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


HBS1L, HBS1, Hbs1p
This gene encodes a member of the GTP-binding elongation factor family. It is expressed in multiple tissues with the highest expression in heart and skeletal muscle. The intergenic region of this gene and the MYB gene has been identified to be a quantitative trait locus (QTL) controlling fetal hemoglobin level, and this region influnces erythrocyte, platelet, and monocyte counts as well as erythrocyte volume and hemoglobin content. DNA polymorphisms at this region associate with fetal hemoglobin levels and pain crises in sickle cell disease. A single nucleotide polymorphism in exon 1 of this gene is significantly associated with severity in beta-thalassemia/Hemoglobin E. Multiple alternatively spliced transcript variants encoding different protein isoforms have been found for this gene. [provided by RefSeq, May 2009] (from NCBI)
Top mentioned proteins: BCL11A, CAN, Beta-globin, caspase-3, mitochondrial intermediate peptidase
Papers on HBS1L
The genetic basis of asymptomatic codon 8 frame-shift (HBB:c25_26delAA) β(0) -thalassaemia homozygotes.
Chui et al., Boston, United States. In Br J Haematol, Feb 2016
On the three major HbF quantitative trait loci (QTL), the twins were homozygous for G>A HBG2 Xmn1 site at single nucleotide polymorphism (SNP) rs7482144, homozygous for 3-bp deletion HBS1L-MYB intergenic polymorphism (HMIP) at rs66650371, and heterozygous for the A>C BCL11A intron 2 polymorphism at rs766432.
Genetic contribution to iron status: SNPs related to iron deficiency anaemia and fine mapping of CACNA2D3 calcium channel subunit.
López-Parra et al., Madrid, Spain. In Blood Cells Mol Dis, Dec 2015
The results replicate the association of SNPs with iron-related traits, and also confirm the protective effect of both A allele of rs1800562 (HFE) and G allele of rs4895441 (HBS1L-MYB).
A systematic review of known mechanisms of hydroxyurea-induced fetal hemoglobin for treatment of sickle cell disease.
Wonkam et al., Cape Town, South Africa. In Expert Rev Hematol, Oct 2015
RESULTS: Studies have provided consistent associations between genomic variations in HbF-promoting loci and variable HbF level in response to HU. Numerous signal transduction pathways have been implicated, through the identification of key genomic variants in BCL11A, HBS1L-MYB, SAR1 or XmnI polymorphism that predispose the response to the treatment, and signal transduction pathways that modulate γ-globin expression (cAMP/cGMP; Giα/c-Jun N-terminal kinase/Jun; methylation and miRNA).
The RNA surveillance complex Pelo-Hbs1 is required for transposon silencing in the Drosophila germline.
Xi et al., Beijing, China. In Embo Rep, Aug 2015
Here, we report that the evolutionarily conserved Pelo (Dom34)-Hbs1 mRNA surveillance complex is required for transposon silencing in the Drosophila germline.
Saccharomyces cerevisiae Ski7 Is a GTP-Binding Protein Adopting the Characteristic Conformation of Active Translational GTPases.
Conti et al., Martinsried, Germany. In Structure, Aug 2015
The C-terminal region of Ski7 (Ski7C) shares overall sequence similarity with the translational GTPase (trGTPase) Hbs1, but whether Ski7 has retained the properties of a trGTPase is unclear.
Sickle cell disease and H3Africa: enhancing genomic research on cardiovascular diseases in African patients.
Members of the H3Africa Consortium et al., Cape Town, South Africa. In Cardiovasc J Afr, Mar 2015
Studies in Tanzania and Cameroon have reported that singlenucleotide polymorphisms in BCL11A and HBS1L-MYB loci and co-inheritance of alpha-thalassaemia impact on foetal haemoglobin levels and clinical severity.
Genetic association of fetal-hemoglobin levels in individuals with sickle cell disease in Tanzania maps to conserved regulatory elements within the MYB core enhancer.
Menzel et al., Dar es Salaam, Tanzania. In Bmc Med Genet, 2014
Here, we present our detailed investigation of HBS1L-MYB intergenic polymorphism block 2 (HMIP-2), the central component of the complex quantitative-trait locus upstream of MYB, in 1,022 individuals with SCD in Tanzania.
