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RNA binding motif protein 8A

Y14, RBM8A
This gene encodes a protein with a conserved RNA-binding motif. The protein is found predominantly in the nucleus, although it is also present in the cytoplasm. It is preferentially associated with mRNAs produced by splicing, including both nuclear mRNAs and newly exported cytoplasmic mRNAs. It is thought that the protein remains associated with spliced mRNAs as a tag to indicate where introns had been present, thus coupling pre- and post-mRNA splicing events. Previously, it was thought that two genes encode this protein, RBM8A and RBM8B; it is now thought that the RBM8B locus is a pseudogene. Two alternative start codons result in two forms of the protein, and this gene also uses multiple polyadenylation sites. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, Magoh, HAD, caspase-3, POLYMERASE
Papers using Y14 antibodies
In vivo BiFC analysis of Y14 and NXF1 mRNA export complexes: preferential localization within and around SC35 domains
Lichter Peter et al., In The Journal of Cell Biology, 1992
... Full-length NXF1 and Y14 sequences were PCR amplified and cloned into peYFP-C1 (CLONTECH Laboratories) using EcoRI–BamHI (New ...
Papers on Y14
Rbm8a haploinsufficiency disrupts embryonic cortical development resulting in microcephaly.
Silver et al., Durham, United States. In J Neurosci, Jun 2015
Here, we show that haploinsufficiency for Rbm8a, an exon junction complex (EJC) component within 1q21.1, causes severe microcephaly and defective neurogenesis in the mouse.
Variations in RBM8A and TBX6 are associated with disorders of the müllerian ducts.
Ledig et al., Münster, Germany. In Fertil Steril, May 2015
INTERVENTION(S): Sequential analysis of RBM8A and TBX6 in a group of 167 clinically well-defined patients with disorders of the müllerian ducts.
Phosphorylation status of human RNA-binding protein 8A in cells and its inhibitory regulation by Magoh.
Tomosugi et al., Kanazawa, Japan. In Exp Biol Med (maywood), Apr 2015
The RNA-binding protein 8A (RBM8A)-mago-nashi homolog, proliferation-associated (Magoh) complex is a component of the exon junction complex (EJC) required for mRNA metabolism involving nonsense-mediated mRNA decay (NMD).
Reconstruction of limb deformities in patients with thrombocytopenia-absent radius syndrome.
Ganger et al., Vienna, Austria. In Orthop Surg, Feb 2015
TAR syndrome is inherited in an autosomal recessive manner and results from compound heterozygosity of RBM8A mutations.
Psoriasis drug development and GWAS interpretation through in silico analysis of transcription factor binding sites.
Gudjonsson et al., Ann Arbor, United States. In Clin Transl Med, 2014
We identified a limited set of DEGs that encode proteins interacting with PRE motifs, including TFs (GATA3, EHF, FOXM1, SOX5) and uDBPs (AVEN, RBM8A, GPAM, WISP2).
Thrombocytopenia-absent radius (TAR) syndrome due to compound inheritance for a 1q21.1 microdeletion and a low-frequency noncoding RBM8A SNP: a new familial case.
Gimelli et al., Genova, Italy. In Mol Cytogenet, 2014
DISCUSSION: The complex inheritance pattern resulted in reduced expression of Y14, the protein encoded by RBM8A, and a component of the core exon-junction complex (EJC) in platelets.
Immunostaining and time-lapse analysis of vinblastine-induced paracrystal formation in human A549 cells.
Ishigaki et al., Kanazawa, Japan. In Oncol Lett, 2014
Additionally, immunostaining with the anti-RBM8A antibody overlapped with paracrystal images obtained from RFP conjugated tubulin.
Overexpression of MLN51 triggers P-body disassembly and formation of a new type of RNA granules.
Gillet et al., Rennes, France. In J Cell Sci, 2014
Unlike the three other EJC core components [eIF4AIII, Magoh and Y14 (also known as RBM8A)], MLN51 is mainly located in the cytoplasm, where it plays a key role in the assembly of stress granules.
A new approach for molecular diagnosis of TAR syndrome.
Poorhosseini et al., Tehrān, Iran. In Clin Biochem, 2014
In most patients chromosomes at 1q21.1 harbor a 200-kb deletion consisted of many genes, including RBM8A.
Update on the causes of platelet disorders and functional consequences.
van Geet et al., Leuven, Belgium. In Int J Lab Hematol, 2014
A major step forward was made during the last 3 years using new-generation genetic approaches that resulted in the discovery of novel genes such as NBEAL2, RBM8A, ACTN1, and GFI1B for the well-known IPD that cause gray platelet syndrome, thrombocytopenia-absent radius syndrome, and autosomal dominant thrombocytopenias, respectively.
The EJC binding and dissociating activity of PYM is regulated in Drosophila.
Ephrussi et al., Heidelberg, Germany. In Plos Genet, 2014
In mammalian cells, the ribosome associated protein PYM (HsPYM) binds the Y14-Mago heterodimer moiety of the EJC core, and disassembles EJCs, presumably during the pioneer round of translation.
Prenatal detection of TAR syndrome in a fetus with compound inheritance of an RBM8A SNP and a 334‑kb deletion: a case report.
Manolakos et al., Thessaloníki, Greece. In Mol Med Report, 2014
Thrombocytopenia‑absent radius syndrome (TAR) is a rare genetic disorder that is characterized by the absence of the radius bone in each forearm and a markedly reduced platelet count that results in life‑threatening bleeding episodes (thrombocytopenia).
New insights into the genetic basis of TAR (thrombocytopenia-absent radii) syndrome.
Ghevaert et al., Cambridge, United Kingdom. In Curr Opin Genet Dev, 2013
Recently it was shown that TAR syndrome is caused by the compound inheritance of a low-frequency noncoding SNP and a rare null allele in RBM8A, a gene encoding the exon-junction complex subunit member Y14 located in the deleted region.
Compound inheritance of a low-frequency regulatory SNP and a rare null mutation in exon-junction complex subunit RBM8A causes TAR syndrome.
Ghevaert et al., Cambridge, United Kingdom. In Nat Genet, 2012
findings show that the two regulatory SNPs result in diminished RBM8A transcription in vitro and that Y14 expression is reduced in platelets from individuals with thrombocytopenia with absent radii (TAR)
Functional interconnections of Arabidopsis exon junction complex proteins and genes at multiple steps of gene expression.
Curi et al., Santa Fe de la Vera Cruz, Argentina. In J Exp Bot, 2011
Overexpression of Mago and Y14 in plants produces an increase in PYM protein levels.
The exon junction complex component Y14 modulates the activity of the methylosome in biogenesis of spliceosomal small nuclear ribonucleoproteins.
Tarn et al., Taipei, Taiwan. In J Biol Chem, 2011
Y14 provides a regulatory link between pre-mRNA splicing and snRNP biogenesis.
Mago Nashi, Tsunagi/Y14, and Ranshi form a complex that influences oocyte differentiation in Drosophila melanogaster.
Boswell et al., Austin, United States. In Dev Biol, 2010
Tsunagi/Y14 forms compllex with Mago Nashi and Ranshi protein that influences oocyte differentiation in Drosophila melanogaster.
Thrombocytopenia Absent Radius Syndrome
Toriello, Seattle, United States. In Unknown Journal, 2010
This deletion involves multiple genes, including RBM8A.
The exon-junction complex proteins, Y14 and MAGOH regulate STAT3 activation.
Matsuda et al., Sapporo, Japan. In Biochem Biophys Res Commun, 2009
These results indicate that MAGOH regulates the transcriptional activation of STAT3 by interfering complex formation between STAT3 and Y14.
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