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Potassium large conductance calcium-activated channel, subfamily M, beta member 4

hbeta4, KCNMB4, hKCNMB4, BKbeta4
MaxiK channels are large conductance, voltage and calcium-sensitive potassium channels which are fundamental to the control of smooth muscle tone and neuronal excitability. MaxiK channels can be formed by 2 subunits: the pore-forming alpha subunit and the modulatory beta subunit. The protein encoded by this gene is an auxiliary beta subunit which slows activation kinetics, leads to steeper calcium sensitivity, and shifts the voltage range of current activation to more negative potentials than does the beta 1 subunit. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: beta-4, KCNMB3, HAD, KCNMB1, OUT
Papers on hbeta4
MEIS3 is repressed in A549 lung epithelial cells by deoxynivalenol and the repression contributes to the deleterious effect.
Kamei et al., Obihiro, Japan. In J Toxicol Sci, Dec 2015
The repression of B3GALT4, MEIS3, AK7, SEMA3A, KCNMB4, and SCARA5 was confirmed by quantitative PCR.
Microarray data analysis of neuroblastoma: Expression of SOX2 downregulates the expression of MYCN.
Zhang et al., Zhengzhou, China. In Mol Med Report, Nov 2015
Functional enrichment analysis indicated that KCNMB4 was involved in the regulation of action potential in neuron term, and the FOS, GLI3 and GLI1 genes were involved in the extracellular matrix‑receptor interaction pathway.
Investigation of osteosarcoma genomics and its impact on targeted therapy: an international collaboration to conquer human osteosarcoma.
Yang, Tianjin, China. In Ai Zheng, 2014
Systematic analysis of genetic/genomic alterations and further functional studies have led to several important findings, including novel rearrangement hotspots, osteosarcoma-specific LRP1-SNRNP25 and KCNMB4-CCND3 fusion genes, VEGF and Wnt signaling pathway alterations, deletion of the WWOX gene, and amplification of the APEX1 and RUNX2 genes.
Predicting the diagnosis of autism spectrum disorder using gene pathway analysis.
Pantelis et al., Melbourne, Australia. In Mol Psychiatry, 2014
Eight SNPs in three genes (KCNMB4, GNAO1, GRM5) had the largest effect in the classifier with some acting as vulnerability SNPs, whereas others were protective.
IFN-γ-mediated reduction of large-conductance, Ca2+-activated, voltage-dependent K+ (BK) channel activity in airway epithelial cells leads to mucociliary dysfunction.
Salathe et al., Miami, United States. In Am J Physiol Lung Cell Mol Physiol, 2014
IFN-γ changed mRNA levels of the BK β-modulatory proteins KCNMB2 (increased) and KCNMB4 (decreased) as well as leucine-rich repeat-containing protein (LRRC)26 (decreased).
Recurrent LRP1-SNRNP25 and KCNMB4-CCND3 fusion genes promote tumor cell motility in human osteosarcoma.
Zhang et al., Tianjin, China. In J Hematol Oncol, 2013
Two recurrent fusion genes associated with the 12q locus, LRP1-SNRNP25 and KCNMB4-CCND3, were identified and validated by RT-PCR, Sanger sequencing and fluorescence in situ hybridization, and were found to be osteosarcoma specific in a validation cohort of 240 other sarcomas.
Failure to confirm association of a polymorphism in KCNMB4 gene with mesial temporal lobe epilepsy.
Gambardella et al., Cosenza, Italy. In Epilepsy Res, 2013
A recent study has implicated a tagging single nucleotide polymorphism (SNP) rs398702 located 3' of KCNMB4 (encoding calcium-activated potassium channel, subfamily M subunit beta 4) as a possible susceptibility allele for mesial temporal lobe epilepsy (mTLE).
Modulation by the BK accessory β4 subunit of phosphorylation-dependent changes in excitability of dentate gyrus granule neurons.
Brenner et al., San Antonio, United States. In Eur J Neurosci, 2011
These results suggest that fast-gating, type I BK channels lacking beta4 can increase neuronal excitability in response to reduced phosphatase activity and activation of calcium channels.