Dom34 rescues ribosomes in 3' untranslated regions.
Green et al., Baltimore, United States. In Cell, 2014
The protein Dom34 and cofactors Hbs1 and Rli1 can dissociate stalled ribosomes in vitro, but the identity of targets in the cell is unknown.
The role of eosinophils and basophils in allergic diseases considering genetic findings.
Matran et al., Villejuif, France. In Curr Opin Allergy Clin Immunol, 2013
At the genome-wide level, studies identified genetic variants belonging to IL1RL1, TSLP and IL-33, and four loci with pleiotropic effects on eosinophil and basophil counts [GATA2 (3q21), MHC (6p21), HBS1L-MYB (6q23), and ERG (21q22)].
Three fingers on the switch: Krüppel-like factor 1 regulation of γ-globin to β-globin gene switching.
Perkins et al., Brisbane, Australia. In Curr Opin Hematol, 2013
Genome-wide association studies (GWAS) have demonstrated that three primary loci are associated with increased HbF levels in the population: the β-globin locus itself, the BCL11A locus, and a site between MYB and HBS1L.
Structural view on recycling of archaeal and eukaryotic ribosomes after canonical termination and ribosome rescue.
Beckmann et al., München, Germany. In Curr Opin Struct Biol, 2012
Both termination and ribosome rescue are mediated by class I release factors (eRF1/aRF1 in eukaryotic/archaeal termination) or their paralogs (Pelota/aPelota for ribosome rescue) and homologs of translational GTPases (eRF3/aEF1α in termination, Hbs1/aEF1α in ribosome rescue).
Dom34:hbs1 plays a general role in quality-control systems by dissociation of a stalled ribosome at the 3' end of aberrant mRNA.
Inada et al., Sendai, Japan. In Mol Cell, 2012
Dom34:Hbs1 facilitates the decay of nonstop mRNAs from the 3' end by exosomes and is required for the complete degradation of nonstop mRNA decay intermediates.
Structure of the no-go mRNA decay complex Dom34-Hbs1 bound to a stalled 80S ribosome.
Beckmann et al., München, Germany. In Nat Struct Mol Biol, 2011
The close structural similarity of Dom34 and Hbs1 to eukaryotic release factors (eRFs) enabled the authors to propose a model for the ribosome-bound eRF1-eRF3 complex.
A 3-bp deletion in the HBS1L-MYB intergenic region on chromosome 6q23 is associated with HbF expression.
Chui et al., Boston, United States. In Blood, 2011
A 3-bp deletion in the HBS1L-MYB intergenic region on chromosome 6q23 is associated with HbF expression.
Dissociation by Pelota, Hbs1 and ABCE1 of mammalian vacant 80S ribosomes and stalled elongation complexes.
Pisarev et al., United States. In Embo J, 2011
Pelota/Hbs1 induced dissociation of elongation complexes from ribosomes and release of peptidyl-tRNA, but only in the presence of ABCE1.
Fine-mapping at three loci known to affect fetal hemoglobin levels explains additional genetic variation.
Lettre et al., Montréal, Canada. In Nat Genet, 2010
We used resequencing and genotyping in African Americans with sickle cell anemia (SCA) to characterize associations with fetal hemoglobin (HbF) levels at the BCL11A, HBS1L-MYB and β-globin loci.
Dom34:Hbs1 promotes subunit dissociation and peptidyl-tRNA drop-off to initiate no-go decay.
Green et al., Baltimore, United States. In Science, 2010
findings show that Dom34:Hbs1 (two interacting factors genetically implicated in no-go decay) interacts with the ribosome to promote subunit dissociation and peptidyl-tRNA drop-off
Multiple loci influence erythrocyte phenotypes in the CHARGE Consortium.
Lin et al., Bethesda, United States. In Nat Genet, 2009
Our findings include loci previously associated with these traits (HBS1L-MYB, HFE, TMPRSS6, TFR2, SPTA1) as well as new associations (EPO, TFRC, SH2B3 and 15 other loci).
Endonucleolytic cleavage of eukaryotic mRNAs with stalls in translation elongation.
Parker et al., Tucson, United States. In Nature, 2006
The cleavage triggered by no-go decay is dependent on translation and involves Dom34p and Hbs1p.
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