gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Mex-3 homolog D

Mex-3, Tino
Top mentioned proteins: FATE, PAL, CAN, HAD, ACID
Papers on Mex-3
A new titinopathy: Childhood-juvenile onset Emery-Dreifuss-like phenotype without cardiomyopathy.
Richard et al., Helsinki, Finland. In Neurology, Jan 2016
The biopsies showed rimmed vacuoles, a dystrophic pattern, and secondary reduction in calpain 3. We identified a novel homozygous mutation in the exon Mex3 of the TTN gene in the first patient.
Transcriptome profiles of Penaeus (Marsupenaeus) japonicus animal and vegetal half-embryos: identification of sex determination, germ line, mesoderm, and other developmental genes.
Hertzler et al., Australia. In Mar Biotechnol (ny), Jun 2015
Some of the genes found included the sex determination genes sex-lethal and transformer; the germ line genes argonaute 1, boule, germ cell-less, gustavus, maelstrom, mex-3, par-1, pumilio, SmB, staufen, and tudor; the mesoderm genes brachyury, mef2, snail, and twist; the axis determination/segmentation genes β-catenin, deformed, distal-less, engrailed, giant, hairy, hunchback, kruppel, orthodenticle, patched, tailless, and wingless/wnt-8c; and a number of cell-cycle regulators.
The RNA binding protein MEX-3 retains asymmetric activity in the early Caenorhabditis elegans embryo in the absence of asymmetric protein localization.
Hunter et al., Colorado Springs, United States. In Gene, Feb 2015
The RNA binding protein MEX-3 is required to restrict translation of pal-1, the Caenorhabditis elegans caudal homolog, to the posterior of the early embryo.
Polarity-dependent asymmetric distribution and MEX-5/6-mediated translational activation of the Era-1 mRNA in C. elegans embryos.
Gönczy et al., Lausanne, Switzerland. In Plos One, 2014
With the exception of mex-3 mRNA, maternally contributed mRNAs are thought to be distributed uniformly in the one-cell embryo.
Germ-granule components prevent somatic development in the C. elegans germline.
Strome et al., Santa Cruz, United States. In Curr Biol, 2014
This is suggested by the loss of P granules from germ cells that transform into somatic cell types, e.g., in germlines lacking MEX-3 and GLD-1 or upon neuronal induction by CHE-1 [7, 8].
The RNA-binding protein Mex3b regulates the spatial organization of the Rap1 pathway.
Billaud et al., Grenoble, France. In Development, 2014
The four related mammalian MEX-3 RNA-binding proteins are evolutionarily conserved molecules for which the in vivo functions have not yet been fully characterized.
MEX-3 proteins: recent insights on novel post-transcriptional regulators.
Almeida et al., Porto, Portugal. In Trends Biochem Sci, 2013
RNA-binding proteins of the evolutionarily-conserved MEX-3 family are mediators of post-transcriptional regulation in different organisms.
Mex3c mutation reduces adiposity and increases energy expenditure.
Lu et al., Winston-Salem, United States. In Mol Cell Biol, 2012
The function of MEX3C, the mammalian homolog of Caenorhabditis elegans RNA-binding protein muscle excess 3 (MEX-3), was unknown until our recent report that MEX3C is necessary for normal postnatal growth and enhances the expression of local bone Igf1 expression.
Mex3c regulates insulin-like growth factor 1 (IGF1) expression and promotes postnatal growth.
Lu et al., Winston-Salem, United States. In Mol Biol Cell, 2012
Caenorhabditis elegans muscle excess 3 (MEX-3) is involved in cell fate specification during early embryonic development through regulating mRNAs involved in specifying cell fate.
Multiple RNA-binding proteins function combinatorially to control the soma-restricted expression pattern of the E3 ligase subunit ZIF-1.
Lin et al., Dallas, United States. In Dev Biol, 2012
POS-1, MEX-3, and SPN-4 function as repressors of ZIF-1 expression, whereas MEX-5 and MEX-6 antagonize this repression.
Salih Myopathy
Salih et al., Seattle, United States. In Unknown Journal, 2012
DIAGNOSIS/TESTING: Diagnosis is based on clinical findings, marginally to moderately increased serum creatine kinase levels, characteristic skeletal muscle histology, and biallelic small frameshift deletions in the exons Mex1 and Mex3 of TTN, the only gene in which mutations are known to cause Salih myopathy.
Microarray analyses of oral punch biopsies from acute myeloid leukemia (AML) patients treated with chemotherapy.
Brennan et al., Charlotte, United States. In Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2011
RESULTS: LIMMA and SAM identified genes potentially affected by the presence of AML, including homeodomain-interacting protein kinase 1 (HIPK1), mex-3 homolog D (MEX3D), and genes potentially affected by chemotherapy, including argininosuccinate synthase 1 (ASS1), notch homolog 1 (NOTCH1), zinc transporter ZIP6 (SLC39A6), and TP53-regulated inhibitor of apoptosis 1 (TRIAP1).
RNA recognition by the embryonic cell fate determinant and germline totipotency factor MEX-3.
Ryder et al., Worcester, United States. In Proc Natl Acad Sci U S A, 2010
The Caenorhabditis elegans RNA binding protein, MEX-3, plays a key role in both processes.
Translational regulators maintain totipotency in the Caenorhabditis elegans germline.
Priess et al., Seattle, United States. In Science, 2006
Here, we show that two conserved translational regulators, MEX-3 and GLD-1, are essential for maintaining totipotency in the Caenorhabditis elegans germline.
MEX-3 is a KH domain protein that regulates blastomere identity in early C. elegans embryos.
Priess et al., Seattle, United States. In Cell, 1996
We show here that maternal-effect lethal mutations in the gene mex-3 cause descendants of the anterior blastomere to produce muscles by a pattern of development similar to that of a descendant of the wild-type posterior blastomere.
share on facebooktweetadd +1mail to friends