Expression of the voltage- and Ca2+-dependent BK potassium channel subunits BKβ1 and BKβ4 in rodent astrocytes.
Prüss et al., Berlin, Germany. In Glia, 2011
BKbeta4 expression in astrocytes likely participates in regulating astrocytic voltage gradients and maintaining poassium homeostasis, hence enabling astrocytes to fulfill their complex regulatory influence on proper brain function.
Intercalated cell BK-alpha/beta4 channels modulate sodium and potassium handling during potassium adaptation.
Sansom et al., Omaha, United States. In J Am Soc Nephrol, 2010
We studied whether BK-beta4-deficient mice (Kcnmb4(-/-)) have altered renal sodium and potassium clearances compared with wild-type mice when fed a regular or potassium-rich diet for ten days.
A large-conductance (BK) potassium channel subtype affects both growth and mineralization of human osteoblasts.
Evans et al., Cardiff, United Kingdom. In Am J Physiol Cell Physiol, 2009
RT-PCR showed the presence of KCNMA1, KCNMB1, KCNMB2, KCNMB3, and KCNMB4 subunits.
Identification of large conductance calcium activated potassium channel accessory beta4 subunit in rat and mouse bladder smooth muscle.
Petkov et al., Columbia, United States. In J Urol, 2009
Our data indicate that, in addition to BKalpha and BKbeta1, neuronal specific BKbeta4 is expressed in mouse and rat bladder smooth muscle cells.
Compartmentalized beta subunit distribution determines characteristics and ethanol sensitivity of somatic, dendritic, and terminal large-conductance calcium-activated potassium channels in the rat central nervous system.
Treistman et al., Worcester, United States. In J Pharmacol Exp Ther, 2009
There is a selective distribution of auxiliary beta1 subunits to the somatic and dendritic compartments and beta4 subunits to the terminal compartment of neurons in the hypothalamic-neurohypophysial system.
{beta} subunit-specific modulations of BK channel function by a mutation associated with epilepsy and dyskinesia.
Cui et al., Saint Louis, United States. In J Physiol, 2009
Report beta subunit (KNMB1-4)-specific modulations of BK channel function by a Slo1 mutation associated with epilepsy and dyskinesia.
Interactions between beta subunits of the KCNMB family and Slo3: beta4 selectively modulates Slo3 expression and function.
Lingle et al., Saint Louis, United States. In Plos One, 2008
results argue that, for native mouse Slo3 channels, the beta4 subunit must be considered as a potential interaction partner and, furthermore, that KCNMB subunits may have functions unrelated to regulation of the Slo1 alpha subunit
The molecular mechanism of "ryegrass staggers," a neurological disorder of K+ channels.
Dalziel et al., Palmerston North, New Zealand. In J Pharmacol Exp Ther, 2008
Unexpectedly, when the response to lolitrem B was examined in mice lacking the beta4 BK channel accessory subunit (Kcnmb4(-/-)), only low-level ataxia was observed.
Structural basis for toxin resistance of beta4-associated calcium-activated potassium (BK) channels.
Ding et al., Wuhan, China. In J Biol Chem, 2008
Structural basis for toxin resistance of beta4-associated calcium-activated potassium (BK) channels
Differential distribution of Ca2+-activated potassium channel beta4 subunit in rat brain: immunolocalization in neuronal mitochondria.
Wilczynski et al., Warsaw, Poland. In Neuroscience, 2008
beta4 subunit is a regulatory component of mitochondrial conductance Ca(2+)-activated potassium channels channels in neurons
Multicentre search for genetic susceptibility loci in sporadic epilepsy syndrome and seizure types: a case-control study.
Goldstein et al., Dublin, Ireland. In Lancet Neurol, 2007
Variations in the genes KCNAB1, GABRR2, KCNMB4, SYN2, and ALDH5A1 were most notable.
Properties of BK(Ca) channels formed by bicistronic expression of hSloalpha and beta1-4 subunits in HEK293 cells.
Davies et al., Leicester, United Kingdom. In J Membr Biol, 2003
Cloning and functional expression of novel large-conductance calcium-activated potassium channel beta subunits, hKCNMB3 and hKCNMB4.
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