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Kelch-like 1

KLHL1, Kelch-like 1
The KLHL1 protein belongs to a family of actin-organizing proteins related to Drosophila Kelch (Nemes et al., 2000 [PubMed 10888605]).[supplied by OMIM, Feb 2010] (from NCBI)
Top mentioned proteins: Actin, V1a, caveolin-3, CAN, CACNA1A
Papers on KLHL1
Down-regulation of endogenous KLHL1 decreases voltage-gated calcium current density.
Piedras-Rentería et al., Maywood, United States. In Cell Calcium, 2014
The actin-binding protein Kelch-like 1 (KLHL1) can modulate voltage-gated calcium channels in vitro.
Genome-wide association study for poor sperm motility in Holstein-Friesian bulls.
Kaminski et al., Olsztyn, Poland. In Anim Reprod Sci, 2014
For five other candidate genes located close to significant markers (in distance of ca. 1 Mb), namely alkaline phosphatase, liver/bone/kidney (ALPL), tripartite motif containing 36 (TRIM36), 3-hydroxyisobutyrate dehygrogenase (HIBADH), kelch-like 1 (KLHL1), protein kinase C, beta (PRKCB), their potential role in sperm motility was confirmed in the earlier studies.
Calcium current homeostasis and synaptic deficits in hippocampal neurons from Kelch-like 1 knockout mice.
Piedras-Rentería et al., Maywood, United States. In Front Cell Neurosci, 2013
Kelch-like 1 (KLHL1) is a neuronal actin-binding protein that modulates voltage-gated CaV2.1 (P/Q-type) and CaV3.2 (α1H T-type) calcium channels; KLHL1 knockdown experiments (KD) cause down-regulation of both channel types and altered synaptic properties in cultured rat hippocampal neurons (Perissinotti et al., 2014).
Elimination of the actin-binding domain in kelch-like 1 protein induces T-type calcium channel modulation only in the presence of action potential waveforms.
Piedras-Rentería et al., Chicago, United States. In J Signal Transduct, 2011
The Kelch-like 1 protein (KLHL1) is a neuronal actin-binding protein that modulates calcium channel function.
Influence of MRP2 on MPA pharmacokinetics in renal transplant recipients-results of the Pharmacogenomic Substudy within the Symphony Study.
Spanish Pharmacogenetic Symphony Substudy Group et al., Spain. In Nephrol Dial Transplant, 2011
Renal transplant recipients T carriers of C24T MRP2 with macrolides treatment were associated with reduced mycophenolic acid area under curve in steady-state conditions
T-type current modulation by the actin-binding protein Kelch-like 1.
Piedras-Rentería et al., Maywood, United States. In Am J Physiol Cell Physiol, 2010
KLHL1 interacts with Cav3.2 and modulates T-type calcium currents by increasing current deactivation kinetics and current density and calcium influx.
Kelch-like 1 protein upregulates T-type currents by an actin-F dependent increase in α(1H) channels via the recycling endosome.
Piedras-Rentería et al., Maywood, United States. In Channels (austin), 2009
KLHL1 requires actin-polymerization to increase T-Type Calcium Channel alpha(1H) currents
Identification of Dlk1, Ptpru and Klhl1 as novel Nurr1 target genes in meso-diencephalic dopamine neurons.
Smidt et al., Utrecht, Netherlands. In Development, 2009
Dlk1 is required to prevent premature expression of Dat in meso-diencephalic dopamine neuronal precursors as part of the multifaceted process of neuronal differentiation driven by Nurr1 and Pitx3.
SCA8 mRNA expression suggests an antisense regulation of KLHL1 and correlates to SCA8 pathology.
Hsieh-Li et al., Taipei, Taiwan. In Brain Res, 2008
KLHL1 was expressed in human brain and kidney, but was also in other tissues, such as prostate gland, small intestine, colon, testis (but not the ovaries), liver and pancreas.
Process elongation of oligodendrocytes is promoted by the Kelch-related protein MRP2/KLHL1.
Avraham et al., Boston, United States. In J Biol Chem, 2007
MRP2/KLHL1 has a role, through its interaction with actin, in the process elongation of oligodendrocytes
The Kelch-like protein 1 modulates P/Q-type calcium current density.
Piedras-Rentería et al., Maywood, United States. In Neuroscience, 2007
modulatory effect of KLHL1 on the P/Q-type calcium channel function, suggesting a possible novel role for KLHL1 in cellular excitability.
KLHL1/MRP2 mediates neurite outgrowth in a glycogen synthase kinase 3beta-dependent manner.
Avraham et al., Boston, United States. In Mol Cell Biol, 2006
This study provides, for the first time, insights into the involvement of MRP2 in neurite outgrowth, which occurs in a GSK3beta-dependent manner.
Targeted deletion of a single Sca8 ataxia locus allele in mice causes abnormal gait, progressive loss of motor coordination, and Purkinje cell dendritic deficits.
Koob et al., Minneapolis, United States. In J Neurosci, 2006
SCA8 is dominantly inherited and is caused by large CTG repeat expansions in the untranslated antisense RNA of the Kelch-like 1 gene (KLHL1), but the molecular mechanism through which this expansion leads to disease is still unknown.
The KLHL1-antisense transcript ( KLHL1AS) is evolutionarily conserved.
Koob et al., Minneapolis, United States. In Mamm Genome, 2002
Spinocerebellar ataxia type 8 (SCA8) is caused by a CTG expansion in an untranslated, endogenous antisense RNA that overlaps the Kelch-like 1 ( KLHL1) gene.
The SCA8 transcript is an antisense RNA to a brain-specific transcript encoding a novel actin-binding protein (KLHL1).
Koob et al., Minneapolis, United States. In Hum Mol Genet, 2000
The sense transcript encodes a 748 amino acid protein with a predicted domain structure typical of a family of actin-organizing proteins related to the Drosophila Kelch gene, and so has been given the name Kelch-like 1 (KLHL1).
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