinity of SERCA.
A polymorphism in CALHM1 is associated with temporal lobe epilepsy.
Liu et al., Beijing, China. In Epilepsy Behav, 2011
The results of this study provide the first evidence that the SNP rs11191692 in CALHM1 confers highly increased susceptibility to temporal lobe epilepsy.
The CALHM1 P86L polymorphism is a genetic modifier of age at onset in Alzheimer's disease: a meta-analysis study.
Amouyel et al., Lille, France. In J Alzheimers Dis, 2009
These results indicate that the CALHM1 Pro86Leu polymorphism may modulate age of onset of Alzheimer's disease by interacting with the effect of the epsilon4 allele of apolipoprotein E.
Linking calcium to Abeta and Alzheimer's disease.
LaFerla et al., Irvine, United States. In Neuron, 2008
[Review] Expression of CALHM1 is found in all brain regions and cells of neuronal lineage; it localizes predominantly to the endoplasmic reticulum but also exists at the plasma membrane, where it forms a novel calcium influx route to the cytosol.
A polymorphism in CALHM1 influences Ca2+ homeostasis, Abeta levels, and Alzheimer's disease risk.
Marambaud et al., North Bay Shore, United States. In Cell, 2008
Study determined that the CALHM1 P86L polymorphism is associated with Alzheimer's disease, further found that the P86L polymorphism increases amyloid-beta levels by interfering with CALHM1-mediated Ca(2+) permeability.
